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中枢神经系统诱导性利钠中的非加压机制。

Nonpressor mechanisms in CNS-induced natriuresis.

作者信息

Mouw D R, Vander A J, Bourgoignie J J, Kutschinski S S, Mathias N P

出版信息

Am J Physiol. 1979 Aug;237(2):157-66. doi: 10.1152/ajprenal.1979.237.2.F157.

DOI:10.1152/ajprenal.1979.237.2.F157
PMID:464123
Abstract

Ventriculocisternal perfusion was performed in pentobarbital-anesthetized dogs. Perfusion of high Na (300 mM NaCl) artificial cerebrospinal fluid (CSF) (E) for 2 h was preceded by 2 h of control (C) and was followed by 2 h of recovery (R) during which normal (150 mM NaCl) artificial CSF was perfused. A time-control group was perfused with normal artificial CSF throughout C, E, and R. High sodium perfusion resulted in a marked natriuresis in each of nine animals and suppression of plasma renin activity. Theere were no simultaneous changes in mean arterial pressure, glomerular filtration rate, or renal plasma flow. Sodium excretion and plasma renin activity showed a slight gradual rise in the time-control group, but no significant differences were observed between the C and E periods; sodium excretion and plasma renin activity were similar in the high Na and time-control groups during C and R, but significantly different during E. It is concluded that when CSF sodium is elevated by perfusing artificial CSF, the resulting natriuresis and suppression of plasma renin activity are not caused by hemodynamic changes.

摘要

在戊巴比妥麻醉的犬身上进行脑室池灌注。在灌注高钠(300 mM NaCl)人工脑脊液(CSF)(E组)2小时之前,先进行2小时的对照灌注(C组),之后进行2小时的恢复灌注(R组),恢复灌注期间灌注正常(150 mM NaCl)人工脑脊液。一个时间对照组在整个C、E和R阶段均灌注正常人工脑脊液。高钠灌注导致9只动物中的每只都出现明显的利钠作用,并抑制血浆肾素活性。平均动脉压、肾小球滤过率或肾血浆流量没有同时发生变化。钠排泄和血浆肾素活性在时间对照组中略有逐渐上升,但在C期和E期之间未观察到显著差异;在C期和R期,高钠组和时间对照组的钠排泄和血浆肾素活性相似,但在E期有显著差异。得出的结论是,当通过灌注人工脑脊液使脑脊液钠升高时,由此产生的利钠作用和血浆肾素活性的抑制不是由血流动力学变化引起的。

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1
Nonpressor mechanisms in CNS-induced natriuresis.中枢神经系统诱导性利钠中的非加压机制。
Am J Physiol. 1979 Aug;237(2):157-66. doi: 10.1152/ajprenal.1979.237.2.F157.
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引用本文的文献

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Natriuretic hormones, endogenous ouabain, and related sodium transport inhibitors.利钠激素、内源性哇巴因及相关钠转运抑制剂。
Front Endocrinol (Lausanne). 2014 Dec 3;5:199. doi: 10.3389/fendo.2014.00199. eCollection 2014.
2
Lack of evidence for a cerebral sodium modulating mechanism in the monkey.猴子大脑中缺乏钠调节机制的证据。
Basic Res Cardiol. 1987 Jul-Aug;82(4):319-25. doi: 10.1007/BF01907019.
3
Cerebral regulation of renal sodium excretion in sheep infused intravenously with hypertonic NaCl.静脉输注高渗氯化钠的绵羊肾钠排泄的脑调节
J Physiol. 1989 Nov;418:273-91. doi: 10.1113/jphysiol.1989.sp017840.