ヒト心房性Na利尿ペプチドと血管内皮細胞のPGI₂産生

抄録

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.