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Inhibitory effect of propofol on endothelium-dependent relaxation and blood pressure lowering in rats  

Kim, Shang-Jin (Department of Pharmacology, College of Veterinary Medicine, Chonbuk National University)
Kim, Jeong-gon (Department of Pharmacology, College of Veterinary Medicine, Chonbuk National University)
Joe, Sung-gun (Department of Pharmacology, College of Veterinary Medicine, Chonbuk National University)
Kang, Hyung-sub (Department of Pharmacology, College of Veterinary Medicine, Chonbuk National University)
Kim, Jin-shang (Department of Pharmacology, College of Veterinary Medicine, Chonbuk National University)
Publication Information
Korean Journal of Veterinary Research / v.44, no.3, 2004 , pp. 357-366 More about this Journal
Abstract
We studied the effect of propofol (PPF) on the endothelium-dependent vascular responses in isolated rat thoracic aorta. In aortic rings with endothelium, PPF inhibited the phenylephrine (PE)-induced contraction in a concentration-dependent manner. In PE-precontracted preparations, PPF attenuated the endothelium-dependent relaxation by acetylcholine but not by A23187. And PPF did not attenuate the endothelium-independent relaxation by sodium nitroprusside (SNP). The relaxation induced by acetylcholine in PE-precontracted aortic rings was significantly augmented by zaprinast, a cGMP-specific phosphodiesterase inhibitor, and this augmentation was inhibited by PPF. Although SNP-induced relaxation was significantly augmented by zaprinast, this augmentation was not inhibited by PPF. In preparations preconstricted with PE, the PPF-induced relaxation was inhibited by atropine. In addition, PPF attenuated the vasorelaxation by phosphodiesterase inhibitors (IBMX, Ro20-1724 or zaprinast except milrinone). In vivo, the infusion of acetylcholine and SNP showed decreased arterial blood pressure in rats. The pre-injection of PPF inhibited the acetylcholine-induced blood pressure lowering, but not the SNP-induced blood pressure lowering. These results suggest that PPF can attenuate in part the acetylcholine-induced vasorelaxation and blood pressure lowering through the inhibition of the acetylcholine receptor-mediated endothelium-derived relaxing factor by acting on endothelium. It is considered that the inhibitory effect of PPF on the vasorelaxation is due to the decreased level of cGMP which can be attributed to the inhibition of the muscarinic receptor and/or receptor-G-protein interaction.
Keywords
propofol; cGMP; endothelium; vasorelaxation; rat aorta;
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