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1.
Characteristics of sodium sensitivity in Korean populations.
Shin, SJ, Lim, CY, Rhee, MY, Oh, SW, Na, SH, Park, Y, Kim, CI, Kim, SY, Kim, JW, Park, HK
Journal of Korean medical science. 2011;(8):1061-7
Abstract
Sodium sensitivity (SS) is a variable response of blood pressure (BP) to changes in sodium intake. The present study evaluated the existence and the characteristics of subjects with SS in Koreans. One hundred one subjects with (n = 31, 57.7 ± 9.8 yr) or without hypertension (n = 70, 40.8 ± 16.5 yr) were given a low-sodium dietary approache to stop hypertension (DASH) diet (LSD) for 7 days and a high-sodium DASH diet (HSD) for the following 7 days. The prevalence of SS in the present study population was 27.7% (17.6% in the non-hypertensive subjects and 51.6% in the hypertensive subjects). Analysis of the non-hypertensive subjects showed that systolic BP, diastolic BP, and mean arterial pressure at baseline and after HSD were higher in the subjects with SS than the subjects without SS, and there were no differences after LSD. In the hypertensive subjects, there was no difference in the BP at baseline and after HSD whether or not the subjects had SS. However, the systolic BP of hypertensive subjects with SS was lower than hypertensive subjects without SS after LSD. In the present study population, subjects with SS have distinctive BP features unlike to subjects without SS.
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2.
Dietary sodium restriction and beta2-adrenergic receptor polymorphism modulate cardiovascular function in humans.
Eisenach, JH, Schroeder, DR, Pike, TL, Johnson, CP, Schrage, WG, Snyder, EM, Johnson, BD, Garovic, VD, Turner, ST, Joyner, MJ
The Journal of physiology. 2006;(Pt 3):955-65
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Abstract
Dietary Na+ intake influences beta2-adrenergic receptor (beta2AR) responsiveness. While receiving a normal Na+ diet (150 mmol day(-1)), subjects homozygous for glycine at amino acid 16 (Gly16) have greater forearm beta2AR-mediated vasodilatation than subjects homozygous for arginine (Arg16), an effect that is mediated by endothelial NO. We tested the hypothesis that dietary Na+ restriction eliminates genotype differences in forearm and systemic beta2AR-mediated dilatation in these groups. We measured heart rate, mean arterial pressure and cardiac output (CO, acetylene breathing) responses to administration of intravenous terbutaline (TRB) before and after 5 days of low dietary Na+ intake (10 mmol day(-1)) in healthy Gly16 (n = 17; age, 31 +/- 7 year) and Arg16 homozygotes (n = 15; age, 29 +/- 8 year). After the low-Na+ diet, a catheter was placed in the brachial artery to measure forearm blood flow (FBF, plethysmography) responses to administration of isoprenaline (isoproterenol) before and after NO inhibition with NG-mono-methyl-L-arginine (L-NMMA). In the Gly16 group, the low-Na+ diet decreased baseline CO from 6.4 +/- 1.4 to 5.5 +/- 1.2 l min(-1) (P = 0.003, paired t test), tended to decrease stroke volume from 97.0 +/- 20.6 to 86.9 +/- 21.7 ml (P = 0.06) and increased peripheral resistance from 1106 +/- 246 to 1246 +/- 222 dynes s cm(-5) (P = 0.02); significant effects of the low-Na+ diet were not observed in Arg16 subjects. In a repeated measures ANOVA, the responses of all cardiovascular measures to systemic administration of TRB were not influenced by genotype or diet. Additionally, the FBF response to incremental doses of isoprenaline did not differ between genotype groups before or after administration of L-NMMA. We conclude that dietary Na+ restriction blunted the increased forearm NO-mediated beta2AR responsiveness in Gly16 homozygotes observed in a previous study after normal dietary Na+ intake, while baseline CO decreased and peripheral resistance increased in this group. This study provides evidence that dietary Na+ modulates effects of the Arg16Gly polymorphism on cardiovascular function.
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3.
Bone remodelling is not affected by consumption of a sodium-rich carbonated mineral water in healthy postmenopausal women.
Schoppen, S, Pérez-Granados, AM, Carbajal, A, de la Piedra, C, Pilar Vaquero, M
The British journal of nutrition. 2005;(3):339-44
Abstract
This study was designed to investigate the possible effects of consuming Na-rich carbonated mineral water on bone remodelling and urinary mineral excretion in postmenopausal women. Women (n 18) included were amenorrhoeic (>1 year), healthy and not obese (BMI <30 kg/m2). No woman was taking oestrogen replacement therapy, mineral and vitamin supplements, phyto-oestrogens or medications known to affect bone and lipid metabolism. In two consecutive interventions that lasted 8 weeks each, women drank 1 litre of control mineral water daily and 1 litre of carbonated mineral water, rich in Na, HCO3- and Cl-, daily. Body weight and height were measured, BMI was calculated and blood pressure was measured. Blood samples were taken from fasting subjects and serum obtained to analyse the biochemical bone markers, procollagen I amino-terminal propeptide (PINP) and beta-carboxy-terminal telopeptide of collagen (beta-CTX). At the end of each period, 24 h urine samples were collected to determine Ca, Mg, P, Na+, K+, Cl-, urine excretion and urinary pH. No changes in body weight, BMI or blood pressure were observed during the experimental period. Ca excretion was lower after the intake of carbonated water than after intake of the control water (P=0.037) while P excretion was higher (P=0.015). Total urine, Na and Cl- excretion did not differ between the two periods but urinary pH was increased after the intake of carbonated mineral water. PINP and beta-CTX did not differ between the two periods. Daily consumption of 1 litre of Na-rich carbonated mineral water for 8 weeks does not affect bone remodelling in healthy postmenopausal women.
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4.
Sodium status and angiotensin-converting enzyme inhibition: effects on plasma angiotensin-(1-7) in healthy man.
Kocks, MJ, Lely, AT, Boomsma, F, de Jong, PE, Navis, G
Journal of hypertension. 2005;(3):597-602
Abstract
OBJECTIVE Angiotensin-converting enzyme (ACE) inhibitors provide effective intervention for cardiovascular and renal disease. Changes in angiotensin-(1-7) have been proposed to be involved in the mechanism of action of ACE inhibition (ACEi). In particular, an altered balance between angiotensin II and angiotensin-(1-7) might be involved. A shift in sodium status modifies the activity of the renin-angiotensin-aldosterone system and the effects of ACEi, but its effects on angiotensin-(1-7) are unknown. We therefore studied the effect of a shift in sodium intake on angiotensin-(1-7), during placebo and ACEi. METHODS A double-blind, placebo-controlled study was conducted in 17 healthy men. The subjects were studied for two 2-week periods: 20 mg/day enalapril and placebo. The first week of each period they used a 50 mmol Na+ diet [low sodium (LS)], the second week a 200 mmol Na+ diet. Angiotensin levels and blood pressure were measured at the end of each week. RESULTS During placebo, LS intake elicited a three-fold rise in ang-(1-7) that paralleled the rise in other components of the renin-angiotensin system. During ACEi LS did not affect angiotensin II, but did induce a clear-cut rise in angiotensin-(1-7)--to the extent that angiotensin-(1-7) was highest during combination of ACEi and LS. Consequently, during ACEi LS shifted the balance between angiotensin-(1-7) and angiotensin II towards angiotensin-(1-7). CONCLUSION The sodium status modifies levels of angiotensin-(1-7). During ACEi angiotensin-(1-7) is still subject to stimulation by sodium restriction, and provides opportunity for therapeutic manipulation. Exploration of this opportunity in patient populations may lead to strategies to improve therapeutic benefits of ACEi.
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A further subgroup analysis of the effects of the DASH diet and three dietary sodium levels on blood pressure: results of the DASH-Sodium Trial.
Bray, GA, Vollmer, WM, Sacks, FM, Obarzanek, E, Svetkey, LP, Appel, LJ, ,
The American journal of cardiology. 2004;(2):222-7
Abstract
This study presents an extensive analysis of the effects on blood pressure (BP) of changes in sodium intake over a wide array of subgroups, including joint subgroups defined by age and hypertension status, race or ethnicity and hypertension status, and gender and race or ethnicity. Participants were given 3 levels of sodium (50, 100, and 150 mmol/2,100 kcal) for 30 days while consuming the Dietary Approaches to Stop Hypertension (DASH) diet (rich in fruits, vegetables, and low-fat dairy) or a more typical American diet. Within each diet and subgroup, there was a general pattern such that the lower the sodium level, the greater the mean reduction in BP. Sodium reduction from 100 to 50 mmol/2,100 kcal generally had twice the effect on BP as reduction from 150 to 100 mmol/2,100 kcal. Age had a strong and graded influence on the effect of sodium within the typical and DASH diets, respectively: -4.8 and -1.0 mm Hg systolic for 23 to 41 years, -5.9 and -1.8 mm Hg for 42 to 47 years, -7.5 and -4.3 mm Hg for 48 to 54 years, and -8.1 and -6.0 mm Hg for 55 to 76 years. The influence of age on the effect of sodium reduction was particularly strong in nonhypertensive patients: -3.7 mm Hg systolic for <45 years and -7.0 mm Hg for >45 years with the typical diet and -0.7 and -2.8 mm Hg with the DASH diet. Reduced sodium intake and the DASH diet should be advocated for the prevention and treatment of high BP, particularly because the benefits to BP strengthen as subjects enter middle age, when the rate of cardiovascular disease increases sharply.
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6.
Effect of sildenafil on renin secretion in human subjects.
Chiu, YJ, Reid, IA
Experimental biology and medicine (Maywood, N.J.). 2002;(8):620-5
Abstract
Sildenafil is a potent and selective inhibitor of the cyclic GMP-specific phosphodiesterase (PDE5) that is very effective in the treatment of male impotence. It inhibits breakdown of cyclic guanosine monophosphate (cGMP) formed in penile smooth muscle cells in response to stimulation by nitric oxide resulting in muscle relaxation. PDE5 is widely distributed in the body, being present in the vasculature, platelets, and kidneys. In the kidney, PDE5 is involved in the regulation of sodium excretion and renin secretion. The aim of the present investigation was to investigate the effect of sildenafil, in doses used clinically, on renin secretion in human subjects. The studies were performed in two groups of healthy normotensive subjects: one in which sodium intake was unrestricted, and one in which sodium intake was restricted to 600 mg/day. Blood pressure and heart rate were monitored throughout the study, and blood samples for the measurement of plasma cGMP and cAMP concentrations and plasma renin activity (PRA) were collected. After control measurements, the subjects ingested a capsule containing sildenafil or placebo. Cardiovascular measurements and blood sampling continued for the next 120 min. Sildenafil had only minor cardiovascular effects. Diastolic pressure tended to be lower and heart rate was generally higher after sildenafil than after placebo, but the differences were small. Sildenafil caused a prompt and sustained increase in plasma cGMP concentration and a more gradual increase in plasma cAMP concentration. After the subjects received placebo, there was a progressive decrease in PRA during the 2-hr observation period, presumably reflecting the circadian rhythm in renin secretion. In contrast, PRA failed to decrease after the subjects received sildenafil, thus indicating that sildenafil exerts a stimulatory action on renin secretion. This action on renin secretion may help explain why sildenafil only has minor effect on blood pressure despite the widespread distribution of PDE5 in vascular tissues.
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7.
Urinary dopamine excretion in healthy volunteers: effect of sodium diet and acute water load.
Luippold, G, Benöhr, P, Piesch, C, Heyne, N, Mühlbauer, B
Pflugers Archiv : European journal of physiology. 2000;(1):28-33
Abstract
The present study was designed to investigate, in human subjects, urinary dopamine excretion under different conditions of sodium and water homeostasis. In a cross-over trial, ten healthy volunteers were subjected to low-salt (LS; dietary salt restriction, sodium chloride (NaCl) intake <5 g per day), normal-salt (NS; normal food ad libitum), and high-salt (HS; normal food plus NaCl 100 mg/kg per day) regimens for 8 days in a randomized order. On day 7, urine was collected for 24 h. The variations in urinary sodium excretion reflected the dietary salt intake (LS: 16.3+/-4.7; NS: 144.1+/-18.2; HS: 221.9+/-12.9 mmol 24 h(-1) 1.73 m(-2)), but were not accompanied by significant changes in urinary dopamine excretion. On day 8, clearance studies showed that an acute oral water load of 1500 ml did not alter glomerular filtration rate or renal plasma flow but significantly increased urinary flow rate without affecting dopamine excretion. Assuming that excreted dopamine is not metabolized or reabsorbed during the tubular passage, both the unchanged urinary dopamine output in spite of 14-fold variations in sodium excretion and its independence of an acute water load argue against the hypothesis that dopamine in the tubular lumen acts as a natriuretic and/or diuretic factor in humans.
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8.
Normal responses of atrial natriuretic factor and renal tubular function to sodium loading in hypertension-prone humans.
Bruun, NE, Dige-Pedersen, H, Skøtt, P
Blood pressure. 2000;(4):206-13
Abstract
BACKGROUND In order to explore the hypothesis of an atrial natriuretic factor (ANF) deficiency in prehypertension, we compared the response to sodium loading on ANF and renal function in subjects with positive and negative histories of hypertension. METHODS Twenty-two offspring of hypertensive parents (OH) and 20 offspring of normotensive parents (ON) were studied after 4 days of low (50 mmol/day) or high (300 mmol/day) dietary sodium intake. The diets were allocated randomly. Blood pressure (BP), renal function, plasma concentration of ANF, cyclic guanosine monophosphate (cGMP), renin, angiotensin I and II, aldosterone, endothelin and catecholamines were determined during a clearance period of 90 min on both diets. Neurohormones were measured by radioimmunoassays. Renal function was determined by simultaneous measurements of 51Cr-ethylenediaminetetraacetate (a marker of glomerular filtration rate), lithium and sodium clearances. RESULTS Supine systolic and diastolic BPs were significantly elevated in OH, with both low and high dietary sodium intake. There was no difference in ANF and cGMP concentrations on the low sodium diet. Increasing sodium intake caused a similar increase in ANF in OH and ON but cGMP did not change significantly. As expected the activity of the renin-angiotensin-aldosterone system was decreased by enhancing sodium intake but with both low and high sodium intake plasma renin concentration was significantly higher in OH than in ON. Activation of the sympathetic nervous system with low sodium intake was indicated by a moderate increase in plasma concentrations of epinephrine and norepinephrine in both groups. The renal effects were characterized by significant increases in GFR, lithium and sodium clearances with increasing sodium intake. There were no differences between OH and ON. Estimated values of fractional proximal and distal tubular sodium reabsorption decreased significantly and in a similar way in both OH and ON. CONCLUSION These results indicate that the renal and neuroendocrine responses to dietary sodium loading are similar in both OH and ON. The only difference was a higher BP and an elevated plasma renin concentration on both dietary regimens in OH compared with ON. In particular, in OH and ON an identical increase in plasma ANF concentration in response to sodium loading was found. Thus, this study cannot support the hypothesis of a dysregulation of ANF in hypertension-prone humans.