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Debra K Moser - One of the best experts on this subject based on the ideXlab platform.
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Factors Related to Nonadherence of a Low Sodium Diet in Heart Failure Patients
2020Co-Authors: Brooke Bentley, Debra K Moser, Marla J. De Jong, Ann R. PedenAbstract:Abstract : A Low Sodium Diet is a cornerstone of nonpharmacologic therapy for heart failure patients. Although nonadherence is common, little is known about why heart failure patients fail to adhere to this Diet. The purpose of this study was to explore the experience of heart failure patients in folLowing a Low Sodium Diet. We conducted a qualitative descriptive study with a convenience sample of 20 participants. Interviews were conducted and analyzed for themes. The data reflected three primary themes about nonadherence to the Low Sodium Diet: lack of knowledge, interference with socialization, and lack of food selections. Participants expressed a need for details about Dietary information, Low Sodium food selection, food preparation, and rationale for the Diet. Lack of knowledge also was manifested as Diet confusion for participants who required additional Dietary restrictions related to other disease processes. Interference with socialization was manifested by patients' experiences with family conflict when family members chose and ate high-Sodium foods at home or family gatherings, and difficulty eating out. The theme of lack of Low Sodium food selections was reflected by comments about limited food choices, and lack of palatability. Researchers and clinicians need to consider patients' perceptions as they generate and evaluate interventions to increase adherence to a Low Sodium Diet.
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Relationship of Heart Failure Patients' Knowledge, Perceived Barriers, and Attitudes Regarding Low‐Sodium Diet Recommendations to Adherence
Progress in Cardiovascular Nursing, 2020Co-Authors: Terry A Lennie, Muna Hammash, Lynn P Roser, Carol S Smith, Robin J Trupp, Misook L Chung, Linda Worrall-carter, Jan Odom-forren, Debra K MoserAbstract:The purposes of this study were to describe heart failure patient perceptions regarding instructions received for folLowing a Low-Sodium Diet and the benefits, barriers, and ease and frequency of folLowing the Diet. A total of 246 patients with heart failure referred from academic medical centers in the United States and Australia participated in the study. A subset of 145 patients provided 24-hour urine samples for Sodium excretion assessment. While most (80%) patients reported receiving recommendations to folLow a Low-Sodium Diet, their recall of specific instructions was poor. Although the majority (75%) reported folLowing a Low-Sodium Diet most or all of the time, 24-hour urine Sodium excretion indicated that only 25% of patients were adherent. Patients who reported being more adherent, however, had Lower urine Sodium excretion levels. Attitudes regarding difficulty in and perceived benefits of folLowing the Diet were not related to Sodium excretion. Data on attitudes and barriers provided guidance for strategies to improve adherence.
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self reported adherence to a Low Sodium Diet and health outcomes in patients with heart failure
Journal of Cardiovascular Nursing, 2016Co-Authors: Eun Kyeung Song, Debra K Moser, Seokmin Kang, Terry A LennieAbstract:BACKGROUND: Most clinicians rely on patients' self-report of folLowing a Low-Sodium Diet to determine adherence of patients with heart failure (HF). Whether self-reported adherence to a Low-Sodium Diet is associated with cardiac event-free survival is unclear. PURPOSES: To determine (1) whether self-reported is concordant with adherence to a Low-Sodium Diet measured by food diaries and 24-hour urinary Sodium excretion and (2) whether self-reported adherence to a Low-Sodium Diet predicts cardiac event-free survival. METHODS: Adherence to a Low-Sodium Diet was measured using 3 measures in 119 HF patients: (1) self-reported adherence, 1 item from the Self-care of Heart Failure Index scale; (2) a 3-day food diary; (3) 24-hour urinary Sodium excretion. Patients were folLowed up for a median of 297 days to determine cardiac hospitalization or emergency department visit. One-way analysis of variance and Cox regression were used to address our purposes. RESULTS: Self-reported adherence was concordant with adherence to a Low-Sodium Diet measured by food diaries and 24-hour urinary Sodium excretion. Thirty-one patients who reported they always folLow a Low-Sodium Diet had an average Sodium intake less than 3 g/d (F = 5.07, P = .002) and 3.3 g of a mean 24-hour urinary Sodium excretion (F = 3.393, P = .020). Patients who reported they never or rarely folLow a Low-Sodium Diet had 4.7 times greater risk of having cardiac events than did those who always folLowed a Low-Sodium Diet (P = .017). CONCLUSION: Self-reported adherence to a Low-Sodium Diet predicted cardiac event-free survival demonstrating clinicians can use this as an indicator of adherence.
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adherence to a Low Sodium Diet in patients with heart failure is best when family members also folLow the Diet a multicenter observational study
Journal of Cardiovascular Nursing, 2015Co-Authors: Misook L Chung, Terry A Lennie, Gia Muddmartin, Debra K MoserAbstract:BACKGROUND: Adherence to a Low-Sodium Diet (LSD) is difficult without continuous support from spouses or family members. Whether having a family member folLow an LSD improves patient adherence has not been tested objectively. OBJECTIVE: The aim of this study was to examine the effect of family adherence to an LSD on patient adherence to an LSD and to examine whether this effect differed by relationship status and living arrangement. METHODS: In this secondary data analysis, we analyzed data from 379 outpatients with heart failure who had objective evidence of adherence to an LSD (ie, a 24-hour urinary Sodium excretion). The t test, analysis of variance, and logistic regressions were used to compare levels of adherence among groups that were categorized by family adherence to an LSD, relationship status, and living arrangement with family member and to predict the likelihood of being adherent to an LSD (24-hour urinary Sodium excretion <3000 mg) by the groups. RESULTS: Compared with patients whose family did not folLow an LSD, patients whose family member folLowed an LSD had Lower average urinary Sodium excretion (3651 vs 4280 mg; P = .003) and were 1.6 times more likely to be adherent to an LSD (95% confidence interval, 1.03-2.4; P = .035). Patients whose spouses folLowed the LSD had Lower Sodium excretion than did patients whose spouses did not folLow the LSD (3730 vs 4534 mg; P = .012). Patients whose nonspousal family member folLowed an LSD were 4 times more likely to be adherent than were patients whose spousal member did not folLow an LSD (odds ratio, 3.94; 95% confidence interval, 1.81-8.58; P = .001). CONCLUSIONS: Living with a spouse or other family member improved patient adherence to LSD only when the spouse or family member also folLowed the LSD. These results suggest that interventions aimed at improving LSD adherence should target patient and family member dyads to encourage family members to folLow the LSD with patients.
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abstract 16922 feasibility of family Sodium watcher program to improve adherence to Low Sodium Diet in patients with heart failure and caregivers
Circulation, 2014Co-Authors: Misook L Chung, Debra K Moser, Terry A LennieAbstract:Introduction: Poor adherence to the Low Sodium Diet (LSD), common in patients with heart failure (HF), is a major predictor of hospitalization for exacerbation of HF. When family member’s consume the same LSD recommended for patients, patient adherence is increased. The Sodium Watcher Program (SWAP) was developed to improve adherence to LSD using a gradual adaptation strategy and an electronic salt monitoring device that alLows detection of Sodium content in food. The purpose of this study was to examine whether the SWAP was feasible and if it resulted in reduction in Sodium intake for patients with HF and their caregivers. Method: In this 2-group randomized controlled trial, 15 patient-caregiver dyads completed 24-hour urine collection for Sodium excretion level (24h UNa) at baseline and 3 months folLow up. Dyads in the SWAP intervention (n=8) received 12 weeks of self-care education for HF and LSD with gradual adaptation strategies in salt intake via 2 home visits and 4 calls. Paired t-test was used to compare adherence to LSD at two data collection times. Only intervention group evaluated use of the electronic salt monitoring devices and the intervention program at 3 months. Results: The intervention group had a significant reduction in 24h UNa (Patients 3894mg vs. 3604mg, p=.02; caregivers 4123mg vs. 3380mg, p<.05). They also reported significant increased level of enjoying eating LSD (M =5.4 on 10-point rating scale vs. M=7.9 p <.01) and 90% noticed a change in their ability to taste salt in their food at the 3-month folLow up. They reported that use of the electronic monitoring devices was easy (M=8.3 on 10-point rating scale) and helpful in supporting LSD adherence (M=8.8 on 10-point rating scale). Caregivers in the intervention reported no significant changes in burden levels. The usual care control group had no change in 24h UNa (patients 4369 mg vs. 4434 mg; caregivers 3301 mg vs. 4826mg). Conclusion: The findings demonstrated that the SWaP is feasible and efficacious for folLowing LSD by dyads. The intervention was feasible for caregivers and did not increase caregiver burden. This family intervention may have potential for promoting long-term adherence and needs to be tested in a larger clinical trial.
Terry A Lennie - One of the best experts on this subject based on the ideXlab platform.
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Relationship of Heart Failure Patients' Knowledge, Perceived Barriers, and Attitudes Regarding Low‐Sodium Diet Recommendations to Adherence
Progress in Cardiovascular Nursing, 2020Co-Authors: Terry A Lennie, Muna Hammash, Lynn P Roser, Carol S Smith, Robin J Trupp, Misook L Chung, Linda Worrall-carter, Jan Odom-forren, Debra K MoserAbstract:The purposes of this study were to describe heart failure patient perceptions regarding instructions received for folLowing a Low-Sodium Diet and the benefits, barriers, and ease and frequency of folLowing the Diet. A total of 246 patients with heart failure referred from academic medical centers in the United States and Australia participated in the study. A subset of 145 patients provided 24-hour urine samples for Sodium excretion assessment. While most (80%) patients reported receiving recommendations to folLow a Low-Sodium Diet, their recall of specific instructions was poor. Although the majority (75%) reported folLowing a Low-Sodium Diet most or all of the time, 24-hour urine Sodium excretion indicated that only 25% of patients were adherent. Patients who reported being more adherent, however, had Lower urine Sodium excretion levels. Attitudes regarding difficulty in and perceived benefits of folLowing the Diet were not related to Sodium excretion. Data on attitudes and barriers provided guidance for strategies to improve adherence.
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long term adherence to Low Sodium Diet in patients with heart failure
Western Journal of Nursing Research, 2017Co-Authors: Misook L Chung, Linda G Park, Susan K Frazier, Terry A LennieAbstract:Although folLowing a Low-Sodium Diet (LSD) for heart failure (HF) has been recommended for decades, little is known about factors related to long-term patient adherence. The purposes of this study were to (a) compare Sodium intake and factors affecting adherence in a long-term adherent group and in a non-adherent group and (b) examine predictors of membership in the long-term adherent group. Patients with HF (N = 74) collected 24-hr urine samples and completed the Dietary Sodium Restriction Questionnaire and the Patient Health Questionnaire-9. Long-term adherence was determined using the Stage of Dietary Behavior Change Scale. The long-term adherent group had Lower Sodium intake (3,086 mg vs. 4,135 mg, p = .01) and perceived more benefits from LSD than the non-adherent group. Only positive attitudes toward LSD predicted membership in the long-term adherence group (odds ratio [OR] = 1.18, p = .005). Interventions focused on enhancing positive perceptions of the benefits of an LSD may improve long-term Diet...
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self reported adherence to a Low Sodium Diet and health outcomes in patients with heart failure
Journal of Cardiovascular Nursing, 2016Co-Authors: Eun Kyeung Song, Debra K Moser, Seokmin Kang, Terry A LennieAbstract:BACKGROUND: Most clinicians rely on patients' self-report of folLowing a Low-Sodium Diet to determine adherence of patients with heart failure (HF). Whether self-reported adherence to a Low-Sodium Diet is associated with cardiac event-free survival is unclear. PURPOSES: To determine (1) whether self-reported is concordant with adherence to a Low-Sodium Diet measured by food diaries and 24-hour urinary Sodium excretion and (2) whether self-reported adherence to a Low-Sodium Diet predicts cardiac event-free survival. METHODS: Adherence to a Low-Sodium Diet was measured using 3 measures in 119 HF patients: (1) self-reported adherence, 1 item from the Self-care of Heart Failure Index scale; (2) a 3-day food diary; (3) 24-hour urinary Sodium excretion. Patients were folLowed up for a median of 297 days to determine cardiac hospitalization or emergency department visit. One-way analysis of variance and Cox regression were used to address our purposes. RESULTS: Self-reported adherence was concordant with adherence to a Low-Sodium Diet measured by food diaries and 24-hour urinary Sodium excretion. Thirty-one patients who reported they always folLow a Low-Sodium Diet had an average Sodium intake less than 3 g/d (F = 5.07, P = .002) and 3.3 g of a mean 24-hour urinary Sodium excretion (F = 3.393, P = .020). Patients who reported they never or rarely folLow a Low-Sodium Diet had 4.7 times greater risk of having cardiac events than did those who always folLowed a Low-Sodium Diet (P = .017). CONCLUSION: Self-reported adherence to a Low-Sodium Diet predicted cardiac event-free survival demonstrating clinicians can use this as an indicator of adherence.
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adherence to a Low Sodium Diet in patients with heart failure is best when family members also folLow the Diet a multicenter observational study
Journal of Cardiovascular Nursing, 2015Co-Authors: Misook L Chung, Terry A Lennie, Gia Muddmartin, Debra K MoserAbstract:BACKGROUND: Adherence to a Low-Sodium Diet (LSD) is difficult without continuous support from spouses or family members. Whether having a family member folLow an LSD improves patient adherence has not been tested objectively. OBJECTIVE: The aim of this study was to examine the effect of family adherence to an LSD on patient adherence to an LSD and to examine whether this effect differed by relationship status and living arrangement. METHODS: In this secondary data analysis, we analyzed data from 379 outpatients with heart failure who had objective evidence of adherence to an LSD (ie, a 24-hour urinary Sodium excretion). The t test, analysis of variance, and logistic regressions were used to compare levels of adherence among groups that were categorized by family adherence to an LSD, relationship status, and living arrangement with family member and to predict the likelihood of being adherent to an LSD (24-hour urinary Sodium excretion <3000 mg) by the groups. RESULTS: Compared with patients whose family did not folLow an LSD, patients whose family member folLowed an LSD had Lower average urinary Sodium excretion (3651 vs 4280 mg; P = .003) and were 1.6 times more likely to be adherent to an LSD (95% confidence interval, 1.03-2.4; P = .035). Patients whose spouses folLowed the LSD had Lower Sodium excretion than did patients whose spouses did not folLow the LSD (3730 vs 4534 mg; P = .012). Patients whose nonspousal family member folLowed an LSD were 4 times more likely to be adherent than were patients whose spousal member did not folLow an LSD (odds ratio, 3.94; 95% confidence interval, 1.81-8.58; P = .001). CONCLUSIONS: Living with a spouse or other family member improved patient adherence to LSD only when the spouse or family member also folLowed the LSD. These results suggest that interventions aimed at improving LSD adherence should target patient and family member dyads to encourage family members to folLow the LSD with patients.
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abstract 16922 feasibility of family Sodium watcher program to improve adherence to Low Sodium Diet in patients with heart failure and caregivers
Circulation, 2014Co-Authors: Misook L Chung, Debra K Moser, Terry A LennieAbstract:Introduction: Poor adherence to the Low Sodium Diet (LSD), common in patients with heart failure (HF), is a major predictor of hospitalization for exacerbation of HF. When family member’s consume the same LSD recommended for patients, patient adherence is increased. The Sodium Watcher Program (SWAP) was developed to improve adherence to LSD using a gradual adaptation strategy and an electronic salt monitoring device that alLows detection of Sodium content in food. The purpose of this study was to examine whether the SWAP was feasible and if it resulted in reduction in Sodium intake for patients with HF and their caregivers. Method: In this 2-group randomized controlled trial, 15 patient-caregiver dyads completed 24-hour urine collection for Sodium excretion level (24h UNa) at baseline and 3 months folLow up. Dyads in the SWAP intervention (n=8) received 12 weeks of self-care education for HF and LSD with gradual adaptation strategies in salt intake via 2 home visits and 4 calls. Paired t-test was used to compare adherence to LSD at two data collection times. Only intervention group evaluated use of the electronic salt monitoring devices and the intervention program at 3 months. Results: The intervention group had a significant reduction in 24h UNa (Patients 3894mg vs. 3604mg, p=.02; caregivers 4123mg vs. 3380mg, p<.05). They also reported significant increased level of enjoying eating LSD (M =5.4 on 10-point rating scale vs. M=7.9 p <.01) and 90% noticed a change in their ability to taste salt in their food at the 3-month folLow up. They reported that use of the electronic monitoring devices was easy (M=8.3 on 10-point rating scale) and helpful in supporting LSD adherence (M=8.8 on 10-point rating scale). Caregivers in the intervention reported no significant changes in burden levels. The usual care control group had no change in 24h UNa (patients 4369 mg vs. 4434 mg; caregivers 3301 mg vs. 4826mg). Conclusion: The findings demonstrated that the SWaP is feasible and efficacious for folLowing LSD by dyads. The intervention was feasible for caregivers and did not increase caregiver burden. This family intervention may have potential for promoting long-term adherence and needs to be tested in a larger clinical trial.
Andre S Mecawi - One of the best experts on this subject based on the ideXlab platform.
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Sodium appetite elicited by Low-Sodium Diet is dependent on p44/42 mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) activation in the brain
Journal of Neuroendocrinology, 2017Co-Authors: Lívia Da Rocha Natalino Monteiro, Lucila Leico Kagohara Elias, Paula Beatriz Marangon, Luís Carlos Reis, José Antunes-rodrigues, Andre S MecawiAbstract:: Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in Sodium appetite. Thus, we addressed the involvement of MAPK signalling in the induction of Sodium appetite after 4 days of Low-Sodium Diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after Low-Sodium Diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that Low-Sodium Diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after Low-Sodium Diet consumption appears to involve another extracellular mediator. We also evaluated whether a Low-Sodium Diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and Low-Sodium Diet groups. These data indicate that Low-Sodium Diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in Sodium appetite after Low-Sodium Diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after Low-Sodium Diet consumption. Thus, the MAPK pathway is involved in promoting the Sodium appetite after Low-Sodium Diet consumption.
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Sodium appetite elicited by Low Sodium Diet is dependent on p44 42 mitogen activated protein kinase extracellular signal regulated kinase 1 2 activation in the brain
Journal of Neuroendocrinology, 2017Co-Authors: Livia Monteiro, L C Reis, Lucila Leico Kagohara Elias, Jose Antunesrodrigues, Paula Beatriz Marangon, Andre S MecawiAbstract:: Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in Sodium appetite. Thus, we addressed the involvement of MAPK signalling in the induction of Sodium appetite after 4 days of Low-Sodium Diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after Low-Sodium Diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that Low-Sodium Diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after Low-Sodium Diet consumption appears to involve another extracellular mediator. We also evaluated whether a Low-Sodium Diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and Low-Sodium Diet groups. These data indicate that Low-Sodium Diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in Sodium appetite after Low-Sodium Diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after Low-Sodium Diet consumption. Thus, the MAPK pathway is involved in promoting the Sodium appetite after Low-Sodium Diet consumption.
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the role of angiotensin ii on Sodium appetite after a Low Sodium Diet
Journal of Neuroendocrinology, 2013Co-Authors: Andre S Mecawi, Tatiane Vilhenafranco, Fabricia Fonseca, L C Reis, Lucila Leico Kagohara Elias, Jose AntunesrodriguesAbstract:: The present study aimed to investigate the role of angiotensin II (Ang II) on Sodium appetite in rats subjected to a normal or a Low-Sodium Diet (1% or > 0.1% NaCl) for 4 days. During Sodium restriction, a reduction in water intake, urinary volume and Sodium excretion was observed. After a Low-Sodium Diet, we observed decreased plasma protein concentrations and haematocrit associated with a slight reduction in arterial pressure, without any significant changes in heart rate, natraemia, corticotrophin-releasing hormone mRNA expression in the paraventricular nucleus and corticosterone levels. After providing hypertonic saline, there was an increase in saline intake folLowed by a small increase in water intake, resulting in an enhanced saline intake ratio and the recovery of arterial pressure. Sodium deprivation increased plasma but not brain Ang I and II concentrations. A Low-Sodium Diet increased kidney renin and liver angiotensinogen mRNA levels but not lung angiotensin-converting enzyme mRNA expression. Moreover, Ang II type 1a receptor mRNA expression was increased in the subfornical organ and the dorsal raphe nucleus and decreased in the medial preoptic nuclei, without changes in the paraventricular nucleus and the nucleus of solitary tract after a Low-Sodium Diet. Blockade of AT(1) receptors or brain Ang II synthesis led to a reduction in Sodium intake after a Low-Sodium Diet. Intracerebroventricular injection of Ang II led to a similar increase in Sodium and water intake in the control and Low-Sodium Diet groups. In conclusion, the results of the present study suggest that Ang II is involved in the increased Sodium appetite after a Low-Sodium Diet.
Jose Antunesrodrigues - One of the best experts on this subject based on the ideXlab platform.
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Sodium appetite elicited by Low Sodium Diet is dependent on p44 42 mitogen activated protein kinase extracellular signal regulated kinase 1 2 activation in the brain
Journal of Neuroendocrinology, 2017Co-Authors: Livia Monteiro, L C Reis, Lucila Leico Kagohara Elias, Jose Antunesrodrigues, Paula Beatriz Marangon, Andre S MecawiAbstract:: Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in Sodium appetite. Thus, we addressed the involvement of MAPK signalling in the induction of Sodium appetite after 4 days of Low-Sodium Diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after Low-Sodium Diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that Low-Sodium Diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after Low-Sodium Diet consumption appears to involve another extracellular mediator. We also evaluated whether a Low-Sodium Diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and Low-Sodium Diet groups. These data indicate that Low-Sodium Diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in Sodium appetite after Low-Sodium Diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after Low-Sodium Diet consumption. Thus, the MAPK pathway is involved in promoting the Sodium appetite after Low-Sodium Diet consumption.
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the role of angiotensin ii on Sodium appetite after a Low Sodium Diet
Journal of Neuroendocrinology, 2013Co-Authors: Andre S Mecawi, Tatiane Vilhenafranco, Fabricia Fonseca, L C Reis, Lucila Leico Kagohara Elias, Jose AntunesrodriguesAbstract:: The present study aimed to investigate the role of angiotensin II (Ang II) on Sodium appetite in rats subjected to a normal or a Low-Sodium Diet (1% or > 0.1% NaCl) for 4 days. During Sodium restriction, a reduction in water intake, urinary volume and Sodium excretion was observed. After a Low-Sodium Diet, we observed decreased plasma protein concentrations and haematocrit associated with a slight reduction in arterial pressure, without any significant changes in heart rate, natraemia, corticotrophin-releasing hormone mRNA expression in the paraventricular nucleus and corticosterone levels. After providing hypertonic saline, there was an increase in saline intake folLowed by a small increase in water intake, resulting in an enhanced saline intake ratio and the recovery of arterial pressure. Sodium deprivation increased plasma but not brain Ang I and II concentrations. A Low-Sodium Diet increased kidney renin and liver angiotensinogen mRNA levels but not lung angiotensin-converting enzyme mRNA expression. Moreover, Ang II type 1a receptor mRNA expression was increased in the subfornical organ and the dorsal raphe nucleus and decreased in the medial preoptic nuclei, without changes in the paraventricular nucleus and the nucleus of solitary tract after a Low-Sodium Diet. Blockade of AT(1) receptors or brain Ang II synthesis led to a reduction in Sodium intake after a Low-Sodium Diet. Intracerebroventricular injection of Ang II led to a similar increase in Sodium and water intake in the control and Low-Sodium Diet groups. In conclusion, the results of the present study suggest that Ang II is involved in the increased Sodium appetite after a Low-Sodium Diet.
Lucila Leico Kagohara Elias - One of the best experts on this subject based on the ideXlab platform.
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Sodium appetite elicited by Low-Sodium Diet is dependent on p44/42 mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) activation in the brain
Journal of Neuroendocrinology, 2017Co-Authors: Lívia Da Rocha Natalino Monteiro, Lucila Leico Kagohara Elias, Paula Beatriz Marangon, Luís Carlos Reis, José Antunes-rodrigues, Andre S MecawiAbstract:: Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in Sodium appetite. Thus, we addressed the involvement of MAPK signalling in the induction of Sodium appetite after 4 days of Low-Sodium Diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after Low-Sodium Diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that Low-Sodium Diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after Low-Sodium Diet consumption appears to involve another extracellular mediator. We also evaluated whether a Low-Sodium Diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and Low-Sodium Diet groups. These data indicate that Low-Sodium Diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in Sodium appetite after Low-Sodium Diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after Low-Sodium Diet consumption. Thus, the MAPK pathway is involved in promoting the Sodium appetite after Low-Sodium Diet consumption.
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Sodium appetite elicited by Low Sodium Diet is dependent on p44 42 mitogen activated protein kinase extracellular signal regulated kinase 1 2 activation in the brain
Journal of Neuroendocrinology, 2017Co-Authors: Livia Monteiro, L C Reis, Lucila Leico Kagohara Elias, Jose Antunesrodrigues, Paula Beatriz Marangon, Andre S MecawiAbstract:: Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in Sodium appetite. Thus, we addressed the involvement of MAPK signalling in the induction of Sodium appetite after 4 days of Low-Sodium Diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after Low-Sodium Diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that Low-Sodium Diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after Low-Sodium Diet consumption appears to involve another extracellular mediator. We also evaluated whether a Low-Sodium Diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and Low-Sodium Diet groups. These data indicate that Low-Sodium Diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in Sodium appetite after Low-Sodium Diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after Low-Sodium Diet consumption. Thus, the MAPK pathway is involved in promoting the Sodium appetite after Low-Sodium Diet consumption.
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the role of angiotensin ii on Sodium appetite after a Low Sodium Diet
Journal of Neuroendocrinology, 2013Co-Authors: Andre S Mecawi, Tatiane Vilhenafranco, Fabricia Fonseca, L C Reis, Lucila Leico Kagohara Elias, Jose AntunesrodriguesAbstract:: The present study aimed to investigate the role of angiotensin II (Ang II) on Sodium appetite in rats subjected to a normal or a Low-Sodium Diet (1% or > 0.1% NaCl) for 4 days. During Sodium restriction, a reduction in water intake, urinary volume and Sodium excretion was observed. After a Low-Sodium Diet, we observed decreased plasma protein concentrations and haematocrit associated with a slight reduction in arterial pressure, without any significant changes in heart rate, natraemia, corticotrophin-releasing hormone mRNA expression in the paraventricular nucleus and corticosterone levels. After providing hypertonic saline, there was an increase in saline intake folLowed by a small increase in water intake, resulting in an enhanced saline intake ratio and the recovery of arterial pressure. Sodium deprivation increased plasma but not brain Ang I and II concentrations. A Low-Sodium Diet increased kidney renin and liver angiotensinogen mRNA levels but not lung angiotensin-converting enzyme mRNA expression. Moreover, Ang II type 1a receptor mRNA expression was increased in the subfornical organ and the dorsal raphe nucleus and decreased in the medial preoptic nuclei, without changes in the paraventricular nucleus and the nucleus of solitary tract after a Low-Sodium Diet. Blockade of AT(1) receptors or brain Ang II synthesis led to a reduction in Sodium intake after a Low-Sodium Diet. Intracerebroventricular injection of Ang II led to a similar increase in Sodium and water intake in the control and Low-Sodium Diet groups. In conclusion, the results of the present study suggest that Ang II is involved in the increased Sodium appetite after a Low-Sodium Diet.
