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心房利钠肽降低培养心肌细胞的收缩性:初步报告。

Atrial natriuretic peptide decreases contractility of cultured heart cell: preliminary report.

作者信息

Vaxelaire J F, Laurent S, Briand V, Michel J B, Schmitt H

机构信息

Laboratory of Cardiovascular Pharmacology, University Broussais-Hotel Dieu, Paris, France.

出版信息

J Hypertens Suppl. 1988 Dec;6(4):S282-3. doi: 10.1097/00004872-198812040-00086.

Abstract

We tested the hypothesis that atrial natriuretic peptide (ANP) has a direct negative inotropic effect on the cultured chick embryo ventricular cell, an experimental system devoid of endogenous neurotransmitters. At 10(-8) and 2.5 x 10(-7) mol/l ANP [rat ANP-(1-23)] significantly and reversibly decreased contractility in spontaneously beating cells. The positive inotropic effect of angiotensin II (2.5 X 10(-7) mol/l) on spontaneously beating cells was fully antagonized by ANP (2.5 X 10(-7) mol/l) and the amplitude of contraction decreased below control levels. In contrast (1) the increase in contractility in response to extracellular calcium was significantly less altered by ANP and (2) the time-course of the positive inotropic effect of the calcium-channel agonist Bay-K-8644 (5 x 10(9) mol/l) or of the beta-adrenergic agonist isoproterenol (10(-6) mol/l) was unchanged by ANP. These results indicate that ANP-(1-23) has a direct negative inotropic effect on cultured chick heart cells and may affect intracellular messengers involved in the cardiac effects of angiotensin II.

摘要

我们检验了如下假设

心房利钠肽(ANP)对培养的鸡胚心室细胞具有直接的负性变力作用,该实验系统不存在内源性神经递质。在浓度为10^(-8)和2.5×10^(-7) mol/L时,ANP [大鼠ANP-(1 - 23)]可显著且可逆地降低自发搏动细胞的收缩性。血管紧张素II(2.5×10^(-7) mol/L)对自发搏动细胞的正性变力作用可被ANP(2.5×10^(-7) mol/L)完全拮抗,且收缩幅度降至对照水平以下。相比之下,(1)ANP对细胞外钙引起的收缩性增加影响较小,(2)钙通道激动剂Bay-K-8644(5×10^(-9) mol/L)或β-肾上腺素能激动剂异丙肾上腺素(10^(-6) mol/L)的正性变力作用的时间进程不受ANP影响。这些结果表明,ANP-(1 - 23)对培养的鸡胚心脏细胞具有直接的负性变力作用,且可能影响参与血管紧张素II心脏效应的细胞内信使。

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