We examined the effects of human α1-acid glycoprotein on isometric tension of mouse aortic rings. α1-Acid glycoprotein (7.5-75 μM) produced a transient, concentration-dependent relaxation of the phenylephrine-precontracted preparation. Although NG-nitro-L- arginine methyl ester or removal of endothelium rarely affected the α1-acid glycoprotein-induced relaxation, extracellular heparin inhibited the α1-acid glycoprotein-induced relaxation. In 10 mM Ca2+-containing external solutions, the α1-acid glycoprotein-induced relaxation was significantly potentiated. In the 60 mM KCl-precontracted preparation, α1-acid glycoprotein produced weaker relaxation than in the phenylephrine-precontracted preparation. These results suggest that the vasorelaxant effect of α1-acid glycoprotein is mainly achieved by block of Ca2+ entry in the vascular smooth muscle cells. The interaction between α1-acid glycoprotein molecules and plasmalemmal Ca2+ entry channels may be modified by extracellular Ca2+ and heparin.
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