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Cytoplasmic and nuclear binding of [3H]triamcinolone acetonide was assessed in isolated rat kidney cortical tubules, enriched in distal (fraction A) or in proximal segments (fraction B). The concentration dependence of specific [3H]triamcinolone acetonide binding in cytoplasm was determined (range = 4.4 X 10(-10) to 2.1 X 10(-7) M) and analyzed by a least-squares curve-fitting method. A single, high-affinity binding class with a dissociation constant of 1 X 10(-8) M (25 degrees C) was obtained in both fractions A and B. Based on competition for the [3H]triamcinolone acetonide sites, the following sequence of affinities was obtained: triamcinolone acetonide = dexamethasone > progesterone = corticosterone > d-aldosterone > 17 beta-estradiol. These specificities imply that these sites are glucocorticoid receptors. Fraction B contained 1.6 times more cytosol sites for [3H]triamcinolone acetonide than fraction A (5.0 +/- 0.5 X 10(-13) vs. 3.0 +/- 0.5 X 10(-13) mol/mg protein). In the presence of a onefold excess of d-aldosterone specific cytoplasmic binding of [3H]triamcinolone acetonide was 1.4-fold greater in fraction B than in fraction A, and specific nuclear binding was 1.3-fold greater in fraction B than in fraction A (5.1 +/- 0.6 X 10(-13) vs 4.0 +/- 0.5 X 10(-13) mol/mg DNA). These results and the measured lengths of proximal and distal tubules yielded estimates of a higher proximal content (three- to sixfold) compared to distal content of glucocorticoid receptors.

Abstract. The influence on plasma aldosterone of plasma volume expansion by hyperosmolar and hyperoncotic solutions and its counterbalance by potassium administration was studied in man. All experiments were done during constant infusion of angiotensin II (All) which consequently excluded changes of the endogenous renin. Hyperosmolar infusion of NaCl, mannitol and NaHCO3 provoked an immediate fall in plasma aldosterone levels and presumably a shift of intracellular potassium to the extracellular compartment. Hyperoncotic solutions of dextran in 0.9% NaCl provoked an immediate fall in plasma aldosterone while dextran in 5% glucose provoked a delayed fall. Administration of minute amounts of potassium could prevent the fall in plasma aldosterone which followed administration of dextran solutions. The same minute amount of potassium, administered without volume expansion, increased plasma aldosterone markedly above the high levels induced by AII. – The data presented add further evidence for the important role of potassium as a mediator in aldosterone regulation. They indicate that intracellular potassium changes at the adrenal level, rather than plasma potassium concentration, probably exert the regulatory function in aldosterone biosynthesis.

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.

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