Abstract

To examine the actions of angiotensin II on regional vascular resistances, we monitored regional blood flows and cardiac output with transit-time flow probes and thermodilution, respectively, in anesthetized rats. To remove the influence of endogenous angiotensin II, rats were pretreated with captopril (30 mg/kg intravenously). Intravenous infusions of angiotensin II were used to produce circulating angiotensin II, and these infusions caused marked dose-related (3, 30, and 300 pmol/min) and sustained (2 h) increases in renal vascular resistance, with lesser effects on mesenteric vascular resistance, little effect on carotid vascular resistance, and no effect on hindquarter or calculated “other tissue” vascular resistances. In contrast, vasopressin caused similar increases in renal, mesenteric, carotid, hindquarter, and other tissue vascular resistances. Infusions of angiotensin II (3, 10, and 30 pmol/min) into the local arterial blood were used to increase selectively local angiotensin II levels. Intrarenal artery infusions of angiotensin II increased renal, but not mesenteric, vascular resistance; and intramesenteric artery infusions of angiotensin II increased mesenteric, but not renal, vascular resistance. Infusions of angiotensin II into the hindquarter and carotid vascular beds caused little change in hindquarter and carotid vascular resistances, respectively, but sufficient angiotensin II escaped the hindquarter and carotid vascular beds to cause increases in renal and mesenteric vascular resistances. In conclusion, angiotensin II constricts primarily the renal vascular bed and to a lesser extent the gut circulation, and those tissues that are most responsive to angiotensin II also metabolize angiotensin II better than tissues that are less responsive to angiotensin II.