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血栓素受体在中枢性血管紧张素II致渴反应中的作用。

Role of thromboxane receptors in the dipsogenic response to central angiotensin II.

作者信息

Kitiyakara Chagriya, Welch William J, Verbalis Joseph G, Wilcox Christopher S

机构信息

Division of Nephrology and Hypertension, and Center for Hypertension and Renal Disease Research, Georgetown University, Washington, District of Columbia 20007, USA.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2002 Mar;282(3):R865-9. doi: 10.1152/ajpregu.00328.2001.

DOI:10.1152/ajpregu.00328.2001
PMID:11832409
Abstract

Central angiotensin II (ANG II) regulates thirst. Because thromboxane A2-prostaglandin H2 (TP) receptors are expressed in the brain and mediate some of the effects of ANG II in the vasculature, we investigated the hypothesis that TP receptors mediate the drinking response to intracerebroventricular (icv) injections of ANG II. Pretreatment with the specific TP-receptor antagonist ifetroban (Ifet) decreased water intake with 50 ng/kg icv ANG II (ANG II + Veh, 7.2 +/- 0.7 ml vs. ANG II + Ifet, 2.8 +/- 0.8 ml; n = 5 rats; P < 0.001) but had no effect on water intake induced by hypertonic saline (NaCl + Veh, 8.4 +/- 1.1 ml vs. NaCl + Ifet, 8.9 +/- 1.8 ml; n = 5 rats; P = not significant). Administration of 0.6 microg/kg icv of the TP-receptor agonist U-46,619 did not induce drinking when given alone but did increase the dipsogenic response to a near-threshold dose of 15 ng/kg icv ANG II (ANG II + Veh, 1.1 +/- 0.7 vs. ANG II + U-46,619, 4.5 +/- 0.9 ml; n = 5 rats; P < 0.01). We conclude that central TP receptors contribute to the dipsogenic response to ANG II.

摘要

中枢血管紧张素II(ANG II)调节口渴。由于血栓素A2 - 前列腺素H2(TP)受体在大脑中表达,并介导ANG II在血管系统中的一些作用,我们研究了TP受体介导对脑室内(icv)注射ANG II的饮水反应这一假说。用特异性TP受体拮抗剂伊非曲班(Ifet)预处理可减少50 ng/kg icv ANG II引起的水摄入量(ANG II + Veh,7.2±0.7 ml对ANG II + Ifet,2.8±0.8 ml;n = 5只大鼠;P < 0.001),但对高渗盐水诱导的水摄入量无影响(NaCl + Veh,8.4±1.1 ml对NaCl + Ifet,8.9±1.8 ml;n = 5只大鼠;P = 无显著性差异)。单独给予0.6 μg/kg icv的TP受体激动剂U - 46,619时不诱导饮水,但确实增加了对15 ng/kg icv ANG II近阈值剂量的致渴反应(ANG II + Veh,1.1±0.7对ANG II + U - 46,619,4.5±0.9 ml;n = 5只大鼠;P < 0.01)。我们得出结论,中枢TP受体促成了对ANG II的致渴反应。

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