RENIN RELEASE OF JUXTAGLOMERULAR CELLS DE PENDING ON ENDOTHELIAL MEDIATORS AND COCULTURE WITH ENDOTHELIAL-CELLS

Endogenous NO formed by vascular endothelial cells is capable of stimu lating renin secretion from juxtaglomerular cells since absence of 1-a rginine or presence of the inhibitor of NO synthase N<(omega)over bar> -nitro-1-arginine (200 mu M) reduces renin release from co-cultures of juxtaglomerular cells with endothelial cells but not from primary cul tures of juxtaglomerular cells. Exogenous NO (10-100 mu M sodium nitro prusside or 100 mu M-10 mM SIN-1) also stimulates renin secretion from primary cultures of juxtaglomerular cells as well as from co-culture with endothelial cells. Co-culture per se is associated with a reducti on of renin release. This inhibition might be caused in part by endoth elin since endothelin isoforms 1-3 (1 mu M each) have been shown to in hibit cAMP-induced (10 mu M forskolin) renin secretion. The made of NO 's action on renin release remains to be clarified (slow-acting, indep endent of cGMP or cAMP, dependent on extracellular calcium).