Halothane attenuates nitric oxide relaxation of rat aortas by competition for the nitric oxide receptor site on soluble guanylyl cyclase.

摘要: Abstract Endothelial cells play an important role in the regulation of vascular activity through release endothelium derived relaxing factor (EDRF) now believed to be nitric oxide (NO). NO and donor drug nitroglycerin relax smooth muscle by stimulating soluble guanylyl cyclase leading elevation intracellular levels cyclic guanosine 3′,5′-monophosphate (cGMP). Halothane has been shown inhibit action on blood vessels. This study was designed further investigate mechanisms which halothane attenuates NO-induced relaxations. done examining effects relaxations presence absence inhibitors cyclase, methylene blue 6-anilino-5,8-quinolinedione (LY 83583). Thoracic aortas from anesthetized male Sprague–Dawley rats were excised cut into rings removed. The aortic suspended organ baths containing Krebs solution equilibrated at their optimal passive tension. When a stable plateau contraction produced EC60 concentrations norepinephrine, increasing or added rings. contraction–relaxation procedure repeated three four times. In some administered calibrated vaporizer 10 min before beginning second procedure. Either LY 83583 20 third combination halothane, fourth Halothane, significantly inhibited nitroglycerin-induced relaxation individually. also (5×10−9–3×10−8 M 5×10−9–3×10−5 M, respectively) relaxation, also, treatment led rightward shift concentration–effect curves. with 83583, inhibition equivalent sum individual effects. present demonstrates that attenuate endothelium-denuded rat suggests may act competitive antagonism common site EDRF/NO pathway.