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내피세포를 제거한 흰쥐 대동맥에서 Phenylephrine이 일으킨 수축반응에 대한 alpha-수용체 길항제의 영향
홍승철(Sung Cheul Hong),강맹희(Maeng Hee Kang),박상일(Sang Il Park),박미선(Mi Sun Park),최수경(Su Kyung Choi),정준기(Joon Ki Chung),서석수(Suk Soo Suh) 대한약학회 1991 약학회지 Vol.35 No.5
The effects of an irreversible or a reversible alpha1-adrenoceptor antagonist (dibenamine or prazosin) on alpha1-adrenoceptor-mediated vasoconstrictions were studied in the endothelium-denuded rat aorta. In these experiments, the mobilization of intracelluler calcium and translocation of extracellular calcium were also studied. To exclude the modulation of endothelium releasing EDRF and EDCF, the endothelium was removed in all rat aortas. Contraction induced by phenylephrine (a full alpha1-adrenoceptor agonist) was separated into a fast phasic component of the response due to the release of intracellular calcium and a slow tonic one due to the influx of extracellular calcium. Pretreatments with increasing doses of reversible alpha1-adrenoceptor antagonist prazosin, as well as irreversible alpha1-adrenoceptor antagonist dibenamine, inhibited the phasic component of phenylephrine-induced contraction more effectively than the tonic one. Pretreatment of dibenamine (0.2 mcM) or prazosin (10 nM) to the rat aorta abolished phasic response but remained tonic one about 41% and 51%, respectively. These results suggest that as the efficiency of phenylephrine was progressively reduced by pretreatments with increasing doses of an irreversible or a reversible alpha1-adrenoceptor antagonist (dibenamine or prazosin), the contraction induced by phenylephrine became progressively more dependent on the influx of extracellular calcium.
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흰쥐 적출 대동맥에서 alpha1-수용체 효능약과 alpha2-수용체 효능약의 혈관수축반응에 대한 내피세포의 영향
정준기(Joon Ki Chung),홍승철(Sung Cheul Hong),최수경(Su Kyung Choi),강맹희(Maeng Hee Kang),구미경(Mi Geong Ku),박상일(Sang Il Park),윤일(Il Yun) 대한약학회 1990 약학회지 Vol.34 No.3
A comparison was made of the effects of selective alpha1-adrenoceptor agonist phenylephrine and selective alpha2-adrenoceptor agonist clonidine on endothelium-containing and endothelium-denuded rings of the rat aorta. In the case of phenylephrine, removal of endothelium increased sensitivity 2.5 fold at EC50 level and maximum contractive response 1.4 fold. In the case of clonidine, which gave only 15% of maximum contractive response given to phenylephrine on endothelium-containing rings, removal of the endothelium increased sensitivity 5.6 fold at EC50 level and maximum contractive response 5 fold, which was about 55% of that given by phenylephrine. In endothelium-denuded ring, phenylephrine-induced contraction tended to be more increased in tonic contraction than in phasic contraction as compared to that in endothelium-containing ring, while clonidine-induced contraction was monophasic and was increased only in tonic contraction. In the calcium-free solution or in the presence, of verapamil, contraction stimulated by clonidine was almost abolished while that stimulated by phenylephrine produced only phasic contraction. The depression of sensitivity to these agonists in rings with endothelium appeared to be due to the vasodepressor action of endothelium derived relaxing factor(EDRF), because hemoglobin, a specific blocking agent of EDRF, abolished this depression. It is unlikely that the endothelium-dependent relaxation was due to stimulation of release of EDRF, because clonidine did not produce endothelium-dependent relaxation in 5-hydroxytryptamine-precontracted ring even when its contractile action was blocked by the alpha1-adrenoceptor antagonist, prazosin. When the efficacy of phenylephrine was reduced to about the initial efficacy of clonidine by pretreatment with dibenamine, the contraction-response curves for phenylephrine became very similar to the corresponding curves obtained for clonidine before receptor inactivation. In the dibenamine-treated rings, contraction of phenylephrine was abolished in calcium-free solution or in the presence of verapamil like that obtained for clonidine before receptor inactivation. These results suggest that EDRF spontaneously released from endothelium depress contraction more profoundly in a case of an agonist with low efficacy and the phenylephrine-induced contraction was totally dependent on extracellular calcium as was that obtained for clonidine when the efficacy of phenylephrine was reduced to that of clonidine by irreversible inactivation of alpha1-adrenoceptor with dibenamine.
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