| Abstrakt: |
The hormonal and cationic regulation of aldosterone production by freshly isolated turkey (Meleagris gallopavo) adrenal steroidogenic cells was investigated. Angiotensin II (AII), ACTH [human ACTH-(1-39)], and K+stimulated aldosterone production in a concentration-dependent manner albeit these agents exhibited considerable differences in lag time for the significant stimulation of aldosterone production over basal production. By contrast, Ca2+was without effect except at a high concentration (10 mM). Although ACTH was more efficacious than AII, it had about one-third the potency of AII for stimulating aldosterone production. However, ACTH potentiated the maximal aldosterone response to AII [maximal enhancement (+499%) at 3 × 10-10MACTH]. Extracellular K+was an absolute requirement for AII-induced aldosterone production (threshold concentration = 3 mM), and maximal enhancement (+200%) occurred with 5 mM(a physiological concentration). Although extracellular Ca2+was not an absolute requirement for inducible aldosterone production, it enhanced AII-induced aldosterone production in a concentration-dependent manner [maximal enhancement (+727%) at 3 mM], albeit it did not alter the half-maximal steroidogenic concentration (EC50) of AII, Ca2+also enhanced maximal ACTH-induced aldosterone production but to a lesser extent (+96% with 1 mMCa2+). However, Ca2+dramatically enhanced ACTH potency (ED50) (nearly 100 times at 1 mMCa2+). The acute augmentation of AII-induced aldosterone production by ACTH, K+, and Ca2+was not accompanied by increases in the cellular concentration and affinity of AII receptors. suggesting that the agents acted at intracellular loci distal to the AII receptor. Several aspects of the present study with isolated turkey adrenal steroidogenic cells differ markedly from those of studies with isolated chicken (Gallus gallus domesticus) adrenal steroidogenic cells and mammalian zona glomerulosa cells, thus suggesting interclass and intraclass differences in homeothermic vertebrate adrenal steroidogenic regulation. |
