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β-肾上腺素能刺激释放的血管紧张素II在大鼠中的作用。

Role of vascular angiotensin II released by beta-adrenergic stimulation in rats.

作者信息

Nakamaru M, Jackson E K, Inagami T

出版信息

J Cardiovasc Pharmacol. 1986;8 Suppl 10:S1-5. doi: 10.1097/00005344-198600101-00002.

Abstract

The effect of a beta-adrenoceptor agonist on the release of the components of the vascular renin-angiotensin system was examined in vitro. Isolated rat mesenteric arteries were perfused in an open system with Krebs-Ringer solution and released immunoreactive angiotensin II (ANG IIir) into the perfusate was directly determined using a Sep-Pak C-18 cartridge connected to the perfusion system. Renin activity in the concentrated perfusate was also determined. Isoproterenol (1 nM-1 microM) increased the release of ANG IIir in a dose-dependent manner. The increase in ANG IIir release during isoproterenol (1 microM) infusion was inhibited by propranolol (1 microM) or captopril (2 microM). Isoproterenol-induced increment of ANG IIir release was blocked by the selective beta 2-adrenoceptor antagonist, ICI 118,551 (1 microM), but not by the selective beta 1-adrenoceptor antagonist, atenolol (1 microM). Renin activity in the perfusate was measurable, but did not increase in response to isoproterenol (1 microM) infusion. There was no significant difference in the response of ANG IIir release to isoproterenol between spontaneously hypertensive rats and Wistar-Kyoto rats. The present results indicate that locally generated ANG II is released by beta 2-adrenoceptor activation. The beta-adrenoceptor agonist and the vascular renin-angiotensin system may play an important role for the regulation of peripheral vascular tone.

摘要

在体外研究了β-肾上腺素能受体激动剂对血管肾素-血管紧张素系统各成分释放的影响。在开放系统中,用 Krebs-Ringer 溶液灌注分离的大鼠肠系膜动脉,并使用连接到灌注系统的 Sep-Pak C-18 柱直接测定灌注液中释放的免疫反应性血管紧张素 II(ANG IIir)。还测定了浓缩灌注液中的肾素活性。异丙肾上腺素(1 nM - 1 μM)以剂量依赖的方式增加了 ANG IIir 的释放。在输注异丙肾上腺素(1 μM)期间,ANG IIir 释放的增加被普萘洛尔(1 μM)或卡托普利(2 μM)抑制。异丙肾上腺素诱导的 ANG IIir 释放增加被选择性β2-肾上腺素能受体拮抗剂 ICI 118,551(1 μM)阻断,但未被选择性β1-肾上腺素能受体拮抗剂阿替洛尔(1 μM)阻断。灌注液中的肾素活性可测量,但对输注异丙肾上腺素(1 μM)无反应。自发性高血压大鼠和 Wistar-Kyoto 大鼠之间,ANG IIir 释放对异丙肾上腺素的反应没有显著差异。目前的结果表明,局部生成的 ANG II 通过β2-肾上腺素能受体激活而释放。β-肾上腺素能受体激动剂和血管肾素-血管紧张素系统可能在外周血管张力的调节中起重要作用。

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