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STEFANO ROCCO, CLARA AMBROZ, GRETI AGUILERA, Interaction between Serotonin and Other Regulators of Aldosterone Secretion in Rat Adrenal Glomerulosa Cells, Endocrinology, Volume 127, Issue 6, 1 December 1990, Pages 3103–3110, https://doi.org/10.1210/endo-127-6-3103
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Although serotonin (5HT) is a recognized stimulator of aldosterone secretion in vivo and in vitro, its physiological role as a regulator of mineralocorticoid secretion and its mechanism of action in the adrenal glomerulosa have not been elucidated. To address these questions we studied the interaction of 5HT with other aldosterone regulators in isolated rat adrenal glomerulosa cells. 5HT stimulated aldosterone production 14-fold, with an ED6o of 20 ± 5 nM, and stimulation was maximal at 0.8 (iM. The stimulation of aldosterone production by 5HT was accompanied by a 5-fold increase in cAMP production, with an ED60 of 1 pM. Threshold levels of 5HT (1 nM) potentiated the effect of submaximal concentrations of angiotensin-II (All), decreasing the ED60 from 1.3 to 0.46 nM and increasing the maximum response in an additive manner. In contrast, the stimulatory effect of 5HT was purely additive to that of submaximal ACTH concentrations. 5HT had no effect on aldosterone secretion stimulated by maximal ACTH concentrations, despite full additivity on cAMP accumulation. Stimulations of steroidogenesis by potassium and 5HT were fully additive at submaximal concentrations, but only partially additive at maximal levels. To determine the mechanism of the synergistic effects of All and 5HT, we analyzed the interaction of both stimuli on cAMP accumulation, intracellular calcium, and inositol phosphate formation. Consistent with the inhibitory effect of All on adenylate cyclase, in the presence of All the stimulation of cAMP by 5HT was reduced by 18 ± 3%. 5HT alone had no effect on cytosolic calcium, but significantly enhanced the peak and later phases of the All-stimulated increase (p> 0.005). This effect of 5HT was due to calcium influx and not to release from intracellular pools, as shown by suppression of the potentiation in the absence of extracellular calcium and the lack of effect of 5HT on basal or All-stimulated inositol phosphate formation. The ability of low concentrations of 5HT to potentiate the stimulatory effect of All on aldosterone secretion suggests that under some physiological conditions, 5HT may play a role in regulating the adrenal sensitivity to AIL (Endocrinology127: 3103–3110, 1990)
