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The role of PGI2 generation originated from vascular endothelial cells in the vasodilatory mechanism of α-hANP was investigated using cultured human vascular endothelial cells (EC). EC were isolated and cultured by the method of Toyoda et al. PGI2 and cyclic nucleotides were assayed by RIA. Ca2+ kinetics were measured by using 45Ca, and the Na+-K+ ATPase activity was measured as ouabain-sensitive 86Rb uptake.The following results were obtained. 1) α-hANP (10-7, 10-5M) had no effect on PGI2 generation. 2) α-hANP (10-5M) did not show any effect on 45Ca uptake, 45Ca release and Na+-K+ ATPase activity. 3) α-hANP (10-5M) did not influence the intracellular cAMP and cGMP concentrations in the absence of 1-metyl-3-isobutylxanthin (MIX; phosphodiesterase inhibitor), but it increased cGMP in the presence of MIX (10-3M), From these results, it was concluded that PGI2 generation by EC might not be implicated to the vasodilatory mechanism of α-hANP from the aspects of its effects on Ca2+ kinetics, Na+-K+ ATPase activity and cyclic nucleotides concentrations in the absence of MIX. However, the increased cGMP cencentration by α-hANP in the presence of MIX was suspected to inhibit PGI2 generation by EC.

Human atrial natriuretic polypeptide and PGI2 generation by vascular endothelial cells.