Fitzgerald S M, Stevenson K M, Evans R G, Anderson W P
Department of Physiology, Monash University, Clayton, Victoria, Australia.
Am J Physiol. 1997 Dec;273(6):R1980-9. doi: 10.1152/ajpregu.1997.273.6.R1980.
Chronic intrarenal infusion of angiotensin II (0.5 ng.kg-1.min-1) in dogs increases arterial pressure. In the present study we determined whether this was associated with changes in cardiac output or in total peripheral resistance. Mean arterial pressure did not change initially but was significantly increased over days 14-28 of the infusion period (+6 +/- 2 mmHg), as was total peripheral resistance (+4 +/- 2 mmHg.min.l-1). Neither cardiac output, renal blood flow, nor glomerular filtration rate was significantly changed over this period. To determine the influence of the autonomic nervous system on the developing hypertension, periodic acute autonomic ganglion blockade was performed. Before angiotensin II infusion ganglion blockade reduced total peripheral resistance and increased cardiac output, and this effect was similar across the 4 wk of angiotensin II infusion. Systemic hemodynamics were not affected by intravenous angiotensin II infusion (0.5 ng.kg-1.min-1). Thus intrarenal infusion of low-dose angiotensin II produced a chronic increase in arterial pressure due to an action within the kidney. The hypertension was associated with increased total peripheral resistance but not with marked changes in cardiac output or renal function or in the influence of the autonomic nervous system on systemic hemodynamics.
给犬慢性肾内输注血管紧张素II(0.5纳克·千克⁻¹·分钟⁻¹)可使动脉压升高。在本研究中,我们确定这是否与心输出量或总外周阻力的变化有关。平均动脉压最初未改变,但在输注期的第14 - 28天显著升高(+6±2毫米汞柱),总外周阻力也是如此(+4±2毫米汞柱·分钟·升⁻¹)。在此期间,心输出量、肾血流量和肾小球滤过率均无显著变化。为了确定自主神经系统对高血压发展的影响,进行了周期性急性自主神经节阻断。在输注血管紧张素II之前,神经节阻断可降低总外周阻力并增加心输出量,且在血管紧张素II输注的4周内这种效应相似。静脉输注血管紧张素II(0.5纳克·千克⁻¹·分钟⁻¹)对全身血流动力学无影响。因此,肾内输注低剂量血管紧张素II由于其在肾内的作用导致动脉压慢性升高。高血压与总外周阻力增加有关,但与心输出量、肾功能或自主神经系统对全身血流动力学的影响无明显变化无关。