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六甲铵预处理后对犬血管紧张素诱导饮水的抑制作用。

Inhibition of angiotensin-induced water intake following hexamethonium pretreatment in the dog.

作者信息

Kucharczyk J

机构信息

Department of Physiology, Health Sciences Centre, Ottawa, Ontario, Canada.

出版信息

Eur J Pharmacol. 1988 Mar 29;148(2):213-9. doi: 10.1016/0014-2999(88)90566-3.

Abstract

The possibility that the pressor effects of angiotensin II influence angiotensin-induced thirst was investigated in dogs pretreated with hexamethonium. Ganglionic blockade reduced drinking elicited by i.c.v. administration of angiotensin II and totally eliminated drinking elicited by i.v. infusion of angiotensin II, whereas the pressor response to i.v. and i.c.v. angiotensin II was significantly increased. In contrast, hexamethonium had no effect on water intake or mean arterial blood pressure following i.c.v. isoproterenol, and produced a significant increase in drinking to s.c. isoproterenol, which was preceded by a large fall in mean arterial pressure. No changes in mean arterial pressure or drinking were observed during NaCl infusion in hexamethonium-pretreated animals. These results suggest that angiotensin II exerts its full dipsogenic activity only during normotensive or hypotensive states, and that the pressor effect of angiotensin II can antagonize its effects on water intake.

摘要

在接受六甲铵预处理的犬中,研究了血管紧张素II的升压作用对血管紧张素诱导的口渴的影响。神经节阻断减少了通过脑室内注射血管紧张素II引起的饮水,并完全消除了通过静脉输注血管紧张素II引起的饮水,而对静脉内和脑室内血管紧张素II的升压反应则显著增加。相比之下,六甲铵对脑室内注射异丙肾上腺素后的水摄入量或平均动脉血压没有影响,并且对皮下注射异丙肾上腺素引起的饮水有显著增加,这之前平均动脉血压有大幅下降。在六甲铵预处理的动物中输注氯化钠期间,未观察到平均动脉血压或饮水的变化。这些结果表明,血管紧张素II仅在正常血压或低血压状态下发挥其完全的致渴活性,并且血管紧张素II的升压作用可以拮抗其对水摄入的影响。

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