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

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 N^G-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.