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澳大利亚肺鱼对血管紧张素、血管紧张素II和氯化钠输注的肾脏反应。

Renal responses of Australian lungfish to vasotocin, angiotensin II, and NaCl infusion.

作者信息

Sawyer W H, Blair-West J R, Simpson P A, Sawyer M K

出版信息

Am J Physiol. 1976 Aug;231(2):593-602. doi: 10.1152/ajplegacy.1976.231.2.593.

DOI:10.1152/ajplegacy.1976.231.2.593
PMID:961912
Abstract

The Australian lungfish (Neoceratodus forsteri) responds to intravenous injections of 0.63 ng/kg or more of arginine vasotocin with increased dorsal aortic blood pressure, inulin clearance, urine flow, and tubular rejection of Na+. Single injections of 1 ng/kg or more of angiotensin II or norepinephrine also increase dorsal aortic pressure but do not cause consistent diuresis and natriuresis, Continuous infusions of angiotensin II or repeated injections of norepinephrine produce sustained hypertension and more modest diuresis and natriuresis than are seen after injections of arginine vasotocin that cause less hypertension. Infusions of isosmolar or hyposmolar NaCl solutions increase blood pressure, inulin clearance, urine flow, and tubular Na+ rejection in a manner resembling the response to argininge vasotocoin injections. These data are consistent with the hypothesis that arginine vasotocin is released in response to volume expansion in lungfishes and that it may act on the kidney as a diuretic and natriuretic hormone. They do not rule out a more direct action of expansion on renal functions.

摘要

澳大利亚肺鱼(新角齿鱼)静脉注射0.63纳克/千克或更多的精氨酸血管加压素后,背主动脉血压、菊粉清除率、尿流量和肾小管对Na + 的重吸收增加。单次注射1纳克/千克或更多的血管紧张素II或去甲肾上腺素也会增加背主动脉血压,但不会引起持续的利尿和利钠作用。持续输注血管紧张素II或重复注射去甲肾上腺素会产生持续的高血压,且与注射精氨酸血管加压素后相比,利尿和利钠作用更弱,而注射精氨酸血管加压素引起的高血压程度较轻。输注等渗或低渗NaCl溶液会使血压、菊粉清除率、尿流量和肾小管对Na + 的重吸收增加,其方式类似于对精氨酸血管加压素注射的反应。这些数据与以下假设一致:精氨酸血管加压素是在肺鱼血容量增加时释放的,并且它可能作为一种利尿和利钠激素作用于肾脏。它们并不排除血容量增加对肾功能有更直接的作用。

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引用本文的文献

1
Hypotensive action of parathyroid hormone preparations on rats and dogs.甲状旁腺激素制剂对大鼠和犬的降压作用。
Proc Natl Acad Sci U S A. 1980 Jan;77(1):675-8. doi: 10.1073/pnas.77.1.675.
2
[Angiotensin-converting enzyme inhibition: direct and indirect mechanisms].[血管紧张素转换酶抑制:直接和间接机制]
Klin Wochenschr. 1985 Sep 16;63(18):897-906. doi: 10.1007/BF01738143.
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Correction of abnormal renal blood flow response to angiotensin II by converting enzyme inhibition in essential hypertensives.通过血管紧张素转换酶抑制纠正原发性高血压患者对血管紧张素II的异常肾血流反应。
J Clin Invest. 1985 Apr;75(4):1285-90. doi: 10.1172/JCI111828.