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精氨酸加压素调节犬体内血管紧张素II的中枢作用。

Arginine vasopressin modulates the central action of angiotensin II in the dog.

作者信息

Michelini L C, Barnes K L, Ferrario C M

出版信息

Hypertension. 1983 Nov-Dec;5(6 Pt 3):V94-100. doi: 10.1161/01.hyp.5.6_pt_3.v94.

Abstract

Endogenous vasopressin may interact with central autonomic nervous system factors in the regulation of cardiovascular function. In 25 morphine/chloralose-anesthetized dogs, we studied the magnitude of the pressor response produced by an infusion of angiotensin II (AII) into the vertebral arteries (VA), before and after intracisternal (n = 10), intravertebral (n = 9), or intravenous (n = 6) administration of a competitive antagonist of arginine vasopressin (AVP) [d(CH2)5Tyr(Me) AVP]. The dose response curve to vertebral artery infusion of AII (range 2-20 ng/kg/min) was significantly (p less than 0.05) shifted to the right of control after injection of the AVP antagonist (10 micrograms/kg) into the cisterna magna; the ED at 20 mm Hg being almost double after central AVP blockade. This effect of AVP blockade was confined only to the cardiovascular response mediated by AII via the vertebral arteries. When pressor doses of AII were injected into either a vein (i.v.) or the cisterna magna of these same dogs, the increases in mean blood pressure were the same before and after AVP antagonist treatment. In another group of anesthetized dogs, we investigated whether the reduced reactivity to intravertebral AII could be duplicated by giving the AVP antagonist either via the vertebral artery or i.v. Only the cisterna magna route was effective in causing a blunting of the pressor response to vertebral artery AII. These data demonstrate a previously unknown interaction between vasopressin and the centrally mediated pressor response to intravertebral AII.

摘要

内源性血管加压素可能在心血管功能调节中与中枢自主神经系统因素相互作用。在25只吗啡/水合氯醛麻醉的犬中,我们研究了在经脑池内(n = 10)、椎体内(n = 9)或静脉内(n = 6)给予精氨酸血管加压素(AVP)竞争性拮抗剂[d(CH2)5Tyr(Me) AVP]之前和之后,向椎动脉(VA)内输注血管紧张素II(AII)所产生的升压反应幅度。向椎动脉输注AII(剂量范围为2 - 20 ng/kg/min)的剂量反应曲线在向脑池内注射AVP拮抗剂(10微克/千克)后显著(p < 0.05)右移至对照曲线右侧;在中心性AVP阻断后,20 mmHg时的半数有效剂量(ED)几乎翻倍。AVP阻断的这种效应仅局限于AII通过椎动脉介导的心血管反应。当向这些犬的静脉(i.v.)或脑池内注射升压剂量的AII时,AVP拮抗剂治疗前后平均血压的升高相同。在另一组麻醉犬中,我们研究了通过椎动脉或静脉给予AVP拮抗剂是否能重现对椎体内AII反应性降低的情况。只有经脑池途径能有效减弱对椎动脉AII的升压反应。这些数据证明了血管加压素与对椎体内AII的中枢介导升压反应之间一种先前未知的相互作用。

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