Kraly F S, Tribuzio R A, Keefe M E, Kim Y M, Lowrance R
Department of Psychology, Colgate University, Hamilton, NY 13346, USA.
Physiol Behav. 1995 Dec;58(6):1137-43. doi: 10.1016/0031-9384(95)02056-x.
A role for endogenous histamine and its receptor subtypes for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats in two experimental paradigms in which drinking was initiated without accompanying change in systemic fluid balance: (a) nondeprived rats eating a small (0.57 g) salted cracker; (b) nondeprived rats receiving IG infusion (through a chronic gastric catheter) of 2 ml 900 mOsm/kg NaCl. The ability of i.p., s.c., or ICV (through a surgically implanted chronic cannula in a lateral ventricle) injections of antagonists to H1, H2, or H3 receptors for histamine to inhibit drinking was examined. For rats ingesting a small cracker: systemic injection of H1 antagonists dexbrompheniramine (DXB) or pyrilamine (PYR) delayed the latency to initiate drinking. Systemic injection of H1 antagonists DXB, PYR, or terfenadine (TER; which fails to penetrate the blood-brain barrier) and ICV injection of DXB or PYR inhibited water intake. The H2 antagonist cimetidine (C) given i.p. or ICV failed to affect drinking. The H3 antagonist thioperamide (Th) given s.c. or ICV delayed the latency to drink and inhibited water intake. For rats receiving IG NaCl: systemic injection of H1 antagonists DXB or PYR or the H3 antagonist Th inhibited water intake, but the H2 antagonist C failed to inhibit drinking. Our findings extend the evidence for the involvement of endogenous histamine in drinking elicited by eating in rats by suggesting roles for peripheral and brain H1 and H3 receptors for drinking initiated by postprandial gastrointestinal osmotic consequences that are subthreshold for changes in systemic fluid balance.
在内源性组胺及其受体亚型介导进食引发的饮水方面的作用，在成年雄性斯普拉格 - 道利大鼠中通过两种实验范式进行了研究。在这两种范式中，饮水开始时全身液体平衡没有伴随变化：（a）未禁食的大鼠食用一小块（0.57克）咸饼干；（b）未禁食的大鼠通过慢性胃导管接受2毫升900毫渗摩尔/千克氯化钠的腹腔内输注。研究了腹腔内、皮下或脑室内（通过手术植入侧脑室的慢性套管）注射组胺H1、H2或H3受体拮抗剂抑制饮水的能力。对于食用小块饼干的大鼠：全身注射H1拮抗剂右溴苯那敏（DXB）或吡拉明（PYR）延迟了开始饮水的潜伏期。全身注射H1拮抗剂DXB、PYR或特非那定（TER；不能穿透血脑屏障）以及脑室内注射DXB或PYR抑制了水的摄入量。腹腔内或脑室内给予H2拮抗剂西咪替丁（C）未能影响饮水。皮下或脑室内给予H3拮抗剂硫代哌酰胺（Th）延迟了饮水潜伏期并抑制了水的摄入量。对于接受腹腔内氯化钠注射的大鼠：全身注射H1拮抗剂DXB或PYR或H3拮抗剂Th抑制了水的摄入量，但H2拮抗剂C未能抑制饮水。我们的研究结果扩展了内源性组胺参与大鼠进食引发饮水的证据，提示外周和脑H1及H3受体在由餐后胃肠道渗透压变化引发的饮水中起作用，而这种变化对全身液体平衡的改变来说阈值较低。
