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1
Renal hypertension in rats immunized against angiotensin I and angiotensin II.用抗血管紧张素I和血管紧张素II免疫的大鼠的肾性高血压
J Exp Med. 1974 Feb 1;139(2):239-48. doi: 10.1084/jem.139.2.239.
2
Role of extrapulmonary conversion in mediating the systemic pressor activity of angiotensin I.肺外转化在介导血管紧张素I的全身升压活性中的作用。
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Alterations in responses to bradykinin, angiotensin I, and angiotensin II during the induction phase of one-kidney, one-wrapped hypertension and associated arterial disease in rabbits.兔单肾单包被高血压及相关动脉疾病诱导期对缓激肽、血管紧张素I和血管紧张素II反应的改变。
Am J Pathol. 1980 Feb;98(2):457-84.
4
Studies on the role of angiotensin in experimental renovascular hypertension: an immunologic approach.血管紧张素在实验性肾血管性高血压中的作用研究:一种免疫学方法。
J Clin Invest. 1969 Aug;48(8):1506-18. doi: 10.1172/JCI106117.
5
Acute changes in the renin-angiotensin system modify bradykinin and angiotensin reactivity and metabolism in conscious rats.肾素-血管紧张素系统的急性变化会改变清醒大鼠体内缓激肽和血管紧张素的反应性及代谢。
Hypertension. 1983 Nov-Dec;5(6 Pt 3):V172-6. doi: 10.1161/01.hyp.5.6_pt_3.v172.
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Mechanism of angiotensin I converting enzyme inhibition by SQ20,881 (less than Glu-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro) in vivo. Further evidence for extrapulmonary conversion.SQ20881(小于Glu-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro)在体内抑制血管紧张素I转换酶的机制。肺外转化的进一步证据。
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引用本文的文献

1
Active immunization with angiotensin I peptide analogue vaccines selectively reduces the pressor effects of exogenous angiotensin I in conscious rats.用血管紧张素I肽类似物疫苗进行主动免疫可选择性降低清醒大鼠中外源性血管紧张素I的升压作用。
Br J Pharmacol. 2000 Mar;129(6):1178-82. doi: 10.1038/sj.bjp.0703178.
2
Role of extrapulmonary conversion in mediating the systemic pressor activity of angiotensin I.肺外转化在介导血管紧张素I的全身升压活性中的作用。
J Exp Med. 1974 Jul 1;140(1):79-86. doi: 10.1084/jem.140.1.79.

本文引用的文献

1
Increased vascular reactivity in experimental hypertension.实验性高血压中血管反应性增加。
Circ Res. 1962 Mar;10:269-73. doi: 10.1161/01.res.10.3.269.
2
Vascular reactivity in hypertension.高血压中的血管反应性。
Circ Res. 1961 May;9:755-61. doi: 10.1161/01.res.9.3.755.
3
Reactivity to pressor agents in hypertension.高血压患者对升压药的反应性。
Circulation. 1955 Dec;12(6):974-80. doi: 10.1161/01.cir.12.6.974.
4
Role of a pressor substance in unilateral renal hypertension.一种升压物质在单侧肾性高血压中的作用。
Proc Soc Exp Biol Med. 1966 Aug-Sep;122(4):941-5. doi: 10.3181/00379727-122-31295.
5
A solid silver clip for induction of predictable levels of renal hypertension in the rat.一种用于在大鼠中诱导可预测水平肾性高血压的实心银夹。
J Appl Physiol. 1971 Jul;31(1):142-4. doi: 10.1152/jappl.1971.31.1.142.
6
Role of the renin-angiotensin system in the pathogenesis of severe hypertension in rats.肾素-血管紧张素系统在大鼠重度高血压发病机制中的作用。
Circ Res. 1971 Dec;29(6):654-63. doi: 10.1161/01.res.29.6.654.
7
Renovascular hypertension in rats immunized with angiotensin II.用血管紧张素II免疫的大鼠的肾血管性高血压
Circ Res. 1972 Feb;30(2):149-57. doi: 10.1161/01.res.30.2.149.
8
Hypertension of renal origin: evidence for two different mechanisms.肾源性高血压:两种不同机制的证据。
Science. 1971 Dec 24;174(4016):1344-6. doi: 10.1126/science.174.4016.1344.
9
The renin-angiotensin system and hypertension.肾素-血管紧张素系统与高血压。
Ann Intern Med. 1971 Nov;75(5):777-87. doi: 10.7326/0003-4819-75-5-777.
10
Renal-clip hypertension in rabbits immunized against angiotensin II.用抗血管紧张素II免疫的家兔肾血管夹性高血压
Circ Res. 1970 Aug;27(2):197-211. doi: 10.1161/01.res.27.2.197.

用抗血管紧张素I和血管紧张素II免疫的大鼠的肾性高血压

Renal hypertension in rats immunized against angiotensin I and angiotensin II.

作者信息

Oates H F, Stokes G S, Storey B G, Glover R G, Snow B F

出版信息

J Exp Med. 1974 Feb 1;139(2):239-48. doi: 10.1084/jem.139.2.239.

DOI:10.1084/jem.139.2.239
PMID:4359399
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2139522/
Abstract

Rats, actively immunized against angiotensin I (AI) and angiotensin II (AII), were subjected to unilateral renal artery constriction to determine whether the resulting hypertension, which may still ensue in the animal immunized against AII, could be prevented by such combined immunity. Sustained immunity to both AI and AII neither changed preoperative blood pressures of the rats from those of control mock-immunized rats nor altered the incidence or severity of renal dip hypertension. Vascular hyperresponsiveness to small quantities of free angiotensin could not be invoked to explain the hypertension, for there was no significant difference between mock-immunized hypertensive animals, and those remaining normotensive, regarding pressor sensitivity to intravenous AI, AII, renin, and norepinephrine. (AI + AII)-immunized hypertensive rats required AI doses averaging 260 times greater than nonimmune hypertensives to elicit equipressor responses, and were refractory to renin, but not to norepinephrine. Thus, while previous studies have not excluded direct participation of endogenous AI in renal clip hypertension in rats, evidence from our experiments makes it extremely difficult to sustain any pressor function therein for circulating AI or AII. Our results also preclude involvement of AII produced from circulating AI by conversion within arteriolar walls, close to receptor sites, since AI immunity would block this mechanism of action.

摘要

用血管紧张素I(AI)和血管紧张素II(AII)对大鼠进行主动免疫后,对其进行单侧肾动脉狭窄手术,以确定在针对AII免疫的动物中可能仍然会出现的高血压是否可以通过这种联合免疫来预防。对AI和AII的持续免疫既没有使大鼠的术前血压与对照假免疫大鼠的血压有所不同,也没有改变肾夹高血压的发生率或严重程度。不能用对少量游离血管紧张素的血管高反应性来解释高血压,因为在假免疫的高血压动物和保持血压正常的动物之间,对静脉注射AI、AII、肾素和去甲肾上腺素的升压敏感性没有显著差异。(AI + AII)免疫的高血压大鼠引发等压反应所需的AI剂量平均比非免疫性高血压大鼠大260倍,并且对肾素不敏感,但对去甲肾上腺素敏感。因此,虽然先前的研究没有排除内源性AI直接参与大鼠肾夹高血压,但我们实验的证据使得很难维持循环中的AI或AII在其中的任何升压功能。我们的结果也排除了在靠近受体部位的小动脉壁内通过循环AI转化产生的AII的参与,因为AI免疫会阻断这种作用机制。