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S Hashimoto, Y Kawai and T Ohhashi
1st Department of Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
The present study examined the responses of isolated pig hepatic lymph vessels to vasoactive substances, the classification of alpha adrenoceptors and the mode of action of acetylcholine (ACh) with special reference to the lymphatic endothelial cells. Contractions of the hepatic lymph vessels were induced by norepinephrine (NE), epinephrine, prostaglandin F2 alpha, histamine and 5-hydroxytryptamine in a dose-dependent manner. NE was the most potent vasoconstrictor agent. 5-bromo-6[2-imidazolin-2-ylamino]-quinoxaline, xylazine and clonidine also produced dose-dependent contractions. NE-induced contractions were inhibited significantly by yohimbine (10(-8)-10(-6) M) but not by prazosin (10(-8)-10(-6) M). Pretreatment with yohimbine (10(-8)-10(-7) M) or rauwolscine (10(-8)-10(-7) M) caused a parallel shift to the right of the dose-response curve for 5-bromo-6[2- imidazolin-2-ylamino]-quinoxaline. These results suggest that the NE- induced contraction in pig hepatic lymph vessels seems to be mediated mainly through stimulation of alpha-2 adrenoceptors. ACh, isoproterenol, histamine, 5-hydroxytryptamine, ATP and adenosine caused dose-dependent relaxations in the hepatic lymph vessels precontracted by 5 x 10(-6) M prostaglandin F2 alpha. ACh was the most potent vasorelaxant agent. Pretreatment with atropine (10(-9)-10(-7) M) inhibited the ACh-induced relaxation in a competitive manner. Removal of endothelium caused a significant reduction of the ACh-induced relaxation. The ACh-induced relaxation was suppressed by pretreatment with N omega-nitro-L-arginine methyl ester (3 x 10(-5) M) and methylene blue (10(-5) M) but was unaffected by aspirin (10(-5) M).(ABSTRACT TRUNCATED AT 250 WORDS)
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