Riegger G A, Albert M, Kochsiek K
Medizinische Universitätsklinik, Würzburg, Federal Republic of Germany.
Am J Physiol. 1988 Mar;254(3 Pt 2):H438-42. doi: 10.1152/ajpheart.1988.254.3.H438.
Our objectives were to examine the role of vasopressin and renin in the regulation of peripheral vascular tone in an animal model of right ventricular failure due to chronic (10 wk) pulmonic stenosis. We tested in chronically instrumented conscious control rats and in rats with pulmonic stenosis on a normal and a high-sodium diet both vasoconstrictor systems by applying specific inhibitors. The rats with pulmonic stenosis showed significant hemodynamic changes, a hypertrophy of the right ventricle, increased levels of plasma renin concentration, and inappropriately elevated plasma levels of vasopressin in comparison to control animals. Plasma renin concentration was suppressed in the sodium-loaded controls. After the administration of a specific inhibitor of the vascular receptors of arginine vasopressin [30 micrograms, d(CH2)5Tyr(Me)AVP], we found no hemodynamic changes in control rats on the normal diet, a reduction of mean arterial pressure in the sodium-loaded controls (4 +/- 4 mmHg; P less than 0.005), and in the animals with pulmonic stenosis and normal sodium intake (5 +/- 5 mmHg; P less than 0.001) and high-salt diet (6 +/- 7 mmHg; P less than 0.02). Intravenous bolus injection of teprotide (1 mg/kg) resulted in a decrease of mean arterial pressure in the control group (normal diet) of 9 +/- 8 mmHg (P less than 0.005). The fall of blood pressure (22 +/- 10 mmHg; P less than 0.001) in the rats with pulmonic stenosis was significantly greater (P less than 0.01) and was strongly related to plasma renin concentration. Therefore, vasopressin and the renin-angiotensin system contribute to an increase of peripheral vascular tone in chronic pulmonic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
我们的目的是在因慢性（10周）肺动脉狭窄导致右心室衰竭的动物模型中，研究血管加压素和肾素在调节外周血管张力中的作用。我们通过应用特异性抑制剂，在长期植入仪器的清醒对照大鼠以及正常饮食和高钠饮食的肺动脉狭窄大鼠中，对这两种血管收缩系统进行了测试。与对照动物相比，肺动脉狭窄大鼠出现了显著的血流动力学变化、右心室肥大、血浆肾素浓度升高以及血浆血管加压素水平不适当升高。钠负荷对照大鼠的血浆肾素浓度受到抑制。在给予精氨酸血管加压素血管受体特异性抑制剂[30微克，d(CH2)5Tyr(Me)AVP]后，我们发现正常饮食的对照大鼠无血流动力学变化，钠负荷对照大鼠平均动脉压降低（4±4 mmHg；P<0.005），钠摄入正常的肺动脉狭窄动物（5±5 mmHg；P<0.001）和高盐饮食的动物（6±7 mmHg；P<0.02）也有降低。静脉推注替普罗肽（1 mg/kg）导致对照组（正常饮食）平均动脉压降低9±8 mmHg（P<0.005）。肺动脉狭窄大鼠的血压下降（22±10 mmHg；P<0.001）显著更大（P<0.01），且与血浆肾素浓度密切相关。因此，血管加压素和肾素-血管紧张素系统在慢性肺动脉狭窄中促使外周血管张力增加。（摘要截短于250字）
