Calcium Efflux and Steroid Output from Superfused Rat Adrenal Cells: Effects of Potassium, Adrenocorticotropic Hormone, 5-Hydroxytryptamine, Adenosine 3′:5′-Cyclic Monophosphate and Angiotensins II and III

The efflux of 45Ca from prelabelled dispersed rat adrenal capsular and decapsulated cell preparations was studied with a column superfusion system. Corticosterone and aldosterone outputs were measured by direct and extraction radioimmunoassays. 2. The stimulants potassium, adrenocorticotropic hormone (ACTH), serotonin and adenosine 3′:5′-cyclic monophosphate (cyclic AMP), at concentrations which gave marked increases in steroid output, had no significant effect on the rate of 45Ca efflux from capsular cell preparations (mainly zona glomerulosa). 3. ACTH, at a concentration which stimulated steriodogenesis similarly, did not alter the rate of 45Ca efflux from decapsulated cell preparations (zona fasciculata/reticularis). 4. Asp1, Val5Angiotensin II caused dose-dependent increases in the rate of 45Ca efflux from capsular cells which correlated with corresponding increases in steroid output, but had no effect either on 45Ca efflux or corticosterone output in decapsulated cell preparations. desAsp1,Ile5Angiotensin II (angiotensin III) caused similar dose-dependent increases in 45Ca efflux from capsular cells, which correlated with its effects on steroidogenesis, but was less potent in both respects than angiotensin II. 5. Lowered extracellular calcium caused a very marked and rapid increase in 45Ca efflux in capsular-cell preparations, which was not significantly modified by raising the extracellular potassium concentration, although stimulation of steriodogenesis was observed. 6. These findings suggest that in zona glomerulosa cells the stimulants potassium, ACTH, serotonin and cyclic AMP are not coupled to changes in calcium transport indicated by alterations in calcium efflux, whereas angiotensins II and III, the only stimulants examined which do not increase cyclic AMP in these cell preparations, appear to act through a calcium-mediated control mechanism. In zona fasciculata/reticularis cell preparations ACTH does not appear to be coupled to such changes in calcium transport.