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血管紧张素I和II对犬窦房结的体内直接作用。

Direct effects in vivo of angiotensins I and II on the canine sinus node.

作者信息

Lambert C, Godin D, Fortier P, Nadeau R

机构信息

Research Centre, Hôpital du Sacré-Coeur de Montréal, Qué., Canada.

出版信息

Can J Physiol Pharmacol. 1991 Mar;69(3):389-92. doi: 10.1139/y91-059.

Abstract

The chronotropic responses to angiotensins I and II (5 micrograms in 1 mL Tyrode's solution) injected into the sinus node artery were assessed before and after the intravenous administration of captopril (2 mg/kg) and saralasin (20 micrograms/kg) in anaesthetized dogs. The effects of angiotensin II given intravenously were also observed. The animals (n = 8) were vagotomized and pretreated with propranolol (1 mg/kg, i.v.) to prevent baroreceptor-mediated responses to increases in blood pressure. Injection of angiotensin I into the sinus node artery induced significant increases in heart rate (114 +/- 6 vs. 133 +/- 6 beats/min) and in systemic systolic (134 +/- 13 vs. 157 +/- 14 mmHg; 1 mmHg = 133.3 Pa) and diastolic (95 +/- 10 vs. 126 +/- 13 mmHg) blood pressures. Similar results were obtained when angiotensin II was injected into the sinus node artery, but intravenous injection induced changes in systolic (138 +/- 8 vs. 180 +/- 25 mmHg) and diastolic (103 +/- 8 vs. 145 +/- 20 mmHg) blood pressures only. Captopril induced a significant decrease in systolic (118 +/- 11 vs. 88 +/- 12 mmHg) and diastolic (84 +/- 9 vs. 59 +/- 9 mmHg) blood pressures without affecting the heart rate (109 +/- 6 vs. 106 +/- 6 beats/min). Saralasin produced a significant increase in systolic (109 +/- 7 vs. 126 +/- 12 mmHg) blood pressure only. Increments in heart rate and systolic and diastolic blood pressures in response to angiotensins I and II were, respectively, abolished by captopril and saralasin. It was concluded that angiotensin II has, in vivo, a direct positive chronotropic effect that can be blocked by saralasin.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在麻醉犬静脉注射卡托普利(2mg/kg)和沙拉新(20μg/kg)前后,评估了注入窦房结动脉的血管紧张素I和II(1mL Tyrode溶液中含5μg)的变时反应。还观察了静脉注射血管紧张素II的效果。动物(n = 8)行迷走神经切断术并预先用普萘洛尔(1mg/kg,静脉注射)处理,以防止压力感受器介导的对血压升高的反应。向窦房结动脉注射血管紧张素I可使心率(114±6对133±6次/分钟)以及全身收缩压(134±13对157±14mmHg;1mmHg = 133.3Pa)和舒张压(95±10对126±13mmHg)显著升高。向窦房结动脉注射血管紧张素II时也得到类似结果,但静脉注射仅引起收缩压(138±8对180±25mmHg)和舒张压(103±8对145±20mmHg)变化。卡托普利使收缩压(118±11对88±12mmHg)和舒张压(84±9对59±9mmHg)显著降低,而不影响心率(109±6对106±6次/分钟)。沙拉新仅使收缩压(109±7对126±12mmHg)显著升高。卡托普利和沙拉新分别消除了对血管紧张素I和II的心率及收缩压和舒张压升高反应。得出结论:血管紧张素II在体内具有直接的正性变时作用,可被沙拉新阻断。(摘要截短至250字)

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