Rioux F, Park W K, Regoli D
Can J Physiol Pharmacol. 1976 Jun;54(3):229-37. doi: 10.1139/y76-035.
Rabbit isolated left atria have been used to study the inotropic action of angiotensin II (ATII). The peptide is active at doses ranging from 1.0 x 10(-9) to 2.8 x 10(-6)M and its inotropic effect is not modified by sotalol, phentolamine, burimamide, and indomethacin. We therefore propose that this effect results from the stimulation of receptors specific for ATII. Dose-response curves of ATII obtained in presence of increasing concentrations of 8-Gly-ATII are gradually displaced to the right, but high doses of the antagonist depressed the maximum contractions caused by ATII. pA2 value for 8-Gly-ATII in this preparation is similar to those observed in vascular and intestinal smooth muscles. Order of potency of analogues of ATII (2-, 3- and 5-Ala-ATII), acting as full agonists, but with reduced affinity, is similar to that found in rabbit aorta strips. It is therefore proposed that receptors for ATII in rabbit isolated left atria are pharmacologically similar to those present in vascular smooth muscles. Positive inotropic effects of angiotensin I, undecapeptide (1-11), dodecapeptide (1-12) and tetradecapeptide (1-14) renin substrate are antagonized by 8-Gly-ATII in similar way as the effect of ATII. This suggests that the action of these peptides is mainly due to stimulation of receptors for ATII. The contribution of myocardial converting enzyme to the action of these peptides is discussed.
兔离体左心房已被用于研究血管紧张素II（ATII）的正性肌力作用。该肽在1.0×10⁻⁹至2.8×10⁻⁶M的剂量范围内具有活性，其正性肌力作用不受索他洛尔、酚妥拉明、丁咪胺和吲哚美辛的影响。因此，我们认为这种作用是由对ATII特异性受体的刺激引起的。在存在浓度不断增加的8-甘氨酰-ATII的情况下获得的ATII剂量-反应曲线逐渐向右移动，但高剂量的拮抗剂会抑制ATII引起的最大收缩。该制剂中8-甘氨酰-ATII的pA2值与在血管和肠道平滑肌中观察到的值相似。作为完全激动剂但亲和力降低的ATII类似物（2-、3-和5-丙氨酰-ATII）的效力顺序与在兔主动脉条中发现的顺序相似。因此，有人提出兔离体左心房中ATII的受体在药理学上与血管平滑肌中的受体相似。血管紧张素I、十一肽（1-11）、十二肽（1-12）和十四肽（1-14）肾素底物的正性肌力作用与ATII的作用一样，被8-甘氨酰-ATII以类似的方式拮抗。这表明这些肽的作用主要是由于对ATII受体的刺激。讨论了心肌转换酶对这些肽作用的贡献。
