Effect of salt intake on endothelium-derived factors in a group of patients with essential hypertension

2001 ◽  
Vol 101 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Ernesto BRAGULAT ◽  
Alejandro de la SIERRA ◽  
María T. ANTONIO ◽  
Wladimiro JIMÉNEZ ◽  
Álvaro URBANO-MÁRQUEZ ◽  
...  

The aim of the present study was to evaluate the effects of the level of salt intake on endothelium-derived factors in a group of patients with essential hypertension. A group of 50 patients with essential hypertension who had never been treated for the condition were placed on a low-sodium (50 mmol/day), low-nitrate (400 µmol/day) diet, which was supplemented, in a single-blind fashion, with placebo tablets for the first 7 days and then with NaCl tablets (200 mmol/day) for a further 7 days (total sodium intake 250 mmol/day). At the end of both periods, 24-h ambulatory blood pressure monitoring was performed. In addition, plasma levels and 24-h urinary excretion of nitrites plus nitrates and cGMP were measured, along with plasma levels of endothelin. A high salt intake promoted significant decreases in plasma levels of nitrites plus nitrates (from 41.0±2.1 to 32.8±1.8 nmol/ml; P < 0.001), 24-h urinary nitrate excretion (from 417±36 to 334±37 µmol/24 h; P = 0.045) and plasma endothelin levels (from 5.6±0.3 to 4.6±0.3 pg/ml; P = 0.007). The plasma concentration and 24-h urinary excretion of cGMP were not altered significantly by a high salt intake. We did not find any relationship between endothelium-derived products and 24-h mean blood pressure, at either low or high salt intakes, or between changes induced by the high-salt diet. A high salt intake also induced significant decreases in plasma renin activity, angiotensin II and aldosterone, and a significant increase in atrial natriuretic peptide. We conclude that a high salt intake decreases the plasma concentration and urinary excretion of nitrates and plasma levels of endothelin in patients with essential hypertension, suggesting that the level of salt intake may affect endothelial cell function. However, these alterations are not correlated with changes in blood pressure induced by the high salt intake.

Medicine ◽  
2020 ◽  
Vol 99 (14) ◽  
pp. e19548
Author(s):  
Wei Cai ◽  
MingJian Lang ◽  
XiaoBo Jiang ◽  
Qian Yu ◽  
Congliang Zhou ◽  
...  

1991 ◽  
Vol 69 (10) ◽  
pp. 1582-1591 ◽  
Author(s):  
P. Weidmann ◽  
P. Ferrari ◽  
Y. Allemann ◽  
C. Ferrier ◽  
S. G. Shaw

The pathogenesis of essential hypertension may possibly involve a deficiency in, or a decreased response to, endogenous vasodilator and natriuretic factor(s). Searching for hereditary or familial defects, it is plausible to evaluate blood pressure (BP) regulating factors in (yet) normotensive offspring of hypertensive parents (OHyp), some of whom are in fact in a stage of prehypertension. Studies by our group demonstrated that compared with healthy offspring of normotensive parents, OHyp have plasma atrial natriuretic (ANF) factor levels that are unaltered on a low salt intake but often fail to increase normally in response to a high salt intake. Plasma levels of cyclic GMP, the presumed second messenger of ANF, also may tend to be decreased in certain OHyp. On the other hand, renal excretory responses of cyclic GMP and electrolytes to ANF infused in "physiological" dose were unchanged in some OHyp tested so far. In borderline to moderate, uncomplicated essential hypertension, plasma ANF levels are often "normal." This may be inappropriately low relative to the existing BP, although the relationship of circulating ANF to atrial pressures in essential hypertension remains to be clarified. A conversion to higher plasma ANF values may occur with cardiac complications such as left ventricular hypertrophy, enlargement, dysfunction, or overt heart failure. Acute or short-term elevation of circulating ANF within the physiological and pathophysiological range by ANF infusion produces an exaggerated natriuresis and lowers BP in essential hypertensive patients. We postulate a syndrome of ANF deficiency, characterized by an impaired response of circulating ANF to high salt intake and by low cyclic GMP levels in certain yet normotensive offspring of essential hypertensive parents and by inappropriately "normal" plasma ANF in some patients with uncomplicated essential hypertension. At the stage of prehypertension, a disturbance in the ANF – cyclic GMP pathway may be expressed primarily at the circulatory rather than at the renal level. Hypertension-prone humans also tend to have an exaggerated vascular reactivity to norepinephrine. Whether the two disturbances may be interrelated is presently unknown. Both defects may potentially predispose to the development of essential hypertension. Relative ANF deficiency, an enhanced natriuretic response to ANF, and a sustained antihypertensive effect of infused ANF may represent a rational basis for treatment of essential hypertension with agents that activate the ANF system.Key words: offspring of hypertensive parents, essential hypertension, ANF, ANF deficiency syndrome, cyclic GMP, blood pressure regulation, vascular reactivity, renal function.


Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Keyona N King-Medina ◽  
Emily Henson ◽  
Pablo Ortiz

Human consumption of fructose as a sweetener has increased in the past 30 years. High fructose intake has been implicated in the development of hypertension, diabetes, and obesity. In the US, the upper 10th percentile of the population consumes up to 40% of their caloric intake from added sugars, in which fructose represents half of these. Fructose metabolism is strikingly different from that of glucose. Yet, the effect of a fructose or glucose-enriched diet in salt handling by the kidney, affecting blood pressure, and its interaction with high salt intake has been poorly studied. In genetic models of salt-sensitive hypertension, the activity of the Na + /K + /2Cl - cotransporter (NKCC2) in the thick ascending limb (TAL) is abnormally enhanced. We hypothesized that chronic fructose in drinking water induces a salt-dependent increase in blood pressure and stimulates NKCC2 during high salt intake in normal rats. Sprague-Dawley rats were given 20% fructose or 20% glucose in drinking water for 1 week after which a high salt (HS) diet (4% Na + in chow) was started for 3 weeks. When we measured systolic blood pressure (SBP) by tail cuff plethysmography in fructose-fed and glucose-fed rats on a HS diet, only the fructose-fed rats had an increased SBP from 120±10 to 132±6 mmHg on day 7 of HS (p<0.01). SBP continued to increase up to 144±18 mmHg after 3 weeks (p<0.01 vs glucose). Fructose or glucose alone did not increase SBP after 4 weeks. We then repeated the protocol using radiotelemetry to monitor the blood pressure (BP). In rats fed fructose, by day 5 of HS the SBP increased by 12±3 mmHg (p<0.02) and SBP remained elevated for 3 weeks (delta: 10±2.5 mmHg, n=3). In rats fed glucose, a HS diet did not significantly change SBP for 3 weeks (n=5). Moreover, NKCC2 activity in the TAL is enhanced by phosphorylation at Thr96, 101. We found that NKCC2 phosphorylation was higher in rats fed fructose plus HS (p<0.02) but not in rats fed glucose plus HS for 3 weeks (HS: 100, fructose+HS: 250±40%, glucose+HS: 95±10%). Therefore, we conclude that a high fructose (but not a glucose) diet in normal rats induces a salt-dependent increase in BP independently from caloric intake. Thus, the increase in BP may in part be due to the stimulation of NKCC2 phosphorylation in the TAL by fructose.


Author(s):  
Christine Y Bakhoum ◽  
Cheryl A M Anderson ◽  
Stephen P Juraschek ◽  
Casey M Rebholz ◽  
Lawrence J Appel ◽  
...  

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.


2020 ◽  
Vol 33 (4) ◽  
pp. 371-371
Author(s):  
Hong-yi Wang ◽  
Yong-jie He ◽  
Wei Li ◽  
Fan Yang ◽  
Ning-ling Sun

Abstract Background To survey the relationship between salt intake and blood pressure in hypertensive patients in Beijing. Methods A cross-sectional survey was used. Essential hypertensive patients were enrolled and divided into three groups (low, medium, and high salt intake) according to their 24 h urinary sodium excretion, which was used to access the salt intake. Blood pressure was measured through office measurement and ambulatory blood pressure monitoring. Results A total of 2,241 patients were enrolled with a mean age of 59.5 ± 13.8 years, mean blood pressure of 141.1 ± 18.5/84.6 ± 12.7 mm Hg, and urinary sodium excretion of 163.9 (95% CI 160.3–167.4) mmol [equal to salt intake 9.59 (9.38–9.79) g/d]. There were 1,544 cases from tertiary hospitals and the other 697 cases from community hospitals. Patients from community hospitals took more salt than patients from tertiary hospitals. Patients with high salt intake were younger than patients with low and medium salt intake. There were more males in high salt intake group than in the other two groups. Ambulatory blood pressure monitoring showed that patients with high salt intake had higher mean blood pressure not only in daytime, but also at night. The diastolic blood pressure in patients with medium salt intake was higher than that in patients with low salt intake. Conclusions Higher salt intake was associated with higher ambulatory blood pressure in hypertensive patients. More effort should be made to lower salt intake to improve blood pressure control rate.


1996 ◽  
Vol 270 (2) ◽  
pp. F301-F310 ◽  
Author(s):  
C. Drummer ◽  
W. Franck ◽  
M. Heer ◽  
W. G. Forssmann ◽  
R. Gerzer ◽  
...  

We examined the effects of a high-salt (100 mmol NaCl) and a low-salt (5 mmol NaCl) meal on the renal excretion of sodium and chloride in 12 healthy male upright subjects. We also measured the urinary excretion of urodilatin [ANP-(95-126)], and the plasma or serum concentrations of atrial natriuretic peptide [ANP-(99-126)], aldosterone, and renin. The high-salt meal produced a postprandial natriuresis (urinary sodium excretion from 59.0 to a peak rate of 204.6 mumol/min in 3rd h after ingestion of meal) and chloride excretion. In parallel, the urinary excretion of urodilatin increased from 35.7 to a peak rate of 105 fmol/min. The effect of high-salt intake on urinary sodium, chloride, and urodilatin excretion was significant (analysis of variance, P < 0.01), and close significant correlations were observed between urodilatin and sodium excretion (mean R = 0.702) as well as between urodilatin and chloride excretion (mean R = 0.776). In contrast, plasma ANP, which was acutely elevated 15 min after high-salt intake, was already back to low-salt values 1 h later. It did not parallel the postprandial natriuretic profile, and no positive correlation between plasma ANP and sodium excretion was observed. These results provide further evidence that urodilatin, not ANP, is the member of this peptide family primarily involved in the regulation of the excretion of sodium and chloride.


Author(s):  
Matthew C. Babcock ◽  
Austin T. Robinson ◽  
Kamila U. Migdal ◽  
Joseph C. Watso ◽  
Christopher R. Martens ◽  
...  

2015 ◽  
Vol 9 (4) ◽  
pp. e72
Author(s):  
Katarzyna Stolarz-Skrzypek ◽  
Adam Bednarski ◽  
Grzegorz Kiełbasa ◽  
Malgorzata Kloch-Badelek ◽  
Danuta Czarnecka

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