Juul B, Aalkjaer C, Mulvany M J
Eur J Pharmacol. 1987 Mar 3;135(1):61-8. doi: 10.1016/0014-2999(87)90757-6.
The effect of angiotensin II and angiotensin I on isolated rat resistance vessels (inner diameter ca. 200 micron) was investigated. Angiotensin II caused a contraction (ED50 = 0.58 +/- 0.17 X 10(-8) M) of rat femoral and cerebral arteries and to a lesser extent of mesenteric and renal arteries. However, all vessels showed strong tachyphylaxis on repeated stimulation with angiotensin II. Tachyphylaxis was avoided by inducing submaximal tone in the vessels with either K, noradrenaline or serotonin. The response to angiotensin II was inhibited by saralasin but not by captopril. Angiotensin I also caused contraction of the femoral arteries (ED50 = 2.68 +/- 0.32 X 10(-8) M). These responses were inhibited by captopril and saralasin. Functional removal of the endothelium had little effect on the contractile responses to either angiotensin I or II. These results indicate that there are functional receptors to angiotensin II in the resistance vessels of the rat and that, in the presence of tone (a more physiological condition), the vessels contract to angiotensin II without tachyphylaxis. In addition, angiotensin II may be formed from angiotensin I by the angiotensin converting enzyme which may be situated in the vessel wall as well as in the endothelium.
研究了血管紧张素II和血管紧张素I对离体大鼠阻力血管(内径约200微米)的作用。血管紧张素II使大鼠股动脉和脑动脉收缩(半数有效剂量[ED50]=0.58±0.17×10⁻⁸M),对肠系膜动脉和肾动脉的收缩作用较小。然而,所有血管在用血管紧张素II反复刺激时均表现出强烈的快速耐受性。通过用钾、去甲肾上腺素或5-羟色胺使血管产生亚最大张力可避免快速耐受性。血管紧张素II的反应被沙拉新抑制,但不被卡托普利抑制。血管紧张素I也使股动脉收缩(ED50=2.68±0.32×10⁻⁸M)。这些反应被卡托普利和沙拉新抑制。功能性去除内皮对血管紧张素I或II的收缩反应影响很小。这些结果表明,大鼠阻力血管中存在血管紧张素II的功能性受体,并且在有张力(更接近生理状态)的情况下,血管对血管紧张素II收缩而无快速耐受性。此外,血管紧张素II可能由血管紧张素I通过血管紧张素转换酶形成,该酶可能位于血管壁以及内皮中。