Quillen E W, Reid I A
Department of Physiology, University of California, San Francisco.
Circ Res. 1988 Oct;63(4):702-11. doi: 10.1161/01.res.63.4.702.
Intravertebral infusion of angiotensin II (Ang II) increases mean arterial pressure (MAP), but the contribution of cardiac output (CO) and total peripheral resistance (TPR) to this increase is unclear. In the present study, the effects of Ang II infusion on CO and regional blood flow was determined by the microsphere technique in eight conscious, chronically catheterized dogs. Ang II was infused into both vertebral arteries at 0.33 and 1.0 ng/kg/min, and intravenously at 0.66, 2.0 and 5.0 ng/kg/min. Intravertebral infusion of Ang II at 0.33 ng/kg/min increased MAP by increasing CO without changing TPR or peripheral plasma Ang II concentration. MAP also was increased with intravertebral infusion of Ang II at 1.0 ng/kg/min, but this resulted from small increases in both CO and TPR. In contrast, intravenous infusion of Ang II at 2.0 and 5.0 ng/kg/min increased MAP by increasing TPR in association with a decrease in CO. The increase in CO with intravertebral infusion of Ang II at 0.33 ng/kg/min was distributed primarily to the muscles, kidneys, heart, and brain. Intravenous infusion of Ang II at 5.0 ng/kg/min and, to a lesser extent, 2.0 ng/kg/min decreased blood flow to the skin, splanchnic region, and kidneys. These data indicate that the increase in MAP produced by a low intravertebral dose of Ang II results from an increase in CO, which is distributed primarily to the muscle, kidney, heart, and brain. In contrast, the increase in MAP produced by a higher intravertebral dose of Ang II results from increases in CO and TPR. This latter action is apparently due to a peripheral action of Ang II to increase resistance in the skin, splanchnic, and renal circulations.
椎体内输注血管紧张素 II（Ang II）可使平均动脉压（MAP）升高，但心输出量（CO）和总外周阻力（TPR）对这种升高的贡献尚不清楚。在本研究中，通过微球技术在8只清醒、长期插管的犬中确定了Ang II输注对CO和局部血流的影响。以0.33和1.0 ng/kg/min的剂量将Ang II输注到双侧椎动脉中，并以0.66、2.0和5.0 ng/kg/min的剂量静脉输注。以0.33 ng/kg/min的剂量椎体内输注Ang II通过增加CO而不改变TPR或外周血浆Ang II浓度来升高MAP。以1.0 ng/kg/min的剂量椎体内输注Ang II时MAP也升高，但这是由于CO和TPR均略有增加所致。相比之下，以2.0和5.0 ng/kg/min的剂量静脉输注Ang II通过增加TPR并伴有CO降低来升高MAP。以0.33 ng/kg/min的剂量椎体内输注Ang II时CO的增加主要分布到肌肉、肾脏、心脏和大脑。以5.0 ng/kg/min的剂量静脉输注Ang II，以及在较小程度上以2.0 ng/kg/min的剂量静脉输注Ang II时，会减少皮肤、内脏区域和肾脏的血流。这些数据表明，低剂量椎体内Ang II引起的MAP升高是由CO增加所致，CO主要分布到肌肉、肾脏、心脏和大脑。相比之下，较高剂量椎体内Ang II引起的MAP升高是由CO和TPR增加所致。后一种作用显然是由于Ang II的外周作用导致皮肤、内脏和肾循环中的阻力增加。
