Effects of α1-acid glycoprotein on isometric tension of mouse aorta

We examined the effects of human alpha(1)-acid glycoprotein on isometric tension of mouse aortic rings. alpha(1)-Acid glycoprotein (7.5-75 microM) produced a transient, concentration-dependent relaxation of the phenylephrine-precontracted preparation. Although N(G)-nitro-L-arginine methyl ester or removal of endothelium rarely affected the alpha(1)-acid glycoprotein-induced relaxation, extracellular heparin inhibited the alpha(1)-acid glycoprotein-induced relaxation. In 10 mM Ca(2+)-containing external solutions, the alpha(1)-acid glycoprotein-induced relaxation was significantly potentiated. In the 60 mM KCl-precontracted preparation, alpha(1)-acid glycoprotein produced weaker relaxation than in the phenylephrine-precontracted preparation. These results suggest that the vasorelaxant effect of alpha(1)-acid glycoprotein is mainly achieved by block of Ca(2+) entry in the vascular smooth muscle cells. The interaction between alpha(1)-acid glycoprotein molecules and plasmalemmal Ca(2+) entry channels may be modified by extracellular Ca(2+) and heparin.