Akademik Veri Yönetim Sistemi
FASEB Journal, cilt.10, sa.3, 1996 (SCI-Expanded)
The puipose of the prêtent study was to detennine the effects of AGM a newtydiscovered clonidine-displacing substance (CDS) in mammals, on pulmonaiy and systemic hemodynamics în the anesthetized, intact-chest rat. In addition, the mechanism of action of AGM was examined using isolated tat thoracic aorta (RTA). Bolus i.v. injection of AGM (1-10 mg) markedly decreased systemic arterial pressure and systemic vascular résistance in a dose-dependent manner. Under conditions of constant pulmonary blood flow, constant left atrial pressure and elevated pulmonary vasomotor tone conditions, intralobar arterial bolus injections of AGM markedly decrested pulmonary vascular resistance in a dose-dependent manner. In RTA precontracted with U-46619, KC1 or phenylephrine, AGM produced concentration-dependent relaxant responses that were not altered by BU224, eraroxane, SFAF 86613. L-NAME , meclotenamate and méthylène blue. The present data suggest that AGM dilates the pulmonary and systemic vascular beds independent of imidazoline (I)i , Iz and ai-receptors, EDRF, cyclooxygenase products as well as activation of soluble guanylate cyclase, respectively. The present data suggest AGM as an endogenous CDS synthesized by endothelium acts to relax vascular smooth muscle in vivo by an unknown mechanism.