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穹窿下器中的心房利钠肽可减少由血管紧张素引起的饮水或对缺水的反应性饮水。

Atrial natriuretic peptide in the subfornical organ reduces drinking induced by angiotensin or in response to water deprivation.

作者信息

Ehrlich K J, Fitts D A

机构信息

Department of Psychology, University of Washington, Seattle 98195.

出版信息

Behav Neurosci. 1990 Apr;104(2):365-72. doi: 10.1037//0735-7044.104.2.365.

DOI:10.1037//0735-7044.104.2.365
PMID:2140687
Abstract

Three experiments tested whether the subfornical organ (SFO) could be a site of action for the antidipsogenic effects of atrial natriuretic peptide (ANP) in rats. Pretreatment with 100, 230, or 500 pmol ANP in the SFO reduced drinking induced by 10 pmol angiotensin II in the SFO. Drinking in response to water deprivation was reduced by ANP in rats having cannulas in or near the SFO, but not in rats having cannulas distant from the SFO or in the ventricles. Finally, ANP had no effect on eating or drinking after food deprivation, suggesting that the rats in the other experiments were not acutely incapacitated. The SFO may mediate the central effects of ANP on drinking induced by angiotensin or in response to water deprivation and could play a similar role in the central effects of ANP on salt appetite, diuresis, vasopressin secretion, and blood pressure.

摘要

三项实验检验了穹窿下器(SFO)是否可能是心房利钠肽(ANP)对大鼠抗利尿作用的作用位点。在SFO中预先注射100、230或500皮摩尔的ANP,可减少由10皮摩尔血管紧张素II在SFO中诱导的饮水。对于在SFO内或其附近植入套管的大鼠,ANP可减少因缺水引起的饮水,但对于套管植入位置远离SFO或位于脑室中的大鼠则无此作用。最后,ANP对禁食后的进食或饮水没有影响,这表明其他实验中的大鼠并未急性丧失能力。SFO可能介导ANP对血管紧张素诱导饮水或缺水引起饮水的中枢作用,并且可能在ANP对盐食欲、利尿、血管加压素分泌和血压的中枢作用中发挥类似作用。

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Atrial natriuretic peptide in the subfornical organ reduces drinking induced by angiotensin or in response to water deprivation.穹窿下器中的心房利钠肽可减少由血管紧张素引起的饮水或对缺水的反应性饮水。
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