Response of Plasma Aldosterone to Angiotensin Ii, Acth and Potassium in Man

Abstract

Plasma aldosterone, corticosterone, cortisol and renin activity have been measured in recumbent normal subjects (n = 3–4) following stimulation with angiotensin II, ACTH and potassium. Control studies on a regular sodium intake show that in the same subject aldosterone and renin activity exhibit no time dependent pattern from 7 a.m. to 11 a.m., while corticosterone and cortisol decrease continuously. Angiotensin II (infusion of 7 ng/kg/min over 1–3 h), ACTH (rapid iv injection of 0.5 mg β1-24 ACTH) and potassium (potassium citrate 30 mEq. po every hour for 3 h) on a regular Na intake induce a reproducible increase of aldosterone. The onset of this increase is observed within 10 min for angiotensin II and ACTH and within 60–90 min for potassium. The range of the rise in aldosterone is about 20–25 ng/100 ml for all 3 stimuli, corresponding to a 3–5 fold increase from basal values. Angiotensin II and potassium are, in the dose used, specific stimuli of aldosterone; ACTH however stimulates aldosterone, corticosterone and cortisol, but to a variable degree and with a different time-course response. On a low sodium intake, a similar aldosterone response pattern is found after stimulation with ACTH, but only exceptionally after stimulation with potassium; after both stimuli values of 55–75 ng/100 ml have been reached.

Effect of Angiotensin Ii on Aldosterone Secretion in the Conscious Rat

“…1). Plasma aldosterone concentration in the conscious rats in this experiment showed a sensitivity to acute infusion of angiotensin that is quantitatively similar to the response observed in man (McCaa, Read, Cowley, Bower, Smith & McCaa, 1973;Schoeler, Birkhauser, Peytremann, Riondel, Vallotton & Müller, 1973;Mendelsohn, Johnson, Doyle, Scoggins, Dentón & Cogían, 1972). These studies in resting, conscious subjects have the advantage that the angiotensin infusion rates used were not much higher than the normal rate of endogenous angiotensin formation.…”

Effect of Calcium-Channel Blockade on the Aldosterone Response to Sodium Depletion and Potassium Loading in Man

“…17 In the present in vivo human study under low salt intake, nifedipine reduced the Aldo/PRA ratio but did not alter K + -induced Aldo secretion. Renin secretion was clearly stimulated as a result of a combined effect of Na + depletion and acute inhibition of slow Ca 2+ chan nels, and as previously reported, 18 it was not modified by KCl administration. The high basal plasma concen tration of Aldo induced by Ang II stimulation was simi lar on nifedipine and placebo.…”

Effect of Volume Expansion by Hyperosmolar and Hyperoncotic Solutions under Constant Infusion of Angiotensin II on Plasma Aldosterone in Man and its Counterbalance by Potassium Administration

“…I n previous studies from our laboratory the roles of AII, ACTH and potassium in the regulation of plasma aldosterone in man have been demonstrated [13].…”