In 1980, studies of the hormone regulation of adrenocortical steroidogenesis had reached a turning point. The important differences in function and responsiveness of the different adrenocortical zones had been recognized (Tait, Tait & Bell, 1980; see also Brown, 1982), and the need for purified cell populations from each zone for in-vitro studies emphasized. Two reviews of that year (Schimmer, 1980; Tait et al. 1980) also highlighted advances which had been made in understanding the mechanisms of hormone-stimulated (particularly adrenocorticotrophin (ACTH)-stimulated) cyclic AMP (cAMP) generation in the adrenal cortex, and how cAMP could bring about an increase in adrenal steroidogenesis. However, these reviews also stressed that not all the known steroidogenic agonists stimulated cAMP production. At least one agonist (angiotensin II (AII)) operated through a mechanism requiring an increase in intracellular Ca2+ concentration ([Ca2+]i).
In many other tissues, agonists such as AII, vasopressin and acetylcholine were known
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