Abstract
We examined the effects of human α 1-acid glycoprotein on isometric tension of mouse aortic rings. α 1-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 α 1-acid glycoprotein-induced relaxation, extracellular heparin inhibited the α 1-acid glycoprotein-induced relaxation. In 10 mM Ca 2+-containing external solutions, the α 1-acid glycoprotein-induced relaxation was significantly potentiated. In the 60 mM KCl-precontracted preparation, α 1-acid glycoprotein produced weaker relaxation than in the phenylephrine-precontracted preparation. These results suggest that the vasorelaxant effect of α 1-acid glycoprotein is mainly achieved by block of Ca 2+ entry in the vascular smooth muscle cells. The interaction between α 1-acid glycoprotein molecules and plasmalemmal Ca 2+ entry channels may be modified by extracellular Ca 2+ and heparin.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
