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依那普利酸对心脏β-肾上腺素能刺激收缩反应的影响。

Effect of enalaprilic acid on cardiac contractile response to beta-adrenergic stimulation.

作者信息

Gomez Llambi H, Taquini C M, Mazzadi A, Gallo A, Fontan M, Taquini A C

机构信息

Facultad de Medicina, Universidad de Buenos Aires, Argentina.

出版信息

Hypertension. 1990 Feb;15(2 Suppl):I51-4. doi: 10.1161/01.hyp.15.2_suppl.i51.

DOI:10.1161/01.hyp.15.2_suppl.i51
PMID:1967591
Abstract

Studies in two-kidney--one clip hypertensive rats have demonstrated that long-term treatment with enalapril induced regression of cardiac hypertrophy, but the cardiac contractile response to beta-adrenergic stimulation remained depressed. In the present study, we evaluate the contractile response to beta-adrenergic stimulation of isolated papillary muscle in normal rats with isoproterenol (10(-11) M to 10(-4) M) in the presence of enalaprilic acid (10(-6) M or 10(-4) M) or enalaprilic acid (10(-4) M) and angiotensin II (10(-6) M). Myocardial contractility was characterized by maximal developed tension and maximal rate of rise of tension (+T), and the relaxant effect of isoproterenol by the ratio of (+T), and the maximal velocity of relaxation (-T)(+T/-T ratio). The rest tension (g/mm2) and the cross-sectional area (mm2) were similar in all the muscles studied. Enalaprilic acid (either 10(-6) M or 10(-4) M) in the bath did not induce any change in contractile and relaxation parameters. The increment in +T and -T (expressed as percentage) in response to cumulative doses of isoproterenol (10(-11) M to 10(-4) M) was significantly depressed in the presence of enalaprilic acid (10(-4) M) when compared with control hearts in which only vehicle was added before isoproterenol (p less than 0.05). The addition of angiotensin II after enalaprilic acid (10(-4) M) did not normalize the response in +T and -T. Enalaprilic acid diminishes the contractile response of the papillary muscle to beta-adrenergic stimulation. The inhibition of the local angiotensin II does not seem to be involved in this result.

摘要

对两肾一夹型高血压大鼠的研究表明,依那普利长期治疗可使心脏肥大消退,但心脏对β-肾上腺素能刺激的收缩反应仍受抑制。在本研究中,我们评估了在依那普利酸(10⁻⁶ M或10⁻⁴ M)或依那普利酸(10⁻⁴ M)与血管紧张素II(10⁻⁶ M)存在的情况下,正常大鼠离体乳头肌对异丙肾上腺素(10⁻¹¹ M至10⁻⁴ M)的β-肾上腺素能刺激的收缩反应。心肌收缩力以最大张力发展和张力上升最大速率(+T)为特征,异丙肾上腺素的舒张作用以(+T)与最大舒张速度(-T)的比值(+T/-T比值)来表示。在所研究的所有肌肉中,静息张力(g/mm²)和横截面积(mm²)相似。浴槽中的依那普利酸(10⁻⁶ M或10⁻⁴ M)未引起收缩和舒张参数的任何变化。与仅在异丙肾上腺素前加入溶媒的对照心脏相比,在依那普利酸(10⁻⁴ M)存在时,对累积剂量异丙肾上腺素(10⁻¹¹ M至10⁻⁴ M)的反应中+T和-T的增加(以百分比表示)明显降低(p<0.05)。在依那普利酸(10⁻⁴ M)后加入血管紧张素II并未使+T和-T的反应恢复正常。依那普利酸降低了乳头肌对β-肾上腺素能刺激的收缩反应。局部血管紧张素II的抑制似乎与该结果无关。

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