The relationship between tissue preparation and function; methods for the study of control of aldosterone secretion: A review

Abstract

The study of the control of aldosterone synthesis and secretion by the rat adrenal gland has over the past thirty years involved the application of many different in vivo and in vitro techniques. In this review the relationship between the data that each of these methods has produced is compared. There are striking differences in overall steroid production rates, and in the qualitative nature of the steroid profile which the various methods produce. In particular, aldosterone is secreted at higher rates in vivo, and when whole tissue preparations are used in vitro, than in incubations of isolated glomerulosa cells. In addition, while corticosterone is a major product of glomerulosa tissue in vitro, the available evidence suggests that it is not a major glomerulosa product in vivo.

Effect of adrenomedullin infusion on basal and stimulated aldosterone secretion in conscious sheep with cervical adrenal autotransplants

“…It was a long-held belief that the actions of ADM may be dependent on the tissue preparation used. It was thought that ADM was inhibitory to aldosterone secretion in dispersed cells and adrenal slices, but stimulatory in intact adrenals and animals, where the integrity of the gland makes it possible for ADM to activate many possible autocrine/ paracrine mechanisms, such as release of catecholamines (for review see Vinson et al 1985). The above idealogy was thrown into doubt recently with the finding that ADM stimulates aldosterone secretion in rat zona glomerulosa cells (Kapas et al 1998).…”

Vascularization of the adrenal cortex: its possible involvement in the regulation of steroid hormone release

“…The time of onset for this effect was reported to be 30-40 minutes, significantly longer than the time required for catecholaminergic substances to exert a vasodilatory effect (Harrison and Hoey, 1960). The association between the corticosteroidogenic effect of ACTH and an increase in adrenal blood flow has subsequently been noted by several authors (Carsia and Malamed, 1979;Maier and Staehelin, 1968;Sibley et al, 1981;Vinson et al, 1985a). The short-term effects of ACTH, which involve an immediate increase in corticosterone secretion, are reported to start within 10 minutes of administration, with the peak effect evident within 15-30 minutes of administration (Bassett and Pollard, 1980;Nussdorfer et al, 1984).…”

“…The adrenal gland is believed to normally operate under conditions of low intraglandular blood pressure, this belief resulting from assessment of the gland's response to changes in extrinsic blood pressure and the delicacy of the intra-adrenal endothelial structures, which appear to be unable to tolerate exposure to systemic levels of arterial blood pressure (Jasper et al, 1990;Vinson et al, 1985a). However, despite this preference for a lower intraglandular pressure, when the animal is experiencing considerable hypotension the gland is capable of maintaining the necessary level of blood flow by lowering intra-glandular vascular resistance (Sparrow and Coupland, 1987).…”

Aldosterone secretion by the rat adrenal cortex is stimulated by the activation of protease-activated receptor 1

“…This discovery challenged many assumptions that had previously been made about methods of tissue preparation, and the interpretation of physiologically relevant results (for review see Vinson et al 1985). However, the mechanism of the effect of trypsin was unclear: it was believed either to break down possible steroid-protein complexes sequestered in the cell membrane, or to cause the transmembrane activation of steroidogenesis by a novel mechanism (Raven et al 1982, Vinson et al 1985. More recent studies revealed that trypsin activated protein kinase C in the adrenal zona glomerulosa (Vinson et al 1990), although the possibility that trypsin may directly activate a phospholipase C-linked receptor was not considered a likely explanation of the effects seen.…”

“…This discovery challenged many assumptions that had previously been made about methods of tissue preparation, and the interpretation of physiologically relevant results (for review see Vinson et al 1985). However, the mechanism of the effect of trypsin was unclear: it was believed either to break down possible steroid-protein complexes sequestered in the cell membrane, or to cause the transmembrane activation of steroidogenesis by a novel mechanism (Raven et al 1982, Vinson et al 1985.…”