Effect Of Sodium Depletion Research Articles

The Influence of Sar1 Ala8 Angiotensin II (Saralasin) on Plasma Aldosterone in Hypertensive Patients

The effect of a 4-hour infusion of the angiotensin II analogue sar1 ala8 angiotensin II (saralasin) on plasma aldosterone concentration (PAC) was assessed in relation to plasma renin activity (PRA) in 12 patients, both on normal sodium intake and after marked sodium depletion. On normal sodium intake the response of PAC to saralasin was variable; following sodium depletion saralasin induced a marked decrease in PAC in 11 of 12 patients. The extent of the change in PAC induced by saralasin correlated closely with log PRA. The data indicate that saralasin is also a competitive antagonist of the effect of the endogenous renin-angiotensin system (RAS) on the adrenal cortex, with agonistic activity appearing at low levels of PRA. The effect of sodium depletion on AC appears to be mediated to a major degree by the RAS.

The effect of sodium depletion on the renal response to short-duration of NH4Cl acid loading.

The effect of sodium depletion on the renal response to short-duration of NH4Cl acid loading.

The effect of aldosterone and the renin-angiotensin system on sodium, potassium and chloride transport by proximal and distal rat colon in vivo.

1. The roles of aldosterone and angiotensin in the direct control of epithelial sodium transport in vivo have been investigated by measurement of electrical p.d. changes and of the fluxes of sodium, potassium and chloride in rat colon, an organ actively involved in electrolyte homoeostasis. Exogenous angiotensin and aldosterone were given by both short- and long-term infusions and endogenous secretion of the hormones was varied by dietary sodium variation and by nephrectomy and/or adrenalectomy. 2. In vitro angiotensin has been shown to influence colonic salt and water absorption but in the present in vivo experiments administered angiotensin had no significant action on p.d. or on the ionic fluxes of the proximal or distal colon. The increase in p.d. produced by infusing aldosterone was unaffected by giving angiotensin concurrently. The effect of sodium depletion in stimulating sodium absorption and potassium secretion was completely abolished by adrenalectomy but was unaffected by nephrectomy. 3. During prolonged infusion of angiotensin into adrenalectomized rats, a small fall in faecal fluid and sodium content was observed, but this change would have little significance in sodium homoeostasis. 4. Aldosterone and sodium depletion stimulated sodium absorption in both proximal and distal colon but significant increase in potassium secretion was demonstrable only in the distal colon. Bicarbonate secretion (by calculation) was unaffected. In the proximal colon, the increased sodium absorption appeared to be accompanied by increased chloride absorption while in the distal colon it was principally the sodium-potassium exchange that was increased. 5. Adrenalectomy reduced potassium secretion in both proximal and distal colon but sodium absorption was only significantly reduced in the proximal colon. 6. It was concluded that there is no evidence that angiotensin in the living animal has a role as an important salt retaining hormone by direct epithelial action. Aldosterone has a considerable effect which is independent of the presence of angiotensin, and which differs in proximal and distal colon in regard to the relative effects on chloride absorption and potassium secretion.

Effects of Sodium Depletion on Plasma Renin Activity and on the Urinary Excretion of Cyclic AMP and Aldosterone in Hypoparathyroid Patients

The effect of sodium depletion on plasma renin activity (PRA), urinary cyclic AMP and urinary aldosterone excretion was studied in hypoparathyroid patients whose basal urinary cylic AMP excretion (urinary cAMP) was less than 50% of that observed in normal subjects. During 7 days of sodium depletion, PRA, urinary aldosterone and urinary cAMP each rose significantly. Administration of the beta-blocker propranolol, 160 mg/day, during 5 further days of sodium depletion produced a fall in PRA and urinary cAMP, but no change in urinary aldosterone excretion. The dissociation in these effects suggests that the increase in aldosterone secretion during sodium depletion may be mediated by pathways other than the renin-angiotensin and adenyl cyclase systems. There was a high degree of correlation between PRA and urinary cAMP (P less than 0.001) during the period of sodium depletion, but not significant relationship between these parameters was found during control and propranolol phases, or in control studies in normal subjects. These findings suggest that beta-adrenergic receptors have a role in mediating the effects of sodium depletion upon renin secretion and adenyl cyclase activity.

Studies on the biosynthesis of aldosterone using the sheep adrenal transplant: effect of sodium depletion on the conversion of corticosterone to aldosterone.

SUMMARY The effect of sodium depletion on the conversion of corticosterone to aldosterone has been examined in vivo using the adrenal transplants of two sheep. [3H]Corticosterone was infused continuously directly into the adrenal gland via the carotid artery over a period of 30 min. and the total adrenal effluent was collected via the jugular vein in six consecutive 5-min. samples. The conversion of [3H]corticosterone to [3H]aldosterone and the endogenous output of aldosterone was measured in each sample using a double isotope derivative method and the specific activity of the aldosterone calculated. Radioactive conversion of B → aldosterone reached equilibrium within 10 min. of the start of infusion and remained constant over a period of 10–25 min. Aldosterone secretion was also constant during the first 25 min. of infusion. In the same sheep the mean percentage conversion increased as aldosterone secretion rose over a range of 2–12 μg./hr. With more severe sodium depletion, i.e. with aldosterone secretion rates of 12–16 μg./hr., conversion decreased to that found in the sodium replete state. The specific activity of the aldosterone was constant throughout the mildly deplete range (2–12 μg./hr.) but fell with severe sodium depletion. In the sodium replete range (0–2 μg./hr.) before the introduction of a parotid fistula, the specific activity was the same as in the mildly deplete state. After the introduction of a parotid fistula the specific activity increased as the secretion decreased from 2 to 0 μg. The validity of the approach and interpretation of the results in terms of the biosynthetic pathways involved are discussed.

Effect of sodium depletion on renin activity of renal venous plasma in renovascular hypertension

Effect of sodium depletion on renin activity of renal venous plasma in renovascular hypertension

Effect of Sodium Depletion on Renin Activity of Renal Venous Plasma in Renovascular Hypertension

In a patient with renovascular hypertension, renal venous renin-activity determinations were carried out during normal sodium intake, after sodium depletion, and after sodium repletion. When the patient was eating a normal sodium diet, renal venous renin-activity levels failed to lateralize, a finding consistent with the results of isotope renography and two separated renal function studies. However, renal venous renin-activity ratios lateralized (ratios greater than 2:1) to the affected side when the patient's severe sodium depletion lasted for three days. From this finding, it was correctly predicted that relief of hypertension would follow nephrectomy for complete occlusion of a branch artery secondary to fibromuscular dysplasia. Acute sodium depletion increases the diagnostic sensitivity of renal venous renin-activity testing in the determination of functional significance of renovascular lesions in hypertensive patients.

The effect of sodium depletion of the renal response to water-loading in dogs.

1. Dogs depleted of sodium by peritoneal dialysis with glucose solution (5 g/100 ml.) showed a significant reduction in plasma sodium concentration, in inulin clearance and in plasma and extracellular fluid volume. The plasma protein concentration and haematocrit were increased.2. By the second day of salt depletion the plasma and extracellular fluid volumes, plasma protein concentration and haematocrit all showed some recovery towards normal values.3. A water-load of 2.5% of body weight did not cause diuresis or natriuresis when given on the first day of depletion, but initiated a water diuresis when given on the second day.4. A water-load of 5% of body weight caused diuresis but not natriuresis, when given on either day of salt depletion.5. The physiological interpretation of these results is discussed.