1. To determine if increases in plasma sodium concentration P[Na] have any sustained effects of the renin-aldosterone system, P[Na] was increased in a group of six dogs over a period of 6 days by increasing sodium intake from 10 to 200 mmol per day while a fixed 700 ml per day water intake was maintained along with a continuous i.v. infusion of antidiuretic hormone (ADH) at a rate of 2.4 units per day. 2. P[Na] rose from 137.3 +/- 2.0 to 153.6 +/- 6.5 mmol/l during the high intake period. Plasma potassium concentration, 22Na space, and mean arterial pressure all remained near control levels in response to Na loading. 3. Plasma renin activity (PRA) averaged 1.0 +/- 0.1 ngAI/ml per hour on the final low Na day and fell transiently to 0.6 +/- 0.2 ngAI/ml per hour on the first day of sodium loading. For the duration of the study it remained at the control level. Plasma aldosterone concentration fell from the low Na level of 15.4 +/- 2.4 ng/100 ml to 10.5 +/- 1.5 ng/100 ml on the final day of high Na intake. 4. We conclude that increases in P[Na] in the absence of concomitant changes in P[K], 22Na space and MAP do not have a sustained effect on control of renin release but may exert a negative effect on aldosterone secretion.

Aldosterone↗

PubMedDate not supplied

Lack of prolonged effect of antidiuretic hormone on the renin-aldosterone system in the dog.

1. The effects of maximally antidiuretic, subpressor antidiuretic hormone (ADH) administration of the renin-aldosterone system were studied in dogs during 4 days of continuous intravenous infusion of ADH at a rate of 0.067 mU/kg per min. Water intake was limited to 700 ml/day to avoid changes in fluid volume status. 2. At the conclusion of the four-day study, plasma sodium concentration had fallen from 140.3 +/- 0.8 to 137.2 +/- 2.0 mmol/l, plasma potassium concentration, 22Na space, and mean arterial pressure remained within the control ranges. 3. Neither plasma renin activity nor plasma aldosterone concentration showed any tendency to change in response to the ADH infusion. 4. The results indicate that physiological levels of ADH have no prolonged, direct effect on the renin-aldosterone system.

Aldosterone↗

PubMedDate not supplied

Regulation of aldosterone biosynthesis during sodium deficiency. Evidence for an essential role of the pituitary gland.

The aldosterone response to adrenocorticotropic hormone (ACTH) and angiotensin II (AII) was evaluated in patients with pituitary insufficiency before and after dietary sodium restriction (10 mEq Na+/day for 12 days). On normal sodium intake, plasma aldosterone concentration and plasma cortisol concentration failed to change from control levels in response to a single injection of ACTH or to a continuous 1-hour infusion of AII in patients with pituitary insufficiency. In response to dietary sodium restriction for 12 days, plasma renin activity (PRA) increased fivefold in patients with pituitary insufficiency, while plasma aldosterone concentration failed to increase significantly, averaging 11.0 +/- 3.1 before and 12.3 +/- 3.7 ng/dl (ns, p greater than 0.05) after sodium deficiency. Although aldosterone secretion failed to increase during sodium deficiency, the patients came into balance at 10 mEq without a significant change in arterial blood pressure (BP). In sharp contrast to the lack of aldosterone response to ACTH before sodium deficiency, plasma aldosterone concentration increased markedly from 12.9 +/- 3.3 to 156 +/- 17.3 ng/dl (p less than 0.001) in response to ACTH after sodium deficiency. Although the adrenal glomerulosa cells were markedly sensitive to ACTH during sodium deficiency, they remained almost totally refractory to AII since aldosterone secretion failed to increase significantly in response to continuous infusion of a pressor dose of AII for 1 hour. Replacement therapy with ACTH gel for 3 months in patients with pituitary insufficiency failed to restore a normal aldosterone response to either ACTH or AII. These data demonstrate that some non-ACTH pituitary factor(s) is essential for a normal aldosterone response to ACTH, AII, and sodium deficiency.

Adrenocorticotropic Hormone↗