Larose P, Ong H, Januszewicz P, Cantin M, du Souich P
Faculty of Pharmacy, University of Montreal, Quebec, Canada.
J Pharmacol Exp Ther. 1988 Mar;244(3):1093-7.
The effects of nicotine on the secretion of arginine vasopressin (AVP) and of the atrial natriuretic factor (ANF) were examined in conscious rabbits. Nicotine was shown to produce significant increases in plasma AVP from 1.7 +/- 0.4 to 75.3 +/- 35.1 pg/ml (P less than .05) and in plasma ANF levels from 39 +/- 11 to 121 +/- 52 pg/ml (P less than .05) within 5 min of an i.v. dose of 0.5 mg/kg. These nicotine-induced stimulations could not be inhibited by muscarinic (atropine), dopaminergic [(+/-)-sulpiride], alpha (phenoxy-benzamine) or beta adrenergic (propranolol) blockers or by a rapid infusion of fluids. Trimetaphan was ineffective in blocking the stimulation of AVP secretion but completely abolished the nicotine-induced secretion of ANF. The more lipophilic ganglionic blocker, mecamylamine, blocked the stimulation of the secretion of both peptides. The effect of nicotine on AVP production was confirmed in vitro using the rat hypothalamo-neurohypophysial system preparation where nicotine increased AVP secretion in a dose-dependent manner. This in vitro stimulation was blocked by the ganglionic blocker hexamethonium. The increase in ANF plasma concentrations was probably due to a primary response to nicotine, for although exogenous AVP (1 microgram i.v.) increased ANF levels by a factor of 3 (P less than .05), the AVP antagonist [-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2- (O-methyl)tyrosine]arginine vasopressin did not prevent the nicotine-induced increase in ANF. Thus, nicotine or its effects appear to stimulate the secretion of ANF and not AVP. It was concluded that nicotine stimulates the secretion of AVP by activating central nicotinic projections to the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
在清醒的兔子身上研究了尼古丁对精氨酸加压素（AVP）和心房利钠因子（ANF）分泌的影响。静脉注射0.5mg/kg尼古丁后5分钟内，血浆AVP从1.7±0.4pg/ml显著增加至75.3±35.1pg/ml（P<0.05），血浆ANF水平从39±11pg/ml增加至121±52pg/ml（P<0.05）。这些尼古丁诱导的刺激不能被毒蕈碱（阿托品）、多巴胺能[（±）-舒必利]、α（酚苄明）或β肾上腺素能（普萘洛尔）阻滞剂抑制，也不能通过快速输注液体来抑制。曲美芬不能有效阻断AVP分泌的刺激，但能完全消除尼古丁诱导的ANF分泌。亲脂性更强的神经节阻滞剂美加明可阻断两种肽分泌的刺激。使用大鼠下丘脑-神经垂体系统制剂在体外证实了尼古丁对AVP产生的影响，其中尼古丁以剂量依赖方式增加AVP分泌。这种体外刺激被神经节阻滞剂六甲铵阻断。血浆ANF浓度的增加可能是对尼古丁的主要反应，因为尽管外源性AVP（静脉注射1μg）使ANF水平增加了3倍（P<0.05），但AVP拮抗剂[-(β-巯基-β,β-环戊亚甲基丙酸)-2-(O-甲基)酪氨酸]精氨酸加压素并不能阻止尼古丁诱导的ANF增加。因此，尼古丁或其作用似乎刺激了ANF的分泌而非AVP的分泌。研究得出结论，尼古丁通过激活下丘脑的中枢烟碱投射来刺激AVP的分泌。（摘要截取自250字）
