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肾血管减压机制:髓质素系统。

Renal vasodepressor mechanisms: the medullipin system.

作者信息

Muirhead E E

机构信息

Department of Pathology, University of Tennessee, Memphis 38163.

出版信息

J Hypertens Suppl. 1993 Dec;11(5):S53-8.

PMID:8158434
Abstract

Renal vasodepressor hormone: Medullipin I is the renomedullary vasodepressor hormone secreted by the renomedullary interstitial cells of the renal papilla. It is conveyed to the liver where it is converted to its active form, medullipin II. Medullipin II is a vasodilator that suppresses sympathetic tone and causes diuresis and natriuresis. Its actions are opposite to those of angiotensin II. These are feedback control systems. The secretion and conversion of medullipin is related to the cytochrome P-450 dependent enzyme system of kidney and liver. Deficiency of medullipin: A deficiency of medullipin is considered to contribute to the pathogenesis of various hypertensive states. There are three known causes for such a deficiency, (1) removal of renomedullary interstitial cells by bilateral nephrectomy, renal surgical papillectomy, chemical papillectomy, papillary atrophy or necrosis; (2) decrease in number and damage to renomedullary interstitial cells in accelerated experimental hypertension and malignant hypertension of humans; and (3) dysfunction of renomedullary interstitial cells as mediated by angiotensin II, by resetting of the effect of increased renal artery perfusion pressure, by stimulation of the renal sympathetic nerve, by inhibition of nitric oxide synthesis and possibly by inhibition of cyclo-oxygenase. Secretion of Medullipin I: The main factor influencing secretion of medullipin I by the kidney appears to be the renal artery perfusion pressure. Elevation of this pressure is attenuated by the presence of medullipin I in the renal venous effluent. Lowering the pressure below normal shuts off this secretion. This is opposite to the effects of perfusion pressure on renin secretion, as elevation shuts off renin secretion while depression turns it on.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

肾血管舒张激素

髓质素I是由肾乳头肾髓质间质细胞分泌的肾髓质血管舒张激素。它被输送到肝脏,在那里转化为其活性形式髓质素II。髓质素II是一种血管舒张剂,可抑制交感神经张力并导致利尿和利钠。其作用与血管紧张素II相反。这些是反馈控制系统。髓质素的分泌和转化与肾脏和肝脏的细胞色素P - 450依赖性酶系统有关。髓质素缺乏:髓质素缺乏被认为与各种高血压状态的发病机制有关。已知这种缺乏有三个原因,(1)通过双侧肾切除术、肾手术乳头切除术、化学乳头切除术、乳头萎缩或坏死去除肾髓质间质细胞;(2)在人类加速实验性高血压和恶性高血压中肾髓质间质细胞数量减少和损伤;(3)血管紧张素II介导的肾髓质间质细胞功能障碍,通过重置肾动脉灌注压升高的效应,通过刺激肾交感神经,通过抑制一氧化氮合成以及可能通过抑制环氧化酶。髓质素I的分泌:影响肾脏分泌髓质素I的主要因素似乎是肾动脉灌注压。肾静脉流出液中存在髓质素I可减弱该压力的升高。将压力降至正常以下会停止这种分泌。这与灌注压对肾素分泌的影响相反,因为压力升高会停止肾素分泌而压力降低则会开启肾素分泌。(摘要截短于250字)

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