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3日和30日肾动脉狭窄家兔对去甲肾上腺素的升压反应。血管紧张素II的作用。

Pressor responses to norepinephrine in rabbits with 3-day and 30-day renal artery stenosis. The role of angiotensin II.

作者信息

Ichikawa S, Johnson J A, Fowler W L, Payne C G, Kurz K, Keitzer W F

出版信息

Circ Res. 1978 Sep;43(3):437-46. doi: 10.1161/01.res.43.3.437.

Abstract

Pressor responses to norepinephrine (NE) infusions were examined in normal rabbits, in rabbits with renal artery stenosis of over 30 days' duration (chronic renal hypertensive rabbits), and in rabbits with renal artery stenosis of 3 days' duration (3-day clipped rabbits). The 3-day clipped rabbits did not have hypertension, but they showed the same increased pressor responses to NE as did the chronic renal hypertensive rabbits, which was about 2.5 times that of the normal rabbits. Plasma renin activity (PRA) was the same in the 3-day clipped rabbits as in the normal group, but in the chronic renal hypertensive rabbits the PRA was significantly below normal. Infusions of angiotensin II (A II) in either subpressor or pressor amounts potentiated the pressor responses to NE in normal rabbits, whereas, in 3-day clipped rabbits and chronic renal hypertensive rabbits, A II in subpressor or pressor doses did not alter the pressor responses to NE. Infusion of the A II antagonist, [1-sarcosine, 8-isoleucine]angiotensin II, did not alter the pressor responses of normal rabbits to NE, but this A II analogue completely abolished the pressor hyperresponsiveness to NE in the 3-day clipped rabbits and greatly reduced the NE hyperresponsiveness in the chronic renal hypertensive rabbits; this A II antagonist did not alter the control arterial pressure in any of the three groups of rabbits. These studies show that the increased pressor response to NE in rabbits with renal artery stenosis occurs before the onset of hypertension and thus is not merely a result of the hypertension. Also, these results provide evidence that A II plays an important role in the increased pressor responses to NE in hypertensive and prehypertensive rabbits.

摘要

在正常兔、肾动脉狭窄超过30天的兔(慢性肾性高血压兔)以及肾动脉狭窄3天的兔(夹闭3天的兔)中检测了对去甲肾上腺素(NE)输注的升压反应。夹闭3天的兔没有高血压,但它们对NE的升压反应增强程度与慢性肾性高血压兔相同,约为正常兔的2.5倍。夹闭3天的兔的血浆肾素活性(PRA)与正常组相同,但慢性肾性高血压兔的PRA显著低于正常水平。以低于升压剂量或升压剂量输注血管紧张素II(A II)可增强正常兔对NE的升压反应,而在夹闭3天的兔和慢性肾性高血压兔中,低于升压剂量或升压剂量的A II不会改变对NE的升压反应。输注A II拮抗剂[1-肌氨酸,8-异亮氨酸]血管紧张素II不会改变正常兔对NE的升压反应,但这种A II类似物完全消除了夹闭3天的兔对NE的升压高反应性,并大大降低了慢性肾性高血压兔对NE的高反应性;这种A II拮抗剂不会改变三组兔中的任何一组的对照动脉血压。这些研究表明,肾动脉狭窄兔对NE的升压反应增强在高血压发作之前就已出现,因此不仅仅是高血压的结果。此外,这些结果提供了证据,表明A II在高血压和高血压前期兔对NE的升压反应增强中起重要作用。

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