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Renin secretion: the difficulty of extrapolating from in vitro to in vivo studies

The renin-angiotensin system plays a pivotal role in blood pressure regulation, both in physiological and pathophysiological conditions. Activation of this system starts by the release of renin from juxtaglomerular cells and culminates in the generation of angiotensin II, a potent vasoconstrictor peptide.

Renin secretion is under the close control of several factors, including hormones (for instance angiotensin II, atrial natriuretic factor and vasopressin), the sympathetic nervous system and intrarenal autoregulatory mechanisms (1, 2). Angiotensin II is known to exert an inhibitory action on renin release, as demonstrated in vivo and in cultured juxtaglomerular cells. This angiotensin II-mediated effect is associated with an increase in intracellular free calcium. The neural control of renin secretion is more complex because it may involve beta — as well as alpha — adrenoceptors. In vivo studies have demonstrated univocally that stimulation of the sympathetic nervous system leads to renin release. This effect can be prevented