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Abstract:
Renin secretion from juxtaglomerular cells of the kidney is controlled by several effector systems, such as renal perfusion pressure, renal nerve activity, salt load to the distal tubule and various humoral agents. The reactive behaviour of juxtaglomerular cells to these mechanisms is homologous to that of vascular smooth muscle cells of the kidney, i.e. manoeuvres inducing vasoconstriction inhibit renin secretion, whereas those inducing vasorelaxation stimulate renin secretion. This homology is partly explained by the fact that juxtaglomerular cells are modified smooth muscle cells. Intracellularly, an increase of cytosolic calcium has been identified as an inhibitory signal, whereas the major stimulatory signal appears to be cAMP (and the decrease of calcium). How intracellular calcium and cAMP are linked to the process of renin secretion, remains obscure.