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Gesche Jurgens - One of the best experts on this subject based on the ideXlab platform.

  • effects of low Sodium Diet versus High Sodium Diet on blood pressure renin aldosterone catecholamines cholesterol and triglyceride
    Cochrane Database of Systematic Reviews, 2017
    Co-Authors: Niels Graudal, Thorbjorn Hubeckgraudal, Gesche Jurgens
    Abstract:

    Background In spite of more than 100 years of investigations the question of whether a reduced Sodium intake improves health is still unsolved. Objectives To estimate the effects of low Sodium intake versus High Sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol, High-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglycerides. Search methods The Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials up to March 2016: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL) (2016, Issue 3), MEDLINE (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We also searched the reference lists of relevant articles. Selection criteria Studies randomising persons to low-Sodium and High-Sodium Diets were included if they evaluated at least one of the above outcome parameters. Data collection and analysis Two review authors independently collected data, which were analysed with Review Manager 5.3. Main results A total of 185 studies were included. The average Sodium intake was reduced from 201 mmol/day (corresponding to High usual level) to 66 mmol/day (corresponding to the recommended level). The effect of Sodium reduction on blood pressure (BP) was as follows: white people with normotension: SBP: mean difference (MD) -1.09 mmHg (95% confidence interval (CI): -1.63 to -0.56; P = 0.0001); 89 studies, 8569 participants; DBP: + 0.03 mmHg (MD 95% CI: -0.37 to 0.43; P = 0.89); 90 studies, 8833 participants. High-quality evidence. Black people with normotension: SBP: MD -4.02 mmHg (95% CI:-7.37 to -0.68; P = 0.002); seven studies, 506 participants; DBP: MD -2.01 mmHg (95% CI:-4.37 to 0.35; P = 0.09); seven studies, 506 participants. Moderate-quality evidence. Asian people with normotension: SBP: MD -0.72 mmHg (95% CI: -3.86 to 2.41; P = 0.65); DBP: MD -1.63 mmHg (95% CI:-3.35 to 0.08; P =0.06); three studies, 393 participants. Moderate-quality evidence. White people with hypertension: SBP: MD -5.51 mmHg (95% CI: -6.45 to -4.57; P < 0.00001); 84 studies, 5925 participants; DBP: MD -2.88 mmHg (95% CI: -3.44 to -2.32; P < 0.00001); 85 studies, 6001 participants. High-quality evidence. Black people with hypertension: SBP MD -6.64 mmHg (95% CI:-9.00 to -4.27; P = 0.00001); eight studies, 619 participants; DBP -2.91 mmHg (95% CI:-4.52, -1.30; P = 0.0004); eight studies, 619 participants. Moderate-quality evidence. Asian people with hypertension: SBP: MD -7.75 mmHg (95% CI:-11,44 to -4.07; P < 0.0001) nine studies, 501 participants; DBP: MD -2.68 mmHg (95% CI: -4.21 to -1.15; P = 0.0006). Moderate-quality evidence. In plasma or serum, there was a significant increase in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.03), cholesterol (P < 0.0005) and triglyceride (P < 0.0006) with low Sodium intake as compared with High Sodium intake. All effects were stable in 125 study populations with a Sodium intake below 250 mmol/day and a Sodium reduction intervention of at least one week. Authors' conclusions Sodium reduction from an average High usual Sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. A few studies showed that these effects in black and Asian populations were greater. The effects on hormones and lipids were similar in people with normotension and hypertension. Renin increased 1.60 ng/mL/hour (55%); aldosterone increased 97.81 pg/mL (127%); adrenalin increased 7.55 pg/mL (14%); noradrenalin increased 63.56 pg/mL: (27%); cholesterol increased 5.59 mg/dL (2.9%); triglyceride increased 7.04 mg/dL (6.3%).

  • effects of low Sodium Diet vs High Sodium Diet on blood pressure renin aldosterone catecholamines cholesterol and triglyceride cochrane review
    American Journal of Hypertension, 2012
    Co-Authors: Niels Graudal, Thorbjorn Hubeckgraudal, Gesche Jurgens
    Abstract:

    BACKGROUND The question of whether reduced Sodium intake is effective as a health prophylaxis initiative is unsolved. The purpose was to estimate the effects of low-Sodium vs. High-Sodium intake on blood pressure (BP), renin, aldosterone, catecholamines, and lipids. METHODS Studies randomizing persons to low-Sodium and High-Sodium Diets evaluating at least one of the above outcome parameters were included. Data were analyzed with Review Manager 5.1. RESULTS A total of 167 studies were included. The effect of Sodium reduction in: (i) Normotensives: Caucasians: systolic BP (SBP) -1.27 mm Hg (95% confidence interval (CI): -1.88, -0.66; P = 0.0001), diastolic BP (DBP) -0.05 mm Hg (95% CI: -0.51, 0.42; P = 0.85). Blacks: SBP -4.02 mm Hg (95% CI: -7.37, -0.68; P = 0.002), DBP -2.01 mm Hg (95% CI: -4.37, 0.35; P = 0.09). Asians: SBP -1.27 mm Hg (95% CI: -3.07, 0.54; P = 0.17), DBP -1.68 mm Hg (95% CI: -3.29, -0.06; P = 0.04). (ii) Hypertensives: Caucasians: SBP -5.48 mm Hg (95% CI: -6.53, -4.43; P < 0.00001), DBP -2.75 mm Hg (95% CI: -3.34, -2.17; P < 0.00001). Blacks: SBP -6.44 mm Hg (95% CI: -8.85, -4.03; P = 0.00001), DBP -2.40 mm Hg (95% CI: -4.68, -0.12; P = 0.04). Asians: SBP -10.21 mm Hg (95% CI: -16.98, -3.44; P = 0.003), DBP -2.60 mm Hg (95% CI: -4.03, -1.16; P = 0.0004). Sodium reduction resulted in significant increases in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.0002), cholesterol (P < 0.001), and triglyceride (P < 0.0008). CONCLUSIONS Sodium reduction resulted in a significant decrease in BP of 1% (normotensives), 3.5% (hypertensives), and a significant increase in plasma renin, plasma aldosterone, plasma adrenaline, and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride.

Ulla C Kopp - One of the best experts on this subject based on the ideXlab platform.

  • role of renal sensory nerves in physiological and pathophysiological conditions
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2015
    Co-Authors: Ulla C Kopp
    Abstract:

    Whether activation of afferent renal nerves contributes to the regulation of arterial pressure and Sodium balance has been long overlooked. In normotensive rats, activating renal mechanosensory nerves decrease efferent renal sympathetic nerve activity (ERSNA) and increase urinary Sodium excretion, an inhibitory renorenal reflex. There is an interaction between efferent and afferent renal nerves, whereby increases in ERSNA increase afferent renal nerve activity (ARNA), leading to decreases in ERSNA by activation of the renorenal reflexes to maintain low ERSNA to minimize Sodium retention. High-Sodium Diet enhances the responsiveness of the renal sensory nerves, while low Dietary Sodium reduces the responsiveness of the renal sensory nerves, thus producing physiologically appropriate responses to maintain Sodium balance. Increased renal ANG II reduces the responsiveness of the renal sensory nerves in physiological and pathophysiological conditions, including hypertension, congestive heart failure, and ischemia-induced acute renal failure. Impairment of inhibitory renorenal reflexes in these pathological states would contribute to the hypertension and Sodium retention. When the inhibitory renorenal reflexes are suppressed, excitatory reflexes may prevail. Renal denervation reduces arterial pressure in experimental hypertension and in treatment-resistant hypertensive patients. The fall in arterial pressure is associated with a fall in muscle sympathetic nerve activity, suggesting that increased ARNA contributes to increased arterial pressure in these patients. Although removal of both renal sympathetic and afferent renal sensory nerves most likely contributes to the arterial pressure reduction initially, additional mechanisms may be involved in long-term arterial pressure reduction since sympathetic and sensory nerves reinnervate renal tissue in a similar time-dependent fashion following renal denervation.

  • Dietary Sodium modulates the interaction between efferent and afferent renal nerve activity by altering activation of α2 adrenoceptors on renal sensory nerves
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2011
    Co-Authors: Ulla C Kopp, Mika Scheinin, Michael Z Cicha, Lori A Smith, Saku Ruohonen, Nicolas Fritz, Tomas Hokfelt
    Abstract:

    Activation of efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which then reflexively decreases ERSNA via activation of the renorenal reflexes to maintain low ERSNA. The ERSNA-ARNA interaction is mediated by norepinephrine (NE) that increases and decreases ARNA by activation of renal α1-and α2-adrenoceptors (AR), respectively. The ERSNA-induced increases in ARNA are suppressed during a low-Sodium (2,470 ± 770% s) and enhanced during a High-Sodium Diet (5,670 ± 1,260% s). We examined the role of α2-AR in modulating the responsiveness of renal sensory nerves during low- and High-Sodium Diets. Immunohistochemical analysis suggested the presence of α2A-AR and α2C-AR subtypes on renal sensory nerves. During the low-Sodium Diet, renal pelvic administration of the α2-AR antagonist rauwolscine or the AT1 receptor antagonist losartan alone failed to alter the ARNA responses to reflex increases in ERSNA. Likewise, renal pelvic release of substance P produced by 250 pM NE (from 8.0 ± 1.3 to 8.5 ± 1.6 pg/min) was not affected by rauwolscine or losartan alone. However, rauwolscine+losartan enhanced the ARNA responses to reflex increases in ERSNA (4,680 ± 1,240%·s), and renal pelvic release of substance P by 250 pM NE, from 8.3 ± 0.6 to 14.2 ± 0.8 pg/min. During a High-Sodium Diet, rauwolscine had no effect on the ARNA response to reflex increases in ERSNA or renal pelvic release of substance P produced by NE. Losartan was not examined because of low endogenous ANG II levels in renal pelvic tissue during a High-Sodium Diet. Increased activation of α2-AR contributes to the reduced interaction between ERSNA and ARNA during low-Sodium intake, whereas no/minimal activation of α2-AR contributes to the enhanced ERSNA-ARNA interaction under conditions of High Sodium intake.

  • afferent renal denervation impairs baroreflex control of efferent renal sympathetic nerve activity
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2008
    Co-Authors: Ulla C Kopp, Susan Y Jones, Gerald F Dibona
    Abstract:

    Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which decreases ERSNA to prevent Sodium retention. High-Sodium Diet enhances ARNA, suggesting an important role for ARNA in suppressing ERSNA during excess Sodium intake. Mean arterial pressure (MAP) is elevated in afferent renal denervated by dorsal rhizotomy (DRX) rats fed High-Sodium Diet. We examined whether the increased MAP in DRX is due to impaired arterial baroreflex function. In DRX and sham DRX rats fed High-Sodium Diet, arterial baroreflex function was determined in conscious rats by intravenous nitroprusside and phenylephrine or calculation of transfer function gain from arterial pressure to ERSNA (spontaneous baroreflex sensitivity). Increasing MAP did not suppress ERSNA to the same extent in DRX as in sham DRX, −60 ± 4 vs. −77 ± 6%. Maximum gain, −4.22 ± 0.45 vs. −6.04 ± 0.90% ΔERSNA/mmHg, and the maximum value of instantaneous gain, −4.19 ± 0.45 vs. −6.04 ± 0.81% ΔERSNA/mmHg, were less in DRX than in sham DRX. Likewise, transfer function gain was lower in DRX than in sham DRX, 3.9 ± 0.2 vs. 6.1 ± 0.5 NU/mmHg. Air jet stress produced greater increases in ERSNA in DRX than in sham DRX, 35,000 ± 4,900 vs. 20,900 ± 3,410%·s (area under the curve). Likewise, the ERSNA responses to thermal cutaneous stimulation were greater in DRX than in sham DRX. These studies suggest impaired arterial baroreflex suppression of ERSNA in DRX fed High-Sodium Diet. There were no differences in arterial baroreflex function in DRX and sham DRX fed normal-Sodium Diet. Impaired arterial baroreflex function contributes to increased ERSNA, which would eventually lead to Sodium retention and increased MAP in DRX rats fed High-Sodium Diet.

  • differential effects of endothelin on activation of renal mechanosensory nerves stimulatory in High Sodium Diet and inhibitory in low Sodium Diet
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2006
    Co-Authors: Ulla C Kopp, Michael Z Cicha, Lori A Smith
    Abstract:

    Activation of renal mechanosensory nerves is enhanced by High and suppressed by low Sodium Dietary intake. Afferent renal denervation results in salt-sensitive hypertension, suggesting that activat...

Niels Graudal - One of the best experts on this subject based on the ideXlab platform.

  • effects of low Sodium Diet versus High Sodium Diet on blood pressure renin aldosterone catecholamines cholesterol and triglyceride
    Cochrane Database of Systematic Reviews, 2017
    Co-Authors: Niels Graudal, Thorbjorn Hubeckgraudal, Gesche Jurgens
    Abstract:

    Background In spite of more than 100 years of investigations the question of whether a reduced Sodium intake improves health is still unsolved. Objectives To estimate the effects of low Sodium intake versus High Sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol, High-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglycerides. Search methods The Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials up to March 2016: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL) (2016, Issue 3), MEDLINE (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We also searched the reference lists of relevant articles. Selection criteria Studies randomising persons to low-Sodium and High-Sodium Diets were included if they evaluated at least one of the above outcome parameters. Data collection and analysis Two review authors independently collected data, which were analysed with Review Manager 5.3. Main results A total of 185 studies were included. The average Sodium intake was reduced from 201 mmol/day (corresponding to High usual level) to 66 mmol/day (corresponding to the recommended level). The effect of Sodium reduction on blood pressure (BP) was as follows: white people with normotension: SBP: mean difference (MD) -1.09 mmHg (95% confidence interval (CI): -1.63 to -0.56; P = 0.0001); 89 studies, 8569 participants; DBP: + 0.03 mmHg (MD 95% CI: -0.37 to 0.43; P = 0.89); 90 studies, 8833 participants. High-quality evidence. Black people with normotension: SBP: MD -4.02 mmHg (95% CI:-7.37 to -0.68; P = 0.002); seven studies, 506 participants; DBP: MD -2.01 mmHg (95% CI:-4.37 to 0.35; P = 0.09); seven studies, 506 participants. Moderate-quality evidence. Asian people with normotension: SBP: MD -0.72 mmHg (95% CI: -3.86 to 2.41; P = 0.65); DBP: MD -1.63 mmHg (95% CI:-3.35 to 0.08; P =0.06); three studies, 393 participants. Moderate-quality evidence. White people with hypertension: SBP: MD -5.51 mmHg (95% CI: -6.45 to -4.57; P < 0.00001); 84 studies, 5925 participants; DBP: MD -2.88 mmHg (95% CI: -3.44 to -2.32; P < 0.00001); 85 studies, 6001 participants. High-quality evidence. Black people with hypertension: SBP MD -6.64 mmHg (95% CI:-9.00 to -4.27; P = 0.00001); eight studies, 619 participants; DBP -2.91 mmHg (95% CI:-4.52, -1.30; P = 0.0004); eight studies, 619 participants. Moderate-quality evidence. Asian people with hypertension: SBP: MD -7.75 mmHg (95% CI:-11,44 to -4.07; P < 0.0001) nine studies, 501 participants; DBP: MD -2.68 mmHg (95% CI: -4.21 to -1.15; P = 0.0006). Moderate-quality evidence. In plasma or serum, there was a significant increase in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.03), cholesterol (P < 0.0005) and triglyceride (P < 0.0006) with low Sodium intake as compared with High Sodium intake. All effects were stable in 125 study populations with a Sodium intake below 250 mmol/day and a Sodium reduction intervention of at least one week. Authors' conclusions Sodium reduction from an average High usual Sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. A few studies showed that these effects in black and Asian populations were greater. The effects on hormones and lipids were similar in people with normotension and hypertension. Renin increased 1.60 ng/mL/hour (55%); aldosterone increased 97.81 pg/mL (127%); adrenalin increased 7.55 pg/mL (14%); noradrenalin increased 63.56 pg/mL: (27%); cholesterol increased 5.59 mg/dL (2.9%); triglyceride increased 7.04 mg/dL (6.3%).

  • effects of low Sodium Diet vs High Sodium Diet on blood pressure renin aldosterone catecholamines cholesterol and triglyceride cochrane review
    American Journal of Hypertension, 2012
    Co-Authors: Niels Graudal, Thorbjorn Hubeckgraudal, Gesche Jurgens
    Abstract:

    BACKGROUND The question of whether reduced Sodium intake is effective as a health prophylaxis initiative is unsolved. The purpose was to estimate the effects of low-Sodium vs. High-Sodium intake on blood pressure (BP), renin, aldosterone, catecholamines, and lipids. METHODS Studies randomizing persons to low-Sodium and High-Sodium Diets evaluating at least one of the above outcome parameters were included. Data were analyzed with Review Manager 5.1. RESULTS A total of 167 studies were included. The effect of Sodium reduction in: (i) Normotensives: Caucasians: systolic BP (SBP) -1.27 mm Hg (95% confidence interval (CI): -1.88, -0.66; P = 0.0001), diastolic BP (DBP) -0.05 mm Hg (95% CI: -0.51, 0.42; P = 0.85). Blacks: SBP -4.02 mm Hg (95% CI: -7.37, -0.68; P = 0.002), DBP -2.01 mm Hg (95% CI: -4.37, 0.35; P = 0.09). Asians: SBP -1.27 mm Hg (95% CI: -3.07, 0.54; P = 0.17), DBP -1.68 mm Hg (95% CI: -3.29, -0.06; P = 0.04). (ii) Hypertensives: Caucasians: SBP -5.48 mm Hg (95% CI: -6.53, -4.43; P < 0.00001), DBP -2.75 mm Hg (95% CI: -3.34, -2.17; P < 0.00001). Blacks: SBP -6.44 mm Hg (95% CI: -8.85, -4.03; P = 0.00001), DBP -2.40 mm Hg (95% CI: -4.68, -0.12; P = 0.04). Asians: SBP -10.21 mm Hg (95% CI: -16.98, -3.44; P = 0.003), DBP -2.60 mm Hg (95% CI: -4.03, -1.16; P = 0.0004). Sodium reduction resulted in significant increases in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.0002), cholesterol (P < 0.001), and triglyceride (P < 0.0008). CONCLUSIONS Sodium reduction resulted in a significant decrease in BP of 1% (normotensives), 3.5% (hypertensives), and a significant increase in plasma renin, plasma aldosterone, plasma adrenaline, and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride.

Lawrence J Appel - One of the best experts on this subject based on the ideXlab platform.

  • the relationship between urine uromodulin and blood pressure changes the dash Sodium trial
    American Journal of Hypertension, 2021
    Co-Authors: Cheryl A M Anderson, Lawrence J Appel, Edgar R Miller, Stephen P Juraschek, Christine Y Bakhoum, Casey M Rebholz, Chirag R Parikh, Wassim Obeid, Dena E Rifkin
    Abstract:

    Background Uromodulin modulates the Sodium-potassium-two-chloride transporter in the thick ascending limb of the loop of Henle, and its overexpression in murine models leads to salt-induced hypertension. We hypothesized that individuals with Higher baseline levels of urine uromodulin would have a greater increase in systolic blood pressure (SBP) for the same increase in Sodium compared with those with lower uromodulin levels. Methods We used data from 157 subjects randomized to the control Diet of the Dietary Approaches to Stop Hypertension (DASH)-Sodium trial who were assigned to 30 days of low (1,500 mg/d), medium (2,400 mg/d), and High salt (3,300 mg/d) Diets in random order. Blood pressure was measured prerandomization and then weekly during each feeding period. We evaluated the association of prerandomization urine uromodulin with change in SBP between Diets, as measured at the end of each feeding period, using multivariable linear regression. Results Baseline urine uromodulin stratified by tertiles was ≤17.64, 17.65-31.97, and ≥31.98 µg/ml. Across the tertiles, there were no significant differences in SBP at baseline, nor was there a differential effect of Sodium Diet on SBP across tertiles (low to High, P = 0.81). After adjusting for age, sex, body mass index, and race, uromodulin levels were not significantly associated with SBP change from low to High Sodium Diet (P = 0.42). Conclusions In a randomized trial of different levels of salt intake, Higher urine uromodulin levels were not associated with a greater increase in blood pressure in response to High salt intake.

  • time course of change in blood pressure from Sodium reduction and the dash Diet
    Hypertension, 2017
    Co-Authors: Mark Woodward, Frank M Sacks, Edgar R Miller, Stephen P Juraschek, Vincent J Carey, Lawrence J Appel
    Abstract:

    Both Sodium reduction and the Dietary Approaches to Stop Hypertension (DASH) Diet lower blood pressure (BP); however, the patterns of their effects on BP over time are unknown. In the DASH-Sodium trial, adults with pre-/stage 1 hypertension, not using antihypertensive medications, were randomly assigned to either a typical American Diet (control) or DASH. Within their assigned Diet, participants randomly ate each of 3 Sodium levels (50, 100, and 150 mmol/d, at 2100 kcal) over 4-week periods. BP was measured weekly for 12 weeks; 412 participants enrolled (57% women; 57% black; mean age, 48 years; mean systolic BP [SBP]/diastolic BP [DBP], 135/86 mm Hg). For those assigned control, there was no change in SBP/DBP between weeks 1 and 4 on the High-Sodium Diet (weekly change, −0.04/0.06 mm Hg/week) versus a progressive decline in BP on the low-Sodium Diet (−0.94/−0.70 mm Hg/week; P interactions between time and Sodium P interactions between time and Sodium=0.56 for SBP and 0.10 for DBP). When comparing DASH to control, DASH changed SBP/DBP by −4.36/−1.07 mm Hg after 1 week, which accounted for most of the effect observed, with no significant difference in weekly rates of change for either SBP ( P interaction=0.97) or DBP ( P interaction=0.70). In the context of a typical American Diet, a low-Sodium Diet reduced BP without plateau, suggesting that the full effects of Sodium reduction are not completely achieved by 4 weeks. In contrast, compared with control, DASH lowers BP within a week without further effect thereafter. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00000608.

  • individual variation in urinary Sodium excretion among adolescent girls on a fixed intake
    Journal of Hypertension, 2016
    Co-Authors: Connie M Weaver, Berdine R Martin, George P Mccabe, Linda D Mccabe, Mark Woodward, Cheryl A M Anderson, Lawrence J Appel
    Abstract:

    BACKGROUND According to traditional understanding of Sodium homeostasis, nearly all of daily Sodium intake is excreted in urine, with intraindividual variability attributed to variability in Dietary Sodium intake and urine collection errors. OBJECTIVE To analyze the variability of urinary Sodium in excretion from a balance study with fixed Sodium intakes. METHODS Daily 24-h urine collections were assessed for Sodium, potassium, and creatinine in 22 black and 13 white adolescent girls (11-15 year, BMI 15-29 kg/m) in a randomized, crossover design with controlled Diets containing either low (57 mmol/day) or High (167 mmol/day) Sodium, each fed for 3 weeks. RESULTS Coefficient of variation analysis indicated Higher variation in urinary Sodium excretion about the mean on low (vs High) Sodium (40 vs 32%, P = 0.02) and in black (vs white) girls (42 vs 30%, P < 0.001). A mixed model showed no Sodium intake × race interaction. Urinary Sodium excretion was not correlated with urinary potassium or creatinine excretion. Excretion of 65 mmol/day (adequate intake) or less was documented on 16% on the days during the High-Sodium Diet. Reliability of the mean of several urine Sodium samples varied from 23% for one sample to 75% for 10 samples for the High-Sodium Diet. CONCLUSION The High intraindividual variability in urinary Sodium excretion on a fixed Diet Highlights the potential for substantial error in (a) using a single 24-h urine collection to estimate an individual's usual Sodium intake and (b) relating Sodium excretion from a single 24-h collection with outcomes. Further research is warranted to understand the causes of such variation.

  • Effects of Sodium intake and Diet on racial differences in urinary potassium excretion: Results from the Dietary approaches to stop hypertension (DASH)-Sodium trial
    American journal of kidney diseases : the official journal of the National Kidney Foundation, 2012
    Co-Authors: Sharon Turban, Carol B. Thompson, Rulan S. Parekh, Lawrence J Appel
    Abstract:

    Background We previously showed that African Americans excreted less urinary potassium than whites, even while consuming similar Diets in the Dietary Approaches to Stop Hypertension (DASH) trial. We hypothesized that a low-Sodium Diet may eliminate these differences. Study Design Data from the DASH-Sodium randomized controlled feeding trial were analyzed. Setting & Participants 412 adults with prehypertension or stage 1 hypertension. Intervention Random assignment to either a typical American "control" Diet (1.7 g [43 mEq] potassium/2,100 kcal/d) or the DASH Diet (4.1 g [105 mEq] potassium/2,100 kcal/d). Within each Diet, participants received 3 levels of Sodium intake in random order for 30 days. Outcomes & Measurements 24-hour urine samples were analyzed at the end of each period. The primary outcome was urinary potassium excretion. Results On the DASH Diet, African Americans consistently excreted significantly less urinary potassium (mean 24-hour urinary potassium excretion, 2,594 ± 961 mg [66 ± 25 mEq]) than whites (3,412 ± 1,016 mg [87 ± 26 mEq]) at the Highest Sodium level; adjusted ( P P = 0.6 comparing white to African American difference in urinary potassium excretion on High- vs low-Sodium Diet). In contrast, there was a smaller but significant white−African American difference in mean daily urinary potassium excretion in participants fed the control/High-Sodium Diet that was not present in the control/low-Sodium Diet (adjusted differences of 281 mg [7 mEq]/d vs 20 mg [0.5 mEq]/d, respectively; P = 0.007). Significant interactions were found between race and Diet ( P P = 0.02). Limitations Single rather than multiple urine collections were available at each time. Lack of stool potassium and sweat potassium values. Conclusions Racial differences in urinary potassium excretion depend on Sodium intake and Diet. Our results may help explain the previously documented large variability in urinary potassium excretion.

Thorbjorn Hubeckgraudal - One of the best experts on this subject based on the ideXlab platform.

  • effects of low Sodium Diet versus High Sodium Diet on blood pressure renin aldosterone catecholamines cholesterol and triglyceride
    Cochrane Database of Systematic Reviews, 2017
    Co-Authors: Niels Graudal, Thorbjorn Hubeckgraudal, Gesche Jurgens
    Abstract:

    Background In spite of more than 100 years of investigations the question of whether a reduced Sodium intake improves health is still unsolved. Objectives To estimate the effects of low Sodium intake versus High Sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol, High-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglycerides. Search methods The Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials up to March 2016: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL) (2016, Issue 3), MEDLINE (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We also searched the reference lists of relevant articles. Selection criteria Studies randomising persons to low-Sodium and High-Sodium Diets were included if they evaluated at least one of the above outcome parameters. Data collection and analysis Two review authors independently collected data, which were analysed with Review Manager 5.3. Main results A total of 185 studies were included. The average Sodium intake was reduced from 201 mmol/day (corresponding to High usual level) to 66 mmol/day (corresponding to the recommended level). The effect of Sodium reduction on blood pressure (BP) was as follows: white people with normotension: SBP: mean difference (MD) -1.09 mmHg (95% confidence interval (CI): -1.63 to -0.56; P = 0.0001); 89 studies, 8569 participants; DBP: + 0.03 mmHg (MD 95% CI: -0.37 to 0.43; P = 0.89); 90 studies, 8833 participants. High-quality evidence. Black people with normotension: SBP: MD -4.02 mmHg (95% CI:-7.37 to -0.68; P = 0.002); seven studies, 506 participants; DBP: MD -2.01 mmHg (95% CI:-4.37 to 0.35; P = 0.09); seven studies, 506 participants. Moderate-quality evidence. Asian people with normotension: SBP: MD -0.72 mmHg (95% CI: -3.86 to 2.41; P = 0.65); DBP: MD -1.63 mmHg (95% CI:-3.35 to 0.08; P =0.06); three studies, 393 participants. Moderate-quality evidence. White people with hypertension: SBP: MD -5.51 mmHg (95% CI: -6.45 to -4.57; P < 0.00001); 84 studies, 5925 participants; DBP: MD -2.88 mmHg (95% CI: -3.44 to -2.32; P < 0.00001); 85 studies, 6001 participants. High-quality evidence. Black people with hypertension: SBP MD -6.64 mmHg (95% CI:-9.00 to -4.27; P = 0.00001); eight studies, 619 participants; DBP -2.91 mmHg (95% CI:-4.52, -1.30; P = 0.0004); eight studies, 619 participants. Moderate-quality evidence. Asian people with hypertension: SBP: MD -7.75 mmHg (95% CI:-11,44 to -4.07; P < 0.0001) nine studies, 501 participants; DBP: MD -2.68 mmHg (95% CI: -4.21 to -1.15; P = 0.0006). Moderate-quality evidence. In plasma or serum, there was a significant increase in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.03), cholesterol (P < 0.0005) and triglyceride (P < 0.0006) with low Sodium intake as compared with High Sodium intake. All effects were stable in 125 study populations with a Sodium intake below 250 mmol/day and a Sodium reduction intervention of at least one week. Authors' conclusions Sodium reduction from an average High usual Sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. A few studies showed that these effects in black and Asian populations were greater. The effects on hormones and lipids were similar in people with normotension and hypertension. Renin increased 1.60 ng/mL/hour (55%); aldosterone increased 97.81 pg/mL (127%); adrenalin increased 7.55 pg/mL (14%); noradrenalin increased 63.56 pg/mL: (27%); cholesterol increased 5.59 mg/dL (2.9%); triglyceride increased 7.04 mg/dL (6.3%).

  • effects of low Sodium Diet vs High Sodium Diet on blood pressure renin aldosterone catecholamines cholesterol and triglyceride cochrane review
    American Journal of Hypertension, 2012
    Co-Authors: Niels Graudal, Thorbjorn Hubeckgraudal, Gesche Jurgens
    Abstract:

    BACKGROUND The question of whether reduced Sodium intake is effective as a health prophylaxis initiative is unsolved. The purpose was to estimate the effects of low-Sodium vs. High-Sodium intake on blood pressure (BP), renin, aldosterone, catecholamines, and lipids. METHODS Studies randomizing persons to low-Sodium and High-Sodium Diets evaluating at least one of the above outcome parameters were included. Data were analyzed with Review Manager 5.1. RESULTS A total of 167 studies were included. The effect of Sodium reduction in: (i) Normotensives: Caucasians: systolic BP (SBP) -1.27 mm Hg (95% confidence interval (CI): -1.88, -0.66; P = 0.0001), diastolic BP (DBP) -0.05 mm Hg (95% CI: -0.51, 0.42; P = 0.85). Blacks: SBP -4.02 mm Hg (95% CI: -7.37, -0.68; P = 0.002), DBP -2.01 mm Hg (95% CI: -4.37, 0.35; P = 0.09). Asians: SBP -1.27 mm Hg (95% CI: -3.07, 0.54; P = 0.17), DBP -1.68 mm Hg (95% CI: -3.29, -0.06; P = 0.04). (ii) Hypertensives: Caucasians: SBP -5.48 mm Hg (95% CI: -6.53, -4.43; P < 0.00001), DBP -2.75 mm Hg (95% CI: -3.34, -2.17; P < 0.00001). Blacks: SBP -6.44 mm Hg (95% CI: -8.85, -4.03; P = 0.00001), DBP -2.40 mm Hg (95% CI: -4.68, -0.12; P = 0.04). Asians: SBP -10.21 mm Hg (95% CI: -16.98, -3.44; P = 0.003), DBP -2.60 mm Hg (95% CI: -4.03, -1.16; P = 0.0004). Sodium reduction resulted in significant increases in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.0002), cholesterol (P < 0.001), and triglyceride (P < 0.0008). CONCLUSIONS Sodium reduction resulted in a significant decrease in BP of 1% (normotensives), 3.5% (hypertensives), and a significant increase in plasma renin, plasma aldosterone, plasma adrenaline, and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride.