Systemic hemodynamic effects of chronic intrarenal infusion of angiotensin II: Role of the autonomic nervous system

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Angiotensin n (Ang II, 0.5 ng/kg/min) was infused into the left renal artery of dogs (n=6) for 28 days. Hemodynamic variables were measured over 3 pre-infusion days, on days 1, 7, 14, 21 and 28 of this infusion and 1 and 10 days after cessation of infusion. Mean arterial pressure did not change significantly in the first 24 hr of Ang n infusion but increased significantly over days 14-28 (+5.8±1.7 mmHg, P=0.002). Total peripheral resistance (TPR) (+3.9±1.8 mmHg.min/l, P=0.03) and renal vascular resistance (+0.04±0.02 mmHg.min/ml, P=0.03) also increased significantly, while cardiac output tended to decrease (-0.4±0.2 l/min, P=0.08). Central venous pressure and glomerular filtration rate were not significantly changed but hematocrit rose steadily (+6±2 % on day 28 of infusion, P<0.001). The role of the autonomie nervous system in the developing hypertension was studied using acute ganglion blockade (pentolinium; 6 mg/kg and 3 mg/kg/hr, i.v.) before and during (on days 7, 14 and 28) the infusion. Before Ang II infusion, pentolinium reduced TPR (4±2 mmHg.min/l) and increased arterial pressure (11±4 mmHg) and cardiac output (1.0±0.3 l/min). The increases in arterial pressure and cardiac output following pentolinium were progressively greater during the 4 weeks of Ang II infusion and by day 28 were 27±8 mmHg and 1.8±0.5 l/min, (P=0.02 & 0.03, respectively). In summary, long-term infusion of Ang II directly into the renal artery at a low dose produces chronic, stable hypertension mediated by increased TPR. The results indicate that the autonomie nervous system buffers the rise in arterial pressure.

Original languageEnglish
JournalThe FASEB Journal
Issue number3
Publication statusPublished - 1 Dec 1997
Externally publishedYes

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