title: Influence of lead (Pb2+) on the reactions of in vitro cultured rat aorta to 5-hydroxytryptamine.
abstract: Although several studies demonstrated that lead induced abnormal vascular responses in low level lead exposed animals, investigations of the direct effects of lead on blood vessels are limited. In this study we tested the hypothesis that lead was able to directly affect the contractile reactivities of vessels. Male Wistar rat aortae were removed and cultured in PMRI 1640 with 1 ppm lead acetate for 0.5, 6, 12, 24 and 48 h, and then their responses to norepinephrine bitartrate (NE) and serotonin (5-hydroxytryptamine, 5-HT) were examined. The contractile responses to 5-HT of lead exposed aortae were significantly increased when the aortae were cultured for 24 and 48 h. Denudation of endothelium was able to abolish the increased contractile response completely. Diphenyleneiodonium (DPI), an inhibitor of the NAD(P)H oxidase, could abolish the increased contractile response to 5-HT. However, Vitamin C (VC) enhanced the contractile response of both groups to higher dosages of 5-HT. The expression of 5-HT(2B) receptor was not significantly altered by incubation with 1 ppm lead for 24 h. These data suggest that exposure to low levels of lead can directly increase the contraction of aorta to 5-HT. This effect is endothelium dependent, which is not mediated by increased expression of the 5-HT 2B receptor. The increased contraction to 5-HT may be related to increased production of superoxide (O2*-) induced by lead exposure.
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, Peking University Health Science Center, Beijing 100083, PR China.
authors.forename: Le-Feng
authors.initials: LF
authors.lastname: Zhang
authors.forename: Shuang-Qing
authors.initials: SQ
authors.lastname: Peng
authors.forename: Sheng
authors.initials: S
authors.lastname: Wang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001013:Aorta, Thoracic / Q000166:cytology / Q000187:drug effects; D001205:Ascorbic Acid / Q000494:pharmacology; D015153:Blotting, Western; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007854:Lead / Q000633:toxicity*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000187:drug effects*; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors; D009638:Norepinephrine / Q000494:pharmacology; D009861:Onium Compounds / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D044403:Receptor, Serotonin, 5-HT2B / Q000096:biosynthesis; D012701:Serotonin / Q000494:pharmacology*; D013481:Superoxides / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D004791:Enzyme Inhibitors; D009861:Onium Compounds; D017382:Reactive Oxygen Species; D044403:Receptor, Serotonin, 5-HT2B; D014662:Vasoconstrictor Agents; D013481:Superoxides; D007854:Lead; D012701:Serotonin; C007517:diphenyleneiodonium; D019255:NADPH Oxidases; D001205:Ascorbic Acid; D009638:Norepinephrine