Time-course and relationship of the early changes in renal sodium excretion and aldosterone secretion during dietary sodium restriction in normal man

1990 ◽  
Vol 78 (6) ◽  
pp. 605-612 ◽  
Author(s):  
D. J. S. Carmichael ◽  
M. S. Sutters ◽  
R. J. Unwin ◽  
D. Gordon ◽  
J. Few ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Low Sodium ◽  
Renal Sodium Excretion ◽  
Plasma Arginine

1. The fall in renal sodium excretion after dietary sodium restriction is prompt and reproducible. The importance of increased aldosterone secretion during the early phase (within 48 h) of this response is unclear. Using two indirect measures of aldosterone secretion (in urine and saliva), we have tried to relate changes in excretion and concentration of this hormone to renal sodium excretion during the abrupt transition from a normal (approximately 150 mmol/day) or high (260 mmol/day) to a low (5–25 mmol/day) sodium intake in 11 and seven male volunteers, respectively. 2. All subjects showed reduced renal sodium excretion within 36 h of dietary restriction, but the times at which increases in renal aldosterone excretion, saliva aldosterone concentration and plasma renin activity became statistically significant varied widely (8–72 h, 2.5–>62.5 h and 38 h for renal aldosterone secretion, saliva aldosterone concentration and plasma renin activity, respectively). Circadian fluctuations in saliva aldosterone concentration were apparent and increased in amplitude during sodium restriction. 3. Urine flow rate tended to increase on the first day of sodium restriction and this reached statistical significance in the group initially on a high sodium intake (64.0 ± 8.8 to 84.3 ± 11.2 ml/h, P <0.01); although the pattern of urine flow did correlate with plasma arginine vasopressin concentration (r = −0.49, P <0.01), there was no significant decrease in mean plasma arginine vasopressin concentration [1.15 (0.92–1.44) to 0.90 (0.72–1.12) pmol/l, P = 0.08; geometric mean and 95% confidence limits]. Renal arginine vasopressin excretion fell significantly after the change from a normal or high to a low sodium diet [2.70 (2.38–8.69) to 2.19 (1.72–4.00) and 3.80 (2.92–5.01) to 2.50 (1.26–2.35) pmol/h, respectively, P <0.05]; in four subjects assayed, plasma atrial natriuretic peptide concentration also fell significantly [20.1 (16.3–24.9)to 13.1 (10.6–16.2) pmol/l, P <0.05]. 4. We conclude that after acute dietary sodium withdrawal: (1) unless enhanced renal sensitivity to aldosterone develops rapidly, increased secretion alone is unlikely to account for the initial decline in renal sodium excretion; (2) decreased atrial natriuretic peptide secretion may have a permissive role in ‘low-sodium’ adaptation; (3) the early ‘low-sodium’ diuresis is probably vasopressin-dependent and is an important mechanism in the preservation of normal plasma osmolality.

Temporal pattern of renin and aldosterone secretion in men: effects of sodium balance

1992 ◽  
Vol 262 (5) ◽  
pp. F871-F877 ◽  
Author(s):  
W. V. Vieweg ◽  
J. D. Veldhuis ◽  
R. M. Carey
Keyword(s):  
Sodium Intake ◽  
Time Lag ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium

To investigate the pulsatile nature of basal and stimulated renin and aldosterone secretion, we sampled blood for plasma renin activity (PRA) and plasma aldosterone concentration at 10-min intervals for 24 h in nine normal supine human male subjects after equilibration in high- and low-sodium balance states. We evaluated serial hormonal measures by a quantitative waveform-independent deconvolution technique designed to compute the number, amplitude, and mass of underlying secretory bursts and simultaneously to estimate the presence and extent of basal secretion. For both PRA and aldosterone: 1) burstlike release accounted for greater than or equal to 60% of total secretion and tonic release for less than 40%; 2) there was an 80- to 85-min interpulse interval unchanged by sodium intake; 3) sodium restriction engendered an increase in plasma hormone concentrations by increasing the amount and maximal rate of hormone secreted per burst; 4) low dietary sodium also induced increases in basal hormone secretory rates, suggesting that there may be two regulatory processes driving renin and aldosterone secretion; and 5) PRA was significantly coupled to plasma aldosterone concentration by a 0-, 10-, or 20-min aldosterone lag time in both high- and low-sodium balance. We conclude that both renin and aldosterone are released via a predominantly burstlike mode of secretion; PRA and plasma aldosterone concentrations are positively coupled by a short time lag (0-20 min); and sodium restriction achieves an increase in mean PRA and plasma aldosterone concentration by selective amplitude enhancement of individual hormone secretory bursts and by increased tonic (interburst) basal secretory rates.

Role of renal nerves in maintaining sodium balance in unrestrained conscious rats

1985 ◽  
Vol 249 (6) ◽  
pp. F819-F826 ◽  
Author(s):  
E. Fernandez-Repollet ◽  
C. R. Silva-Netto ◽  
R. E. Colindres ◽  
C. W. Gottschalk
Keyword(s):  
Blood Pressure ◽  
Renal Denervation ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Restriction ◽  
Low Sodium ◽  
Dietary Sodium Restriction

This study was designed to investigate the effects of bilateral renal denervation on sodium and water balance, the renin-angiotensin system, and systemic blood pressure in unrestrained conscious rats maintained on a normal- or low-sodium diet. Renal denervation was proven by chemical and functional tests. Both bilaterally denervated rats (n = 18) and sham-denervated rats (n = 15) maintained positive sodium balance while on a normal sodium intake. Both groups were in negative sodium balance for 1 day after dietary sodium restriction was instituted but were in positive sodium balance for the following 9 days. Systolic blood pressure was higher in sham-denervated (115 +/- 3 mmHg) than in denervated rats (102 +/- 3 mmHg) while on a normal diet (P less than 0.05) and remained so during sodium restriction. Plasma renin concentration (PRC) and plasma aldosterone concentration (PAC) were significantly diminished in the denervated rats during normal sodium intake (P less than 0.05). After dietary sodium restriction, PRC increased in both groups but remained significantly lower in the denervated rats (P less than 0.05). Following dietary sodium restriction, PAC also increased significantly to levels that were similar in both groups of rats. These results demonstrate that awake unrestrained growing rats can maintain positive sodium balance on a low sodium intake even in the absence of the renal nerves. However, efferent renal nerve activity influenced plasma renin activity in these animals.

Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

2008 ◽  
Vol 294 (1) ◽  
pp. R17-R25 ◽  
Author(s):  
Mads Kjolby ◽  
Peter Bie
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Ang Ii ◽  
Low Sodium ◽  
Arterial Blood ◽  
Body Sodium ◽  
Custom Made ◽  
Total Body

Responses to acute sodium loading depend on the load and on the level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response, which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low-sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03–0.75 mmol·kg−1·day−1for 7 days. Acute NaCl administration increased PV (+6.3–8.9%) and plasma sodium concentration (∼2%) and decreased plasma protein concentration (−6.4–8.1%). Plasma ANG II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, and plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms that are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down-regulated within 2 h. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines that are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake.

Enhanced adrenal renin and aldosterone biosynthesis during sodium restriction in TGR (mREN2)27

1994 ◽  
Vol 267 (4) ◽  
pp. E515-E520 ◽  
Author(s):  
S. Rubattu ◽  
I. Enea ◽  
D. Ganten ◽  
D. Salvatore ◽  
G. Condorelli ◽  
...  
Keyword(s):  
Adrenal Cortex ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Transgenic Rat ◽  
Sodium Restriction ◽  
Sprague Dawley ◽  
Low Sodium ◽  
Sd Rats

The aim of the study was to investigate the relationships between tissue renin and the steroid production in the adrenal cortex during dietary sodium restriction in the transgenic rat (TGR) (mREN2)27. Thus the effects of a 1-wk low-sodium intake (0.04% NaCl) were studied in 5-wk-old male TGR (n = 33, systolic blood pressure = 151 +/- 3 mmHg) and in 24 age- and sex-matched outbred normotensive Sprague-Dawley (SD) rats. Measurements of plasma and tissue hormones were obtained at 0, 4, and 7 days of a low-sodium diet. Sodium restriction caused sustained increases of adrenal renin activity (from 28.5 +/- 3.5 to 87.5 +/- 4.5 ng.mg protein-1.h-1 on day 7) and of adrenal renin mRNA (+63 +/- 13 and +43 +/- 7% on days 4 and 7, respectively), whereas plasma renin activity (from 3.3 +/- 0.3 to 4.4 +/- 0.6 ng.ml-1.h-1) and renal renin activity (from 0.85 +/- 0.25 to 0.7 +/- 0.4 microgram.mg protein-1.h-1) did not change. The stimulation of the adrenal renin-angiotensin system was associated with a large increase of the aldosterone synthase cytochrome P-450 mRNA (+165 +/- 35 and +184 +/- 44%, on days 4 and 7) and of plasma aldosterone levels (from 125 +/- 32 to 338 +/- 59 pg/ml, P < 0.01). In SD rats, in spite of a more consistent increase in renal and circulating renin, mineralocorticoid production did not increase significantly. These results demonstrate that the exaggerated biosynthesis of aldosterone in TGR during sodium restriction is associated with an activation of renin in the adrenal cortex but not in the kidney.

Development of two-kidney Goldblatt hypertension in rats under dietary sodium restriction

1980 ◽  
Vol 238 (6) ◽  
pp. H889-H894 ◽  
Author(s):  
H. Munoz-Ramirez ◽  
R. E. Chatelain ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Goldblatt Hypertension

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.

Adrenergic control of renin during dietary sodium deprivation in conscious dogs

1989 ◽  
Vol 256 (6) ◽  
pp. E863-E871 ◽  
Author(s):  
H. Hisa ◽  
Y. H. Chen ◽  
K. J. Radke ◽  
J. L. Izzo ◽  
C. D. Sladek ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Conscious Dogs ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Adrenergic Stimulation ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Dietary Sodium Restriction

These experiments evaluated the contribution of alpha- and beta-adrenergic stimulation to plasma renin activity (PRA) during early and long-term dietary sodium restriction, compared with normal sodium intake. Uninephrectomized conscious dogs with catheters in the aorta, vena cava, and remaining renal artery were studied during normal sodium diet (approximately 70 meq/day), after 2-3 days of low-sodium diet (5-7 meq/day), and after greater than or equal to 2 wk of low-sodium diet. Direct renal arterial (ira) infusion of phenoxybenzamine plus propranolol decreased PRA by similar proportions (39-48%) during all three states of dietary sodium intake. The PRA achieved after adrenergic blockade remained higher (P less than 0.05) during early and long-term sodium restriction than during normal sodium intake. The effect on PRA of ira infusion of propranolol alone was not different from that of phenoxybenzamine plus propranolol during normal or low-sodium diet, and the magnitude of decrease in PRA during low-sodium diet was the same whether propranolol (1 microgram.kg-1.min-1) was infused ira or intravenously. In summary, beta-adrenergic stimulation accounts for similar proportions of PRA during early and long-term dietary sodium restriction and during normal sodium intake. Renal alpha-adrenoceptors appear to play little or no role in control of PRA under these conditions.

Unaltered dopaminergic modulation of aldosterone secretion in cirrhosis

1988 ◽  
Vol 74 (2) ◽  
pp. 137-143 ◽  
Author(s):  
M. Bernardi ◽  
Rossana De Palma ◽  
F. Trevisani ◽  
R. Malatesta ◽  
M. Baraldini ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Plasma Renin Activity ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Plasma Prolactin ◽  
Aldosterone Secretion ◽  
Renal Sodium Excretion ◽  
Cirrhotic Patients

1. The responses of plasma aldosterone and plasma prolactin concentrations to metoclopramide (10 mg intravenously) were evaluated over 2 h in eight healthy controls and in 23 patients with cirrhosis (10 without and 13 with ascites). Plasma renin activity, glomerular filtration rate and renal sodium excretion were also determined. 2. Metoclopramide did not significantly influence plasma renin activity, whereas both plasma aldosterone and plasma prolactin rose significantly. The incremental areas under the curves did not differ among controls and cirrhotic patients without and with ascites. No significant correlations between plasma prolactin and aldosterone, either under basal conditions or after metoclopramide administration, were found in either controls or patients. 3. Glomerular filtration rate did not change after metoclopramide. Renal sodium excretion in controls and cirrhotic patients without ascites was also unaffected, whereas it decreased significantly in cirrhotic patients with ascites. In the latter, renal sodium excretion was inversely correlated with plasma aldosterone both under basal conditions and after metoclopramide administration. 4. The dopaminergic control of aldosterone secretion does not appear to be significantly altered in cirrhosis. Metoclopramide administration to cirrhotic patients with ascites leads to an increase in plasma aldosterone that may enhance renal sodium retention.

scholarly journals Dietary Sodium Restriction Increases the Risk of Misinterpreting Mild Cases of Primary Aldosteronism

2016 ◽  
Vol 101 (11) ◽  
pp. 3989-3996 ◽  
Author(s):  
Rene Baudrand ◽  
Francisco J. Guarda ◽  
Jasmine Torrey ◽  
Gordon Williams ◽  
Anand Vaidya
Keyword(s):  
Primary Aldosteronism ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Positive Screen ◽  
Serum Aldosterone ◽  
Optimal Screening ◽  
Dietary Sodium Restriction ◽  
Aldosterone To Renin Ratio

Context: The aldosterone to renin ratio (ARR) is recommended to screen for primary aldosteronism (PA). Objective: To evaluate whether dietary sodium restriction results in misinterpretation of PA screening. Participants: Untreated hypertensives with ARR more than 20 on a high dietary sodium intake (HS) were also evaluated on a low dietary sodium intake (LS) (n = 241). Positive screening for PA was defined as: plasma renin activity (PRA) less than or equal to 1.0 ng/mL · h with serum aldosterone more than or equal to 6 ng/dL. PA was confirmed by a 24-hour urinary aldosterone excretion more than or equal to 12 mcg with urinary sodium more than 200 mmol. Results: Only 33% (79/241) of participants with an ARR more than 20 had a positive PA screen on HS. On LS, 56% (44/79) of these participants no longer met criteria for positive PA screening. When compared with participants with positive PA screening on both diets, participants with a positive screen on HS but negative on LS exhibited a significantly higher PRA on both diets. Remarkably, of the 48/79 participants who had PA confirmed, 52% had negative PA screening on LS. The distinguishing feature of these participants with “discordant” screening results was a larger rise in PRA on LS resulting in normalization of the ARR and higher Caucasian race prevalence. Conclusions: Sodium restriction is recommended in hypertension; however, it can significantly raise PRA, normalize the ARR, and result in false interpretation of PA screening. Milder phenotypes of PA, where PRA is not as suppressed, are most susceptible to dietary sodium influences on renin and ARR. Optimal screening for PA should occur under conditions of HS.

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