Studies on Cyclic Nucleotides in the Adrenal Gland. XI. Adrenergic Regulation of Adenylate Cyclase Activity in the Adrenal Cortex*

Abstract

Adrenergic regulation of adenylate cyclase activities in the zona glomerulosa (the capsular fraction) and the zona fasciculata-reticularis (the decapsulated fraction) from rat adrenocortical glands has been investigated. Specific binding of [3H]dihydroalprenolol to the membrane from the capsular and the decapsulated fractions was saturable with dissociation constant (Kd) of 4.67 and 5.1 microM, respectively. The receptor density in the capsular and the decapsulated fractions was 230 and 235 fmol/mg protein, respectively. The potencies which isoproterenol, epinephrine, salbutamol, and norepinephrine competed with [3H]dihydroalprenolol binding sites indicted that adrenergic receptors of the capsular and the decapsulated membranes were of the beta 2-type. beta-Adrenergic stimulation of the adenylate cyclase system was observed only in the capsular fraction. This suggests that beta-adrenergic receptors of the capsular membrane are associated with their adenylate cyclase system, but those of the decapsulated membrane are not. Maximum stimulatory concentrations of ACTH and isoproterenol had no additive effect on the capsular adenylate cyclase, indicating that receptors for ACTH and beta-adrenergic agonists are coupled to a common pool of the cyclase.

Morphological and functional studies of the paracrine interaction between cortex and medulla in the adrenal gland

“…The a-agonist phenylephrine does not stimulate steroid release from isolated perfused pig adrenals, suggesting that the stimulatory effect of epinephrine is mediated by a b-adrenergic mechanism. Consistent with these results, in bovine (Ehrhart- and rat adrenocortical cells (Pratt et al, 1985;Shima et al, 1984) the stimulatory effects of epinephrine are not influenced by a-blockade, whereas the effect is completely abolished by the b-adrenergic antagonist propranolol. Therefore, the catecholamines released in large amounts are further possible transmitters which could be responsible for the observed stimulation of the functions of the mammalian adrenal gland by activation of the sympathoadrenal system.…”

Actions of vasoactive intestinal peptide on the rat adrenal zona glomerulosa

“…The question as to whether the catecholamines are able to influence aldosterone secretion was not directly addressed by the present study, as there is already much evidence to support the contention that adrenergic agonists stimulate aldosterone secretion in a variety of different rat adrenal preparations, including adrenal slices (Andreis et al 1995), capsular preparations in vitro (Shima et al 1984, Pratt et al 1985, Pratt & McAteer 1989, the isolated perfused adrenal preparation ( J P Hinson, unpublished observations) and dispersed zona glomerulosa cell preparations (Horiuchi et al 1987). The question of the physiological role of the VIP-catecholamine system in the regulation of zona glomerulosa function remains unclear.…”

Splanchnic Nerve Stimulation Modulates Steroid Secretion in Hypophysectomized Dogs

“…Similar experiments have not been done using dog adrenals. Beta-adrenergic agonists stimulate aldosterone and corticosterone release from rat and bovine zona glomerulosa cells [34,35]. However, corticosterone release from rat zona fasciculata cells was not affected [36].…”

“…Catecholamines would act on the adrenal cortex to elicit a stero idogenic response. This possibility also seems unlikely since there is little evidence for an adrenergic influence on cortico steroid secretion from the zona fascieulata [34]. However, further experiments are required to determine if blockade of adrenergic receptors affects the steroid responses observed after nerve stimulation.…”