In vitro study demonstrates bradykinin-stimulated nitric oxide and cyclic GMP production in bovine endothelial cells, suggesting autocrine regulation of vascular tone.
The cellular mechanism by which bradykinin induces nitric oxide (NO) formation was studied in cultured bovine endothelial cells. The basal release of nitrate/nitrite (NOx) from endothelial cells increased linearly during one-min incubation and reached plateau levels thereafter. Bradykinin dose-dependently and similarly stimulated NOx release and cyclic GMP production, both of which were abolished by NG-monomethyl L-arginine. D-Arg-[Hyp3, Thio5′8, D-Phe7]-bradykinin (B2-antagonist), but not Leu8-des Arg9-bradykinin (B1-antagonist), inhibited bradykinin-induced production of both NOx and cyclic GMP. Removal of extracellular Ca2+ by EGTA failed to affect bradykinin-induced NOx and cyclic GMP production, whereas intracellular Ca2+ release inhibitor (TMB-8) completely abolished NOx and cyclic GMP production stimulated by bradykinin. A relatively selective calmodulin inhibitor (W-7) blocked bradykinin-induced production of NOx and cyclic GMP. Our data suggest that bradykinin stimulates B2 receptor-mediated NO formation via activation of Ca2+/calmodulin-dependent constitutive NO synthase, and that NO may function as an autocrine/paracrine factor in endothelial cells. (Hypertens Res 1993; 16: 131-137)
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Emori et al. (1993) studied this question.
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