EFFECTS OF VASOACTIVE SUBSTANCES ON THE PIG ISOLATED HEPATIC LYMPH VESSELS

Citation
S. Hashimoto et al., EFFECTS OF VASOACTIVE SUBSTANCES ON THE PIG ISOLATED HEPATIC LYMPH VESSELS, The Journal of pharmacology and experimental therapeutics, 269(2), 1994, pp. 482-488
Citations number
28
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00223565
Volume
269
Issue
2
Year of publication
1994
Pages
482 - 488
Database
ISI
SICI code
0022-3565(1994)269:2<482:EOVSOT>2.0.ZU;2-B
Abstract
The present study examined the responses of isolated pig hepatic lymph vessels to vasoactive substances, the classification of alpha adrenoc eptors and the mode of action of acetylcholine (ACh) with special refe rence to the lymphatic endothelial cells. Contractions of the hepatic lymph vessels were induced by norepinephrine (NE), epinephrine, prosta glandin F-2 alpha histamine and 5-hydroxytryptamine in a dose-dependen t manner. NE was the most potent vasoconstrictor agent. 5-bromo-6[2-im idazolin-2-ylamino]-quinoxaline, xylazine and clonidine also produced dose-dependent contractions. NE-induced contractions were inhibited si gnificantly 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 rauwolsci ne (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. Thes e results suggest that the NE-induced contraction in pig hepatic lymph vessels seems to be mediated mainly through stimulation of alpha-2 ad renoceptors. ACh, isoproterenol, histamine, 5-hydroxytryptamine, ATP a nd adenosine caused dose-dependent relaxations in the hepatic lymph ve ssels precontracted by 5 x 10(-6) M prostaglandin F-2 alpha. ACh was t he 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-ind uced relaxation. The ACh-induced relaxation was suppressed by pretreat ment with N omega-nitro-L-arginine methyl ester (3 x 10(-5) M) and met hylene blue (10(-5) M) but was unaffected by aspirin (10(-5) M). Addit ional treatment with L-arginine (10(-3) M) in the presence of 3 x 10(- 5)M Nw-nitro-L-arginine methyl ester reversed completely the Nw-nitro- L-arginine methyl ester-induced reduction of the relaxation. These res ults suggest that ACh causes the release of nitric oxide or its relate d compounds from the endothelial cells, which results in the relaxatio n of the hepatic lymph vessels via the accumulation of cellular guanos ine 3',5'-cyclic monophosphate.