Plasma and Urine Dopamine in Man Given Sodium Chloride in the Diet

1979 ◽  
Vol 56 (3) ◽  
pp. 261-264 ◽  
Author(s):  
N. S. Oates ◽  
S. G. Ball ◽  
C. M. Perkins ◽  
M. R. Lee
Keyword(s):  
Sodium Chloride ◽  
Dietary Supplements ◽  
Renal Clearance ◽  
Sodium Excretion ◽  
Normal Subjects ◽  
Dietary Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Excretion Rates

1. Plasma and urine free dopamine were measured daily for 5 days in six normal subjects maintained on a low sodium diet. The subjects were then given dietary supplements of sodium chloride for 5 days and the measurements repeated. 2. Throughout the experiment the 24 h free dopamine excretion rates for all the subjects were higher than could be accounted for by renal clearance. Dopamine excretion increased significantly in response to the added sodium chloride whereas plasma dopamine remained unchanged. The rise in dopamine excretion preceded that of sodium excretion. 3. It is concluded that free dopamine is formed within the kidney in response to increased dietary sodium and may have a role in the control of sodium excretion.

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.

Effect of Chronic Hemorrhage on Urinary Aldosterone-Like Activity and Sodium Excretion in Dogs

1957 ◽  
Vol 189 (1) ◽  
pp. 181-184 ◽  
Author(s):  
M. Jay Goodkind ◽  
Wilmot C. Ball ◽  
James O. Davis
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Sodium Content ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renal Sodium Excretion

Chronic hemorrhage in normal dogs resulted in increased urinary aldosterone-like activity and a reduction in renal sodium excretion which was approximately equivalent to the sodium content of the blood removed. Glomerular filtration rate either increased or did not change. A comparable increase in aldosterone-like activity was observed in urine from normal dogs fed a low sodium diet equivalent to the net sodium intake of dogs subjected to hemorrhage.

EFFECT OF PROSTAGLANDIN SYNTHETASE INHIBITORS ON RENIN AND ALDOSTERONE IN MAN ON A NORMAL OR LOW SODIUM DIET

1978 ◽  
Vol 87 (3) ◽  
pp. 577-588 ◽  
Author(s):  
G. Norbiato ◽  
M. Bevilacqua ◽  
U. Raggi ◽  
P. Micossi ◽  
C. Moroni ◽  
...  
Keyword(s):  
Diclofenac Sodium ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Upright Position ◽  
Synthetase Activity ◽  
Prostaglandin Synthetase ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Before And After

ABSTRACT The effect of two inhibitors of prostaglandin synthetase activity (acetylsalicylic acid (ASA) and diclofenac sodium (DCFS)) on plasma renin activity (PRA) and plasma aldosterone (PA) was studied in normal subjects kept on a diet with constant sodium and potassium intake or on a low-salt diet for 7 days. In 9 subjects, 2 days of treatment with ASA (3 g/day) was followed by a significant decrease of PA in the supine position (after overnight rest); there was no significant decrease of PRA. However, both PA and PRA with the subjects in the upright position were significantly reduced after ASA. In 9 subjects treated with DCFS (200 mg for 2 days), both PA and PRA with the subjects in the supine and upright positions decreased significantly. Similar results were obtained from 4 subjects on a low-sodium diet (15–30 mEq./day) treated with DCFS (150 mg/day for 3 days). In contrast, no significant changes in PA or PRA with the subjects in the supine or upright position were observed in 4 subjects on a very low sodium diet (< 15 mEq./day) treated with DCFS (150 mg/day for 3 days). Covariance analysis (with PRA as independent variable and PA as dependent variable) of the data obtained in the upright position before and after treatment with ASA or DCFS showed that the decrease in PA remained significant after adjustment for the PRA effect. These results suggest a direct effect of prostaglandins on PA. The data obtained from subjects on a low sodium diet indicate that sodium deprivation may counteract the effects of DCFS on PRA and PA.

Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1–7) administration in anesthetized rats

2013 ◽  
Vol 304 (3) ◽  
pp. R260-R266 ◽  
Author(s):  
Julie O'Neill ◽  
Alan Corbett ◽  
Edward J. Johns
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renal Hemodynamic

Angiotensin II at the kidney regulates renal hemodynamic and excretory function, but the actions of an alternative metabolite, angiotensin (1–7), are less clear. This study investigated how manipulation of dietary sodium intake influenced the renal hemodynamic and excretory responses to intrarenal administration of angiotensin (1–7). Renal interstitial infusion of angiotensin (1–7) in anesthetized rats fed a normal salt intake had minimal effects on glomerular filtration rate but caused dose-related increases in urine flow and absolute and fractional sodium excretions ranging from 150 to 200%. In rats maintained for 2 wk on a low-sodium diet angiotensin (1–7) increased glomerular filtration rate by some 45%, but the diuretic and natriuretic responses were enhanced compared with those in rats on a normal sodium intake. By contrast, renal interstitial infusion of angiotensin (1–7) in rats maintained on a high-sodium intake had no effect on glomerular filtration rate, whereas the diuresis and natriuresis was markedly attenuated compared with those in rats fed either a normal or low-sodium diet. Plasma renin and angiotensin (1–7) were highest in the rats on the low-sodium diet and depressed in the rats on a high-sodium diet. These findings demonstrate that the renal hemodynamic and excretory responses to locally administered angiotensin (1–7) is dependent on the level of sodium intake and indirectly on the degree of activation of the renin-angiotensin system. The exact way in which angiotensin (1–7) exerts its effects may be dependent on the prevailing levels of angiotensin II and its receptor expression.

Renal nerves in renal adaptation to dietary sodium restriction

1983 ◽  
Vol 245 (3) ◽  
pp. F322-F328 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Renal Denervation ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Body Sodium ◽  
Renal Adaptation

To assess the physiologic importance of the renal nerves in the renal mechanisms for the maintenance of body sodium balance, renal adaptation to normal and low sodium diet was evaluated in conscious Sprague-Dawley male rats before and 8 days after recovery from bilateral surgical-pharmacological renal denervation. Renal denervation was confirmed in every rat at the end of the study by absence of renal vasoconstriction to splanchnic nerve stimulation and loss of renal tissue norepinephrine content. Daily sodium balance, defined as the difference between dietary sodium intake and urinary sodium excretion, was positive with the normal sodium diet before and after bilateral renal denervation. Prior to bilateral renal denervation, changing to the low sodium diet was associated with a diminishingly negative sodium balance for 3 days that became progressively positive thereafter. After bilateral renal denervation, changing to the low sodium diet was associated with a continuous and progressively negative sodium balance. We conclude that intact renal innervation is required for normal renal sodium conservation and maintenance of body sodium balance during dietary sodium restriction.

Long-Term Adherence to Low-Sodium Diet in Patients With Heart Failure

2017 ◽  
Vol 39 (4) ◽  
pp. 553-567 ◽  
Author(s):  
Misook L. Chung ◽  
Linda Park ◽  
Susan K. Frazier ◽  
Terry A. Lennie
Keyword(s):  
Heart Failure ◽  
Patient Adherence ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Factors Affecting ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Positive Attitudes

Although following a low-sodium diet (LSD) for heart failure (HF) has been recommended for decades, little is known about factors related to long-term patient adherence. The purposes of this study were to (a) compare sodium intake and factors affecting adherence in a long-term adherent group and in a non-adherent group and (b) examine predictors of membership in the long-term adherent group. Patients with HF ( N = 74) collected 24-hr urine samples and completed the Dietary Sodium Restriction Questionnaire and the Patient Health Questionnaire-9. Long-term adherence was determined using the Stage of Dietary Behavior Change Scale. The long-term adherent group had lower sodium intake (3,086 mg vs. 4,135 mg, p = .01) and perceived more benefits from LSD than the non-adherent group. Only positive attitudes toward LSD predicted membership in the long-term adherence group (odds ratio [OR] = 1.18, p = .005). Interventions focused on enhancing positive perceptions of the benefits of an LSD may improve long-term dietary adherence in patients with HF.

Aldosterone response to sodium deprivation and angiotensin II in patients with hypopituitarism

1981 ◽  
Vol 96 (3) ◽  
pp. 361-369 ◽  
Author(s):  
Cornelia Seifert ◽  
Wolfgang Oelkers
Keyword(s):  
Angiotensin Ii ◽  
Pituitary Gland ◽  
Blood Pressure Response ◽  
Normal Subjects ◽  
Zona Glomerulosa ◽  
Sodium Balance ◽  
Sodium Deficiency ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Abstract. Unknown pituitary factor(s) apart from ACTH may participate in the regulation of aldosterone (aldo) secretion in man. We investigated whether the 'sensitization' of the zona glomerulosa against angiotensin II (A II) by sodium deficiency was mediated by the pituitary gland. A II was infused in stepwise increasing doses (2, 4, 8 ng/kg/min) into 5 normal subjects (N) and into 8 patients with hypopituitarism (H) before and after 4 days on a low sodium diet. Mean cumulative sodium balance after the low sodium diet was − 145 mm in N and − 165mm in H. Plasma-aldo and aldo-exretion rate on the normal sodium diet were slightly lower in H than in N but rose less than normal during sodium depletion in H. Plasma A II and renin activity on normal sodium were slightly higher in H than in N, but the increase on the low sodium diet was blunted in H. The stimulation of plasmaaldo by A II infusion was similar in both groups on the normal sodium diet. In both groups, the response of P-aldo to A II infusion was greater in the sodium deplete than in the replete state, although 'sensitization' was slightly less marked in H than in N. This may be due to the blunted rise of plasma-A II after sodium loss in H, which may also account for abnormalities in the blood pressure response in the H group. Altogether, the results speak against a direct involvement of the pituitary gland in 'sensitization', but an indirect influence through unexplained abnormalities in renin secretion is possible.

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