Capponi A M, Lew P D, Wüthrich R, Vallotton M B
J Hypertens Suppl. 1986 Jun;4(2):S61-5.
The effects of the synthetic (1-24) atrial natriuretic peptide (atriopeptin III) on angiotensin II-induced changes in cytosolic free calcium and biological responses have been examined in three cell types: adrenal glomerulosa cells, vascular smooth muscle cells and renal cortical tubular cells. Atriopeptin III did not affect the transient changes in cytosolic free calcium induced by angiotensin II in adrenal glomerulosa and vascular smooth muscle cells, nor did it alter resting cytosolic free calcium levels. In contrast with its known inhibitory effects on angiotensin II-induced aldosterone production and vasoconstriction, atriopeptin III did not prevent either angiotensin II-stimulated prostaglandin 6-keto-F1 alpha or prostaglandin E2 (PGE2) synthesis in cultured vascular smooth muscle cells and dispersed renal cortical tubular cells, respectively. These data show that atrial natriuretic peptide is not an endogenous calcium-blocking agent, and indicate that the atrial peptide is not a general inhibitor of all angiotensin II-induced biological responses.
