Impaired Response of Atrial Natriuretic Factor to High Salt Intake in Persons Prone to Hypertension

1988 ◽  
Vol 319 (18) ◽  
pp. 1223-1224 ◽  
1990 ◽  
Vol 68 (3) ◽  
pp. 408-412
Author(s):  
Jiri Widimsky Jr. ◽  
Otto Kuchel ◽  
Waldemar Debinski ◽  
Gaétan Thibault

The influence of prolonged high salt intake on intravascular volume, right atrial pressure, plasma atrial natriuretic factor, and extra-atrial tissue (lung, kidney, and liver) COOH- and NH2-terminal atrial natriuretic factor content was investigated in normotensive rats. Despite prolonged high salt (8% NaCl) intake for 5 weeks, total intravascular volume was not impaired. However, right atrial pressure was increased by 54% (p < 0.01) after salt loading. Although this increment in right atrial pressure should favor atrial natriuretic factor release after NaCl intake, plasma atrial natriuretic factor (COOH-terminal) concentrations markedly decreased from 97.8 ± 27 to 38.9 ± 8 pg/mL. Sodium and circulatory homeostasis was, however, well preserved. The lungs contained the highest levels of COOH- and NH2-terminal atrial natriuretic factor. Salt loading resulted in increased concentrations of low as well as high molecular weight atrial natriuretic factor in the lung but not in the kidney or the liver. Our study indicates a limited role of atrial natriuretic factor in adaptation to prolonged salt consumption in rats. Dissociation between right atrial pressure and plasma atrial natriuretic factor after salt intake implicates other factors regulating circulating peptide levels. Prolonged salt intake increases lung generation of atrial natriuretic factor.Key words: atrial natriuretic factor, volume, atrial pressure, high salt diet.


1990 ◽  
Vol 258 (6) ◽  
pp. F1579-F1583
Author(s):  
A. Dal Canton ◽  
G. Romano ◽  
G. Conte ◽  
L. De Nicola ◽  
A. Caglioti ◽  
...  

This study was performed to define the extent to which atrial natriuretic factor (ANF) contributes to upregulate salt excretion in subjects eating a high-salt diet. Eight normal volunteers were first studied at low-salt diet (80 mmol NaCl/day); urinary sodium excretion (UNaV) and plasma ANF (PANF) were measured in the basal condition and during stepwise infusion of human alpha-ANF at 2, 4, 8, and 16 ng.min-1.kg-1. Then the same subjects were shifted to a high-salt diet (400 mmol/day), and UNaV and PANF were measured in the new balance condition. At low-salt diet, UNaV averaged 0.069 meq/min, and PANF averaged 21 pg/ml; infusion of human alpha-ANF raised stepwise both UNaV and PANF (means in meq/min and pg/ml, respectively, were 0.177 and 46, 0.218 and 76, 0.360 and 86, and 0.601 and 182). Infusion of ANF caused a progressive fall of plasma aldosterone and plasma renin activity. Mean UNaV and PANF at high-salt diet were 0.301 meq/min and 35 pg/ml. Thus, by increasing experimentally PANF in a low-salt diet condition to the levels occurring physiologically in a high-salt diet condition, a significant rise in UNaV is evoked, which accounts for approximately 50% of the rise of UNaV that is necessary to balance the increased salt intake.


1996 ◽  
Vol 7 (7) ◽  
pp. 1045-1051
Author(s):  
D Leosco ◽  
N Ferrara ◽  
P Landino ◽  
G Romano ◽  
S Sederino ◽  
...  

The effects of normal, low, and high dietary salt intake on basal atrial natriuretic factor plasma levels, plasma renin activity, and aldosterone were evaluated in seven young (Group 1), seven middle-aged (Group 2), and seven elderly healthy volunteers (Group 3). In all subjects, progressively higher doses of human alpha-atrial natriuretic factor were infused at low-sodium diet conditions to obtain hormone plasma values during infusion similar to those obtained in the same subjects at high-sodium diet conditions. Atrial natriuretic factor plasma values were significantly higher in Group 3 than in the other two groups at both normal- and high-salt diet conditions, and at all steps of the infusion study. At low-sodium diet conditions, peptide concentrations averaged 23.2 +/- 6.2 in Group 3, 26.2 +/- 1.9 in Group 2, and 19.1 +/- 3.9 pg/mL in Group 1 (P = not significant between groups). Hormone plasma values at high-salt diet conditions averaged 47 +/- 6.9 pg/mL in Group 1, 60 +/- 6.5 pg/mL in Group 2, and 136.3 +/- 14.6 pg/mL in Group 3. Each value was not significantly different from the corresponding value gained at an infusion step of 2 ng/min per kg in Group 1 and 2 (57.1 +/- 11.9 and 62.7 +/- 6.5 pg/mL, respectively), and of 1 ng/min per kg (139.1 +/- 22.2 pg/mL) in Group 3. At these infusion steps and at high-salt diet conditions, the urinary sodium excretion rate was, respectively, 0.185 +/- 0.02 and 0.311 +/- 0.02 mEq/min in Group 1, 0.168 +/- 0.01 and 0.300 +/- 0.02 mEq/min in Group 2, and 0.110 +/- 0.01 and 0.256 +/- 0.01 mEq/min in Group 3. Hormone infusion induced a progressive fall of plasma renin activity and aldosterone level in all groups. By experimentally increasing plasma concentrations of atrial natriuretic factor in a low-salt diet condition to the levels occurring physiologically in a high-salt diet condition, a significant rise in urinary sodium excretion rate is evoked, which accounts for 52% in young, 47% in middle-aged, and 30% in older subjects of the rise that is necessary to balance the increased salt intake.


1989 ◽  
Vol 161 (6) ◽  
pp. 1620-1623 ◽  
Author(s):  
Lony C. Castro ◽  
Chander P. Arora ◽  
Jane L. Davis ◽  
Calvin J. Hobel ◽  
Hassan Parvez

Peptides ◽  
1990 ◽  
Vol 11 (3) ◽  
pp. 501-506
Author(s):  
Jiri Widimsky ◽  
Waldemar Debinski ◽  
Otto Kuchel ◽  
Nguyen T. Buu ◽  
Patrick Du Souich

1990 ◽  
Vol 194 (3) ◽  
pp. 251-257 ◽  
Author(s):  
W. Debinski ◽  
O. Kuchel ◽  
N. T. Buu ◽  
M. Nemer ◽  
J. Tremblay ◽  
...  

1996 ◽  
Vol 91 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Alejandro De La Sierra ◽  
María Del Mar Lluch ◽  
Antonio Coca ◽  
María Teresa Aguilera ◽  
Vicente Giner ◽  
...  

1. The aim of the study was to detect differences between salt-sensitive and salt-resistant hypertensive patients in the response of the renin—aldosterone axis, plasma noradrenaline and atrial natriuretic peptide to high salt intake. 2. Fifty essential hypertensive patients followed 2 weeks of a standard diet with 20 mmol of NaCl daily, supplemented by placebo tablets for the first 7 days and by NaCl tablets for the last 7 days, in a single-blind fashion. Salt sensitivity was defined as a significant rise (P < 0.05) in 24 h mean blood pressure obtained by ambulatory blood pressure monitoring from the low- to the high-salt period. Biochemical and hormonal measurements were performed on the last day of both periods. 3. Twenty-two (44%) patients fulfilled criteria of salt-sensitive hypertension, whereas the remaining 28 (56%) were considered salt-resistant. High salt intake promoted a significant decrease (P < 0.05) in plasma creatinine, potassium, glucose, cholesterol, low-density lipoprotein-cholesterol, triacylglycerols, uric acid and plasma renin activity, and a significant increase in plasma atrial natriuretic peptide and 24 h urinary calcium excretion. The direction of these changes did not differ between salt-sensitive and salt-resistant patients. Salt-resistant hypertensive patients exhibited a significant decrease in plasma aldosterone induced by high salt intake (from 446 ∓ 35 to 226 ± 35 pmol/l; P < 0.001), whereas this parameter was not significantly modified in salt-sensitive patients (from 485 ± 76 to 364 ± 83 pmol/l; P not significant). Salt-sensitive patients showed an increase in plasma noradrenaline after high salt intake (from 1.15 ± 0.11 to 1.56 ± 0.14 nmol/l; P < 0.05), whereas salt-resistant patients presented a decrease in this parameter (from 1.48 ± 0.08 to 1.12 ± 0.08 nmol/l; P < 0.05). The change in plasma noradrenaline was directly correlated with the change in mean blood pressure induced by high salt intake (r = 0.479; P = 0.003). 4. We conclude that the increase in blood pressure induced by high salt intake in salt-sensitive patients is associated with a stimulation of the sympathetic nervous system and a blunted decrease in plasma aldosterone. Conversely, changes in renal function, electrolyte excretion and plasma concentrations of atrial natriuretic peptide induced by high salt intake seem to be similar in both salt-sensitive and salt-resistant patients.


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