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Carina Aparecida Fabrício De ,andrade - One of the best experts on this subject based on the ideXlab platform.
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Alpha2-adrenergic activation in the lateral parabrachial nucleus induces NaCl intake under conditions of systemic hyperOsmolarity.
Neuroscience, 2006Co-Authors: Carina Aparecida Fabrício De ,andrade, L. A. De Luca, Debora S. A. Colombari, José Vanderlei MenaniAbstract:The inhibition of sodium intake by increased Plasma Osmolarity may depend on inhibitory mechanisms present in the lateral parabrachial nucleus. Activation of α2-adrenergic receptors in the lateral parabrachial nucleus is suggested to deactivate inhibitory mechanisms present in this area increasing fluid depletion-induced 0.3 M NaCl intake. Considering the possibility that lateral parabrachial nucleus inhibitory mechanisms are activated and restrain sodium intake in animals with increased Plasma Osmolarity, in the present study we investigated the effects on water and 0.3 M NaCl intake produced by the activation of α2-adrenergic receptors in the lateral parabrachial nucleus in rats with increased Plasma Osmolarity. Male Holtzman rats with stainless steel cannulas implanted bilaterally into the lateral parabrachial nucleus were used. One hour after intragastric 2 M NaCl load (2 ml), bilateral injections of moxonidine (α2-adrenergic/imidazoline receptor agonist, 0.5 nmol/0.2 μl, n=10) into the lateral parabrachial nucleus induced a strong ingestion of 0.3 M NaCl intake (19.1±5.5 ml/2 h vs. vehicle: 1.8±0.6 ml/2 h), without changing water intake (15.8±3.0 ml/2 h vs. vehicle: 9.3±2.0 ml/2 h). However, moxonidine into the lateral parabrachial nucleus in satiated rats not treated with 2 M NaCl produced no change on 0.3 M NaCl intake. The pre-treatment with RX 821002 (α2-adrenergic receptor antagonist, 20 nmol/0.2 μl) into the lateral parabrachial nucleus almost abolished the effects of moxonidine on 0.3 M NaCl intake (4.7±3.4 ml/2 h). The present results suggest that α2-adrenergic receptor activation in the lateral parabrachial nucleus blocks inhibitory mechanisms, thereby allowing ingestion of hypertonic NaCl under conditions of extracellular hyperOsmolarity. We suggest that during cell dehydration, circuits subserving sodium appetite are activated, but at the same time strongly inhibited through the lateral parabrachial nucleus.
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Participação dos receptores adrenérgicos Alfa2 do núcleo parabraquial lateral no controle da ingestão de sódio
Programa de Pós-graduação em Ciências Fisiológicas, 2006Co-Authors: Carina Aparecida Fabrício De ,andradeAbstract:Water and NaCl intake is strongly inhibited by the activation of α2-adrenergic receptors with clonidine or moxonidine (α2-adrenergic/imidazoline agonists) injected peripherally or into the forebrain and by serotonin and cholecystokinin into the lateral parabrachial nucleus (LPBN), a pontine structure. Serotonergic and cathecolaminergic neurons are present in the projection from AP/NTS to the LPBN and the presence of α2- adrenergic sites in the LPBN has been shown. The aim of the present study was to investigate the possible involvement of α2-adrenergic receptors of the LPBN in the control of water and 0.3 M NaCl intake induced by the treatment with subcutaneous furosemide (FURO, 10 mg/kg of body weight) + captopril (CAP, 5 mg/kg of body weight) and also during cellular dehydration induced by intragastric 2 M NaCl load (2 ml). In addition, the possible interaction between α2-adrenergic receptors and serotoninergic, GABAergic or opioidergic mechanisms in the LPBN to control of water and 0.3 M NaCl intake was also investigated. Male Holtzman rats with cannulas implanted bilaterally in the LPBN were used. Contrary to forebrain injections, bilateral LPBN injections of moxonidine produced a strong and surprising increase in FURO + CAP-induced 0.3 M NaCl intake and a small increase in water intake, without change mean arterial pressure and heart rate or FURO + CAP-induced c-fos expression in forebrain areas related to the control of fluid-electrolyte balance. Prior injections of RX 821002 (α2-adrenergic antagonist, 10 and 20 nmol/0.2 µl) abolished the effect of moxonidine (0.5 nmol) on 0.3 M NaCl intake. Bilateral injections of moxonidine (0.5 nmol/0.2 µl) into the LPBN also induced a strong ingestion of 0.3 M NaCl intake, without changing water intake in rats with increased Plasma Osmolarity. However, moxonidine into the LPBN in satiated rats not treated with 2 M NaCl produced no change on 0.3 M NaCl intake. The activation of the LPBN α2-adrenoceptors inhibited the LPBN serotonergic inhibitory mechanism involved in the control of water and NaCl intake, and the increase in FURO+CAP-induced sodium intake produced by the activation of the α2-adrenergic receptors in the LPBN was partially dependent on GABAergic or opioidergic mechanisms in the LPBN. In rats submitted to the taste reactivity test to oral infusions of a 0.3 M sodium solution, the blockage serotonergic receptors into the LPBN enhanced positive hedonic taste reactivity patterns. In conclusion, previous and present results indicate opposite roles for α2-adrenergic receptors in the control of sodium and water intake according to their distribution in the rat brain. The α2-adrenergic activation into the LPBN produces a potent increase in hypertonic sodium intake during extracellular and cellular dehydration. These effects of α2-adrenergic activation into the LPBN is possibly due to the inhibitory serotoninergic mechanisms blockage into the LPBN and at least part of these effects is also dependent of an interaction with GABAergic and opioidergic mechanisms into the same area. Finally, the blockade of serotonergic receptors in the LPBN can enhance sodium palatability thus contributing to the increase in sodium intake during cell dehydration.Universidade Federal de Minas GeraisA ingestão de água e de NaCl 0,3 M é fortemente inibida pela ativação de receptores adrenérgicos α2 com clonidina ou moxonidina (agonistas de receptores adrenérgicos α2/imidazólicos) injetadas perifericamente ou em áreas prosencefálicas, ou pela serotonina e colecistocinina no núcleo parabraquial lateral (NPBL), estrutura bilateral localizada na ponte. Neurônios serotoninérgicos e catecolaminérgicos estão presentes nas projeções da área postrema e núcleo do trato solitário para o NPBL e a presença de receptores adrenérgicos α2 no NPBL já foi demonstrada. O objetivo do presente estudo foi investigar o possível envolvimento dos receptores adrenérgicos α2 do NPBL no controle da ingestão de água e de NaCl 0,3 M induzida pelo tratamento com furosemida (FURO, 10 mg/kg de peso corporal) + captopril (CAP, 5 mg/kg de peso corporal) subcutaneamente e durante desidratação celular, induzida pela sobrecarga intragástrica de NaCl 2 M (2 ml). Além disso, também foi investigada a possível interação entre os receptores adrenérgicos α2 e os mecanismos serotoninérgicos, GABAérgicos e opioidérgicos do NPBL no controle da ingestão de água de NaCl 0,3 M. Foram usados ratos Holtzman com cânulas implantadas bilateralmente em direção ao NPBL. Contrariamente aos efeitos produzidos pelas injeções prosencefálicas, as injeções de moxonidina (0,1; 0,5 e 1,0 nmol/0,2 µl) produziram um forte e surpreendente aumento da ingestão de NaCl 0,3 M induzida por FURO + CAP, e um pequeno aumento da ingestão de água, sem alterações cardiovasculares e da expressão da proteína c-fos em áreas prosencefálicas envolvidas no controle do equilíbrio hidroeletrolítico. Injeções prévias de RX 821002 (antagonista de receptores adrenérgicos α2, 10 e 20 nmol/0,2 µl) aboliram o efeito da moxonidina (0,5 nmol) sobre a ingestão de NaCl 0,3 M. Em ratos previamente tratados com sobrecarga intragástrica de NaCl 2 M, as injeções bilaterais de moxonidina no NPBL induziram uma forte ingestão de NaCl 0,3 M, sem alterar a ingestão de água. Injeções de moxonidina no NPBL não alteram a ingestão de sódio e de água em animais saciados. A ativação de receptores adrenérgicos α2 no NPBL inibiu os efeitos da ativação do mecanismo serotoninérgico inibitório do NPBL. O aumento da ingestão de sódio produzido pela ativação de receptores adrenérgicos α2 no NPBL foi parcialmente dependente de mecanismos GABAérgicos e opioidérgicos do NPBL. O bloqueio de receptores serotoninérgicos no NPBL promoveu aumento das respostas hedônicas a infusão intra-oral ao sódio hipertônico em animais desidratados. Em conclusão, os prévios e presentes resultados indicam papéis opostos para os receptores adrenérgicos α2 no controle da ingestão e de água de acordo com sua distribuição no cérebro do rato. A ativação de receptores adrenérgicos α2 no NPBL promove um potente aumento da ingestão de sódio em condições de desidratação extracelular ou intracelular. Os efeitos da ativação dos receptores adrenérgicos α2 do NPBL possivelmente se devem ao bloqueio dos mecanismos serotoninérgicos inibitórios do NPBL e pelo menos parte dos efeitos também depende de uma interação com mecanismos GABAérgicos e opioidérgicos do NPBL. Finalmente, os receptores serotoninérgicos do NPBL podem estar envolvidos na modulação da palatabilidade ao sódio hipertônico
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Participação dos receptores adrenérgicos Alfa2 do núcleo parabraquial lateral no controle da ingestão de sódio.
Universidade Federal de São Carlos, 2006Co-Authors: Carina Aparecida Fabrício De ,andradeAbstract:A ingestão de água e de NaCl 0,3 M é fortemente inibida pela ativação de receptores adrenérgicos α2 com clonidina ou moxonidina (agonistas de receptores adrenérgicos α2/imidazólicos) injetadas perifericamente ou em áreas prosencefálicas, ou pela serotonina e colecistocinina no núcleo parabraquial lateral (NPBL), estrutura bilateral localizada na ponte. Neurônios serotoninérgicos e catecolaminérgicos estão presentes nas projeções da área postrema e núcleo do trato solitário para o NPBL e a presença de receptores adrenérgicos α2 no NPBL já foi demonstrada. O objetivo do presente estudo foi investigar o possível envolvimento dos receptores adrenérgicos α2 do NPBL no controle da ingestão de água e de NaCl 0,3 M induzida pelo tratamento com furosemida (FURO, 10 mg/kg de peso corporal) + captopril (CAP, 5 mg/kg de peso corporal) subcutaneamente e durante desidratação celular, induzida pela sobrecarga intragástrica de NaCl 2 M (2 ml). Além disso, também foi investigada a possível interação entre os receptores adrenérgicos α2 e os mecanismos serotoninérgicos, GABAérgicos e opioidérgicos do NPBL no controle da ingestão de água de NaCl 0,3 M. Foram usados ratos Holtzman com cânulas implantadas bilateralmente em direção ao NPBL. Contrariamente aos efeitos produzidos pelas injeções prosencefálicas, as injeções de moxonidina (0,1; 0,5 e 1,0 nmol/0,2 l) produziram um forte e surpreendente aumento da ingestão de NaCl 0,3 M induzida por FURO + CAP, e um pequeno aumento da ingestão de água, sem alterações cardiovasculares e da expressão da proteína c-fos em áreas prosencefálicas envolvidas no controle do equilíbrio hidroeletrolítico. Injeções prévias de RX 821002 (antagonista de receptores adrenérgicos α2, 10 e 20 nmol/0,2 l) aboliram o efeito da moxonidina (0,5 nmol) sobre a ingestão de NaCl 0,3 M. Em ratos previamente tratados com sobrecarga intragástrica de NaCl 2 M, as injeções bilaterais de moxonidina no NPBL induziram uma forte ingestão de NaCl 0,3 M, sem alterar a ingestão de água. Injeções de moxonidina no NPBL não alteram a ingestão de sódio e de água em animais saciados. A ativação de receptores adrenérgicos α2 no NPBL inibiu os efeitos da ativação do mecanismo serotoninérgico inibitório do NPBL. O aumento da ingestão de sódio produzido pela ativação de receptores adrenérgicos α2 no NPBL foi parcialmente dependente de mecanismos GABAérgicos e opioidérgicos do NPBL. O bloqueio de receptores serotoninérgicos no NPBL promoveu aumento das respostas hedônicas a infusão intra-oral ao sódio hipertônico em animais desidratados. Em conclusão, os prévios e presentes resultados indicam papéis opostos para os receptores adrenérgicos α2 no controle da ingestão e de água de acordo com sua distribuição no cérebro do rato. A ativação de receptores adrenérgicos α2 no NPBL promove um potente aumento da ingestão de sódio em condições de desidratação extracelular ou intracelular. Os efeitos da ativação dos receptores adrenérgicos α2 do NPBL possivelmente se devem ao bloqueio dos mecanismos serotoninérgicos inibitórios do NPBL e pelo menos parte dos efeitos também depende de uma interação com mecanismos GABAérgicos e opioidérgicos do NPBL. Finalmente, os receptores serotoninérgicos do NPBL podem estar envolvidos na modulação da palatabilidade ao sódio hipertônico.Water and NaCl intake is strongly inhibited by the activation of α2-adrenergic receptors with clonidine or moxonidine (α2-adrenergic/imidazoline agonists) injected peripherally or into the forebrain and by serotonin and cholecystokinin into the lateral parabrachial nucleus (LPBN), a pontine structure. Serotonergic and cathecolaminergic neurons are present in the projection from AP/NTS to the LPBN and the presence of α2- adrenergic sites in the LPBN has been shown. The aim of the present study was to investigate the possible involvement of α2-adrenergic receptors of the LPBN in the control of water and 0.3 M NaCl intake induced by the treatment with subcutaneous furosemide (FURO, 10 mg/kg of body weight) + captopril (CAP, 5 mg/kg of body weight) and also during cellular dehydration induced by intragastric 2 M NaCl load (2 ml). In addition, the possible interaction between α2-adrenergic receptors and serotoninergic, GABAergic or opioidergic mechanisms in the LPBN to control of water and 0.3 M NaCl intake was also investigated. Male Holtzman rats with cannulas implanted bilaterally in the LPBN were used. Contrary to forebrain injections, bilateral LPBN injections of moxonidine produced a strong and surprising increase in FURO + CAP-induced 0.3 M NaCl intake and a small increase in water intake, without change mean arterial pressure and heart rate or FURO + CAP-induced c-fos expression in forebrain areas related to the control of fluid-electrolyte balance. Prior injections of RX 821002 (α2-adrenergic antagonist, 10 and 20 nmol/0.2 l) abolished the effect of moxonidine (0.5 nmol) on 0.3 M NaCl intake. Bilateral injections of moxonidine (0.5 nmol/0.2 l) into the LPBN also induced a strong ingestion of 0.3 M NaCl intake, without changing water intake in rats with increased Plasma Osmolarity. However, moxonidine into the LPBN in satiated rats not treated with 2 M NaCl produced no change on 0.3 M NaCl intake. The activation of the LPBN α2-adrenoceptors inhibited the LPBN serotonergic inhibitory mechanism involved in the control of water and NaCl intake, and the increase in FURO+CAP-induced sodium intake produced by the activation of the α2-adrenergic receptors in the LPBN was partially dependent on GABAergic or opioidergic mechanisms in the LPBN. In rats submitted to the taste reactivity test to oral infusions of a 0.3 M sodium solution, the blockage serotonergic receptors into the LPBN enhanced positive hedonic taste reactivity patterns. In conclusion, previous and present results indicate opposite roles for α2-adrenergic receptors in the control of sodium and water intake according to their distribution in the rat brain. The α2-adrenergic activation into the LPBN produces a potent increase in hypertonic sodium intake during extracellular and cellular dehydration. These effects of α2-adrenergic activation into the LPBN is possibly due to the inhibitory serotoninergic mechanisms blockage into the LPBN and at least part of these effects is also dependent of an interaction with GABAergic and opioidergic mechanisms into the same area. Finally, the blockade of serotonergic receptors in the LPBN can enhance sodium palatability thus contributing to the increase in sodium intake during cell dehydration
Sushrut S Waikar - One of the best experts on this subject based on the ideXlab platform.
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association of predialysis calculated Plasma Osmolarity with intradialytic blood pressure decline
American Journal of Kidney Diseases, 2015Co-Authors: Finnian Mc R Causland, Sushrut S WaikarAbstract:Background The rapid reduction in Plasma osmolality during hemodialysis (HD) may induce temporary gradients that promote the movement of water from the extracellular to the intracellular compartment, predisposing to the development of intradialytic hypotension (IDH). Study Design Observational cohort study. Setting & Participants 3,142 prevalent patients receiving thrice-weekly HD from a single dialysis provider organization. Predictor Predialysis calculated Plasma Osmolarity (calculated after the 2-day interval as 2 × serum sodium + serum urea nitrogen/2.8 + serum glucose/18). Outcome Magnitude of systolic blood pressure (SBP) decline (predialysis SBP − nadir intradialytic SBP) and risk of IDH (SBP decline > 35 or nadir SBP Measurements Unadjusted and multivariable-adjusted generalized linear models were fit to estimate the association of calculated Osmolarity with intradialytic SBP decline and the odds of developing IDH. Results Mean age of participants was 62.6±15.2 (SD) years, 57.1% were men, and 61.0% had diabetes. Mean predialysis calculated Osmolarity during follow-up was 306.4 ± 9.5mOsm/L. After case-mix adjustment, each 10-mOsm/L increase in predialysis calculated Osmolarity was associated with 1.48 (95% CI, 0.86-2.09) mm Hg ( P Limitations Measured serum osmolality, timing of changes in intradialytic osmolality, dialysate osmolality, and dialysate temperature were not available. Conclusions Higher predialysis calculated Osmolarity is associated with greater decline in intradialytic SBP and greater risk of IDH in maintenance HD patients. Strategies to minimize rapid shifts in osmolality should be tested prospectively to minimize excess SBP decline in susceptible patients.
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Original Investigation Association of Predialysis Calculated Plasma Osmolarity With Intradialytic Blood Pressure Decline
2015Co-Authors: Finnian Mc R Causland, Sushrut S WaikarAbstract:Background: The rapid reduction in Plasma osmolality during hemodialysis (HD) may induce temporary gradients that promote the movement of water from the extracellular to the intracellular compartment, predisposing to the development of intradialytic hypotension (IDH). Study Design: Observational cohort study. Setting & Participants: 3,142 prevalent patients receiving thrice-weekly HD from a single dialysis provider organization. Predictor: Predialysis calculated Plasma Osmolarity (calculated after the 2-day interval as 2 3 serum sodium 1 serum urea nitrogen/2.8 1 serum glucose/18). Outcome: Magnitude of systolic blood pressure (SBP) decline (predialysis SBP 2 nadir intradialytic SBP) and risk of IDH (SBP decline . 35 or nadir SBP , 90 mm Hg). Measurements: Unadjusted and multivariable-adjusted generalized linear models were fit to estimate the association of calculated Osmolarity with intradialytic SBP decline and the odds of developing IDH. Results: Mean age of participants was 62.6 6 15.2 (SD) years, 57.1% were men, and 61.0% had diabetes. Mean predialysis calculated Osmolarity during follow-up was 306.4 6 9.5 mOsm/L. After case-mix adjustment, each 10-mOsm/L increase in predialysis calculated Osmolarity was associated with 1.48 (95% CI, 0.86-2.09) mm Hg (P , 0.001) greater decline in intradialytic SBP and 10% greater odds of IDH (OR, 1.10; 95% CI, 1.05-1.15). In adjusted models, lower predialysis sodium and higher serum urea nitrogen and serum glucose levels were associated with greater decline in intradialytic SBP. Limitations: Measured serum osmolality, timing of changes in intradialytic osmolality, dialysate osmolality, and dialysate temperature were not available. Conclusions: Higher predialysis calculated Osmolarity is associated with greater decline in intradialytic SBP and greater risk of IDH in maintenance HD patients. Strategies to minimize rapid shifts in osmolality should be tested prospectively to minimize excess SBP decline in susceptible patients. Am J Kidney Dis. 66(3):499-506. a 2015 by the National Kidney Foundation, Inc.
Finnian Mc R Causland - One of the best experts on this subject based on the ideXlab platform.
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association of predialysis calculated Plasma Osmolarity with intradialytic blood pressure decline
American Journal of Kidney Diseases, 2015Co-Authors: Finnian Mc R Causland, Sushrut S WaikarAbstract:Background The rapid reduction in Plasma osmolality during hemodialysis (HD) may induce temporary gradients that promote the movement of water from the extracellular to the intracellular compartment, predisposing to the development of intradialytic hypotension (IDH). Study Design Observational cohort study. Setting & Participants 3,142 prevalent patients receiving thrice-weekly HD from a single dialysis provider organization. Predictor Predialysis calculated Plasma Osmolarity (calculated after the 2-day interval as 2 × serum sodium + serum urea nitrogen/2.8 + serum glucose/18). Outcome Magnitude of systolic blood pressure (SBP) decline (predialysis SBP − nadir intradialytic SBP) and risk of IDH (SBP decline > 35 or nadir SBP Measurements Unadjusted and multivariable-adjusted generalized linear models were fit to estimate the association of calculated Osmolarity with intradialytic SBP decline and the odds of developing IDH. Results Mean age of participants was 62.6±15.2 (SD) years, 57.1% were men, and 61.0% had diabetes. Mean predialysis calculated Osmolarity during follow-up was 306.4 ± 9.5mOsm/L. After case-mix adjustment, each 10-mOsm/L increase in predialysis calculated Osmolarity was associated with 1.48 (95% CI, 0.86-2.09) mm Hg ( P Limitations Measured serum osmolality, timing of changes in intradialytic osmolality, dialysate osmolality, and dialysate temperature were not available. Conclusions Higher predialysis calculated Osmolarity is associated with greater decline in intradialytic SBP and greater risk of IDH in maintenance HD patients. Strategies to minimize rapid shifts in osmolality should be tested prospectively to minimize excess SBP decline in susceptible patients.
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Original Investigation Association of Predialysis Calculated Plasma Osmolarity With Intradialytic Blood Pressure Decline
2015Co-Authors: Finnian Mc R Causland, Sushrut S WaikarAbstract:Background: The rapid reduction in Plasma osmolality during hemodialysis (HD) may induce temporary gradients that promote the movement of water from the extracellular to the intracellular compartment, predisposing to the development of intradialytic hypotension (IDH). Study Design: Observational cohort study. Setting & Participants: 3,142 prevalent patients receiving thrice-weekly HD from a single dialysis provider organization. Predictor: Predialysis calculated Plasma Osmolarity (calculated after the 2-day interval as 2 3 serum sodium 1 serum urea nitrogen/2.8 1 serum glucose/18). Outcome: Magnitude of systolic blood pressure (SBP) decline (predialysis SBP 2 nadir intradialytic SBP) and risk of IDH (SBP decline . 35 or nadir SBP , 90 mm Hg). Measurements: Unadjusted and multivariable-adjusted generalized linear models were fit to estimate the association of calculated Osmolarity with intradialytic SBP decline and the odds of developing IDH. Results: Mean age of participants was 62.6 6 15.2 (SD) years, 57.1% were men, and 61.0% had diabetes. Mean predialysis calculated Osmolarity during follow-up was 306.4 6 9.5 mOsm/L. After case-mix adjustment, each 10-mOsm/L increase in predialysis calculated Osmolarity was associated with 1.48 (95% CI, 0.86-2.09) mm Hg (P , 0.001) greater decline in intradialytic SBP and 10% greater odds of IDH (OR, 1.10; 95% CI, 1.05-1.15). In adjusted models, lower predialysis sodium and higher serum urea nitrogen and serum glucose levels were associated with greater decline in intradialytic SBP. Limitations: Measured serum osmolality, timing of changes in intradialytic osmolality, dialysate osmolality, and dialysate temperature were not available. Conclusions: Higher predialysis calculated Osmolarity is associated with greater decline in intradialytic SBP and greater risk of IDH in maintenance HD patients. Strategies to minimize rapid shifts in osmolality should be tested prospectively to minimize excess SBP decline in susceptible patients. Am J Kidney Dis. 66(3):499-506. a 2015 by the National Kidney Foundation, Inc.
Craig E. Franklin - One of the best experts on this subject based on the ideXlab platform.
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freshwater to seawater acclimation of juvenile bull sharks carcharhinus leucas Plasma osmolytes and na k atpase activity in gill rectal gland kidney and intestine
Journal of Comparative Physiology B-biochemical Systemic and Environmental Physiology, 2005Co-Authors: Richard D. Pillans, Jonathan P Good, Gary W Anderson, Neil Hazon, Craig E. FranklinAbstract:This study examined the osmoregulatory status of the euryhaline elasmobranch Carcharhinus leucas acclimated to freshwater (FW) and seawater (SW). Juvenile C. leucas captured in FW (3 mOsm l−1 kg−1) were acclimated to SW (980–1,000 mOsm l−1 kg−1) over 16 days. A FW group was maintained in captivity over a similar time period. In FW, bull sharks were hyper-osmotic regulators, having a Plasma Osmolarity of 595 mOsm l−1 kg−1. In SW, bull sharks had significantly higher Plasma osmolarities (940 mOsm l−1 kg−1) than FW-acclimated animals and were slightly hypo-osmotic to the environment. Plasma Na+, Cl−, K+, Mg2+, Ca2+, urea and trimethylamine oxide (TMAO) concentrations were all significantly higher in bull sharks acclimated to SW, with urea and TMAO showing the greatest increase. Gill, rectal gland, kidney and intestinal tissue were taken from animals acclimated to FW and SW and analysed for maximal Na+/K+-ATPase activity. Na+/K+-ATPase activity in the gills and intestine was less than 1 mmol Pi mg−1 protein h−1 and there was no difference in activity between FW- and SW-acclimated animals. In contrast Na+/K+-ATPase activity in the rectal gland and kidney were significantly higher than gill and intestine and showed significant differences between the FW- and SW-acclimated groups. In FW and SW, rectal gland Na+/K+-ATPase activity was 5.6±0.8 and 9.2±0.6 mmol Pi mg−1 protein h−1, respectively. Na+/K+-ATPase activity in the kidney of FW and SW acclimated animals was 8.4±1.1 and 3.3±1.1 Pi mg−1 protein h−1, respectively. Thus juvenile bull sharks have the osmoregulatory plasticity to acclimate to SW; their preference for the upper reaches of rivers where salinity is low is therefore likely to be for predator avoidance and/or increased food abundance rather than because of a physiological constraint.
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Plasma osmolyte concentrations and rectal gland mass of bull sharks carcharhinus leucas captured along a salinity gradient
Comparative Biochemistry and Physiology A-molecular & Integrative Physiology, 2004Co-Authors: Richard D. Pillans, Craig E. FranklinAbstract:Bull sharks (Carcharhinus leucas) were captured across a salinity gradient from freshwater (FW) to seawater (SW). Across all salinities, C leucas were hyperosmotic to the environment. Plasma Osmolarity in FW-captured animals (642 +/- 7 mosM) was significantly reduced compared to SW-captured animals (1067 +/- 21 mosM). In FW animals, sodium, chloride and urea were 208 +/- 3, 203 +/- 3 and 192 +/- 2 mmol l(-1), respectively. Plasma sodium, chloride and urea in SW-captured C leucas were 289 +/- 3, 296 +/- 6 and 370 +/- 10 mmol l(-1), respectively. The increase in Plasma Osmolarity between FW and SW was not linear. Between FW (3 mosM) and 24%o SW (676 mosM), Plasma Osmolarity increased by 22% or 0.92% per 1parts per thousand rise in salinity. Between 24%o and 33parts per thousand, Plasma Osmolarity increased by 33% or 4.7% per 1 parts per thousand rise in salinity, largely due to a sharp increase in Plasma urea between 28parts per thousand and 33parts per thousand. C. leucas moving between FW and SW appear to be faced with three major osmoregulatory challenges, these occur between 0-10parts per thousand, 11-20parts per thousand and 21-33parts per thousand. A comparison between C leucas captured in FW and estuarine environments (20-28%o) in the Brisbane River revealed no difference in the mass of rectal glands between these animals. However, a comparison of rectal gland mass between FW animals captured in the Brisbane River and Rio San Juan/Lake Nicaragua showed that animals in the latter system had a significantly smaller rectal gland mass at a given length than animals in the Brisbane River. The physiological challenges and mechanisms required for C leucas moving between FW and SW, as well as the ecological implications of these data are discussed. (C) 2004 Elsevier Inc. All rights reserved.
H Takahashi - One of the best experts on this subject based on the ideXlab platform.
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the correlation between Plasma Osmolarity and tear Osmolarity
International Ophthalmology, 2018Co-Authors: Maika Kobayashi, Chiaki Fujimoto, Hisaharu Suzuki, Tsutomu Igarashi, H TakahashiAbstract:Purpose To the correlation between Plasma Osmolarity (Posm) and tear Osmolarity (Tosm) in patients (54 patients, 88 eyes) who underwent cataract surgery was evaluated.