Influence of mineralocorticoids and cations on the inotropic effect of angiotensin and norepinephrine in isolated cardiac muscle.
Influence of mineralocorticoids and cations on the inotropic effect of angiotensin and norepinephrine in isolated cardiac muscle.
复制标题
盐皮质激素和阳离子对离体心肌中血管紧张素和去甲肾上腺素正性肌力作用的影响。
DOI：
10.1016/0002-8703(67)90177-9
复制
发表时间：
1967
影响因子：
4.8
通讯作者：
A. M. Lefer
中科院分区：
文献类型：
--
作者：
A. M. Lefer
醛固酮和脱氧皮质酮（DOC）在一个相对较宽的浓度范围内未能加强血管紧张素和去甲肾上腺素在离体猫乳头肌的正性肌力作用。降低沐浴介质中的钙浓度并没有改变这种关系。降低培养基中的钠浓度本身就降低了离体心肌对5×10− 7 M血管紧张素的变力性反应。增加钠浓度可增强血管紧张素的正性肌力作用。这种增强似乎是独立的溶液的渗透压的变化。改变钾的浓度对血管紧张素反应没有任何显著影响。猫的既往利血平化没有改变对血管紧张素的变力性反应，也没有阻断在钠水平升高的情况下观察到的增强效应。因此，这种增强可能不依赖于储存在心脏组织中的儿茶酚胺的释放。改变培养基中钠的浓度并不能改变对4×10−8M去甲肾上腺素的正性变力反应，本研究的结果不能完全解释体内盐皮质激素增强血管紧张素的机制。然而，他们强烈认为，在完整犬中观察到的血管紧张素心脏效应的增强是由这些激素在体内的钠保留效应介导的。
Both aldosterone and desoxycorticosterone (DOC) over a relatively wide range of concentrations failed to potentiate the positive inotropic effect of angiotensin and of norepinephrine in the isolated cat papillary muscle. Lowering the concentration of calcium in the bathing medium did not alter this relationship. Lowering the concentration of sodium in the medium itself reduced the inotropic responsiveness of the isolated cardiac muscle to 5×10−7M angiotensin. Raising the concentration of sodium enhanced the positive inotropic effect of angiotensin. This enhancement seems to be independent of changes in osmolarity of the solution. Altering the concentration of potassium did not have any significant influence on the angiotensin response. Prior reserpinization of the cat did not alter the inotropic response to angiotensin, nor did it block the enhanced effect seen in the presence of an elevated level of sodium. Therefore, the enhancement probably does not depend on the release of catecholamines stored in cardiac tissue. Altering the concentration of sodium in the medium did not modify the positive inotropic response to 4×10−8M norepinephrine.The findings in this study do not completely account for the mechanism of potentiation of angiotensin by mineralocorticoids reported in vivo. However, they strongly suggest that the potentiation of the cardiac effects of angiotensin seen in the intact dog is mediated by the sodium-retaining effects of these hormones in vivo.