Abstract
The stimulatory effect of angiotensin II (AT) on the accumulation of inositol phosphates and on aldosterone production is abolished by the AT 1 selective receptor antagonist DuP753 while PD123177, an AT 2 antagonist, is ineffective. Similarly, a depolarizing effect of AT (inhibition of K +/ 86Rb efflux) is prevented by DuP753. While mediators derived from phospholipase C activation have a central role in the stimulation of aldosterone production by AT, the effect of AT on K + permeability is mimicked neither by elevation of cytoplasmic [Ca 2+]by ionomycin nor by kinase C activation with phorbol ester. Our results suggest that AT stimulates phospholipase C and the subsequent steroid production by glomerulosa cells through AT 1 receptors. In addition some events induced by the activation of AT 1 receptors may not be mediated by the activation of phospholipase C.
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