Liu Yu, Chang Hailiang, Niu Longgang, Xue Wenxin, Zhang Xuanping, Liang Yueqin, Zhang Mingsheng
Department of Pharmacology, Shanxi Medical University, Xinjiannanlu 56, Taiyuan 030001, Shanxi Province, China.
Vascul Pharmacol. 2009 Aug-Sep;51(2-3):182-9. doi: 10.1016/j.vph.2009.06.003. Epub 2009 Jun 21.
Rat renal arterial rings were suspended in organ chambers for isometric tension recording. The effects of propofol on the resting tone, KCl-, norepinephrine (NE)-, serotonin- and thromboxane A(2) analog U46619-induced contractions were observed. The relaxation responses to propofol on KCl-, NE- and U46619-induced contractions were assessed in the absence or presence of cyclooxygenase inhibitor, nitric oxide synthetase inhibitor or specific K(+) channel inhibitors. Propofol did not significantly affect the resting tone, but inhibited the contractions induced by KCl-, NE-, serotonin- and U46619. Propofol (1-100 microM) concentration-dependently relaxed 60 mM KCl-, 10 microM NE-, and 1 microM U46619-induced contractions with the values of RC(50) (concentration to decline the precontraction by 50%) being 18.9 microM, 70.6 microM and 12.7 microM, respectively. Propofol-induced relaxation was attenuated by indomethacin, but not by either N(G) nitro-l-arginine methyl ester (L-NAME) or any K(+) channel specific inhibitors used. The vasorelaxations induced by acetylcholine, sodium nitroprusside and amrinone were not affected by the presence of propofol. The present results indicate that propofol antagonizes provoked contractions of the arteriole and suggest that inhibition of extracellular Ca(2+) influx and synthesis of vasodilator prostanoid may be involved in propofol-induced relaxation of the arteriole.
