Cellular mechanisms of renin release.

The renin-angiotensin system plays a central role in salt and water balance and in the regulation of arterial blood pressure. The level of activity of this system is determined primarily by the rate at which the granulated juxtaglomerular cells (JG cells) secrete renin into the blood. Physiologically, renin secretory rate is controlled by a number of first messengers: afferent arteriolar transmural pressure or some function of it, such as stretch (the baroreceptor mechanism); solute transport in the macula densa segment of the nephron (the macula densa mechanism); catecholamines released from the renal nerves and the adrenal medulla (the beta-adrenergic mechanism); extracellular concentrations of many organic and inorganic substances including angiotensin II, vasopressin, K, and Mg (1-3). In addition to these physiological first messengers, a number of pharmacological agents affect renin secretion (3). It is an accepted principle of cellular biology that first messengers act by affecting the intracellular concentrations of only a few second messengers. The evidence that intracellular free ionic calcium, cyclic AMP, and cyclic GMP are second messengers in renin secretion has been reviewed in detail recently (4-9). These reviews are cited extensively, since space limitations precluded citing all the original literature.