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血管紧张素诱导的变力作用的温度敏感性。

Temperature sensitivity of angiotensin-induced inotropic effects.

作者信息

Trachte G J, Peach M J

出版信息

Proc Soc Exp Biol Med. 1984 Oct;177(1):47-54. doi: 10.3181/00379727-177-41910.

DOI:10.3181/00379727-177-41910
PMID:6473355
Abstract

Temperatures in the range of 30 to 37 degrees C were examined for effects on angiotensin (Ang) peptide-induced inotropic actions in rabbit isolated aortic rings and left atria. Both transmurally-stimulated and punctate-stimulated atria were employed to examine neurogenic and direct cardiac actions of the Ang, respectively. The peptides examined were Ang II, Ang III, and sarcosyl1-Ang II. Ang III was more potent at 33 degrees C than at 37 degrees C in the transmurally stimulated atria, in which the Ang III concentration-response curve was shifted roughly 10-fold to the left at 33 degrees C in comparison to 37 degrees C. Sarcosyl1-Ang II responses were maximal at 37 degrees C and significantly reduced at lower temperatures in aortic rings (30 degrees C) and in transmurally stimulated atria (30 and 33 degrees C). Ang II actions were not significantly altered by temperature changes in the 30 to 37 degrees C range except in transmurally stimulated atria, in which angiotensin II was more potent at 30 degrees C than at 33 degrees C. The results indicate that relatively small temperature alterations can profoundly affect potency ratios and maximal responses among the angiotensin peptides particularly when the angiotensin response is mediated in part by activation of sympathetic neurons, as in the transmurally stimulated atria. The data are consistent with either different mechanisms of cellular stimulation or multiple populations of receptors for the angiotensins. The greater effect of temperature alterations on angiotensin responses in the transmurally stimulated atria suggests that the peptides influence sympathetic nerves and cardiac or smooth muscle differently.

摘要

研究了30至37摄氏度范围内的温度对兔离体主动脉环和左心房中血管紧张素(Ang)肽诱导的变力作用的影响。分别采用经壁刺激心房和点状刺激心房来检测Ang的神经源性和直接心脏作用。所检测的肽为血管紧张素II(Ang II)、血管紧张素III(Ang III)和肌氨酰 - Ang II。在经壁刺激的心房中,Ang III在33摄氏度时比在37摄氏度时更有效,与37摄氏度相比,33摄氏度时Ang III浓度 - 反应曲线大致向左移动了10倍。肌氨酰 - Ang II在37摄氏度时反应最大,在主动脉环(30摄氏度)和经壁刺激的心房(30和33摄氏度)中,较低温度下反应显著降低。在30至37摄氏度范围内,除了经壁刺激的心房中血管紧张素II在30摄氏度时比在33摄氏度时更有效外,Ang II的作用并未因温度变化而显著改变。结果表明,相对较小的温度变化可深刻影响血管紧张素肽之间的效价比和最大反应,特别是当血管紧张素反应部分由交感神经元激活介导时,如在经壁刺激的心房中。这些数据与细胞刺激的不同机制或血管紧张素的多种受体群体一致。温度变化对经壁刺激心房中血管紧张素反应的更大影响表明,这些肽对交感神经与心脏或平滑肌的影响不同。

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