Regional vascular selectivity of angiotensin II

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 t he influence of endogenous angiotensin II, rats were pretreated with captop ril (30 mg/kg intravenously). Intravenous infusions of angiotensin II were used to produce circulating angiotensin II, and these infusions caused mark ed dose-related (3, 30, and 300 pmol/min) and sustained (2 h) increases in renal vascular resistance, with lesser effects on mesenteric vascular resis tance, little effect on carotid vascular resistance, and no effect on hindq uarter or calculated "other tissue" vascular resistances. In contrast, vaso pressin 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 sele ctively local angiotensin II levels. Intrarenal artery infusions of angiote nsin II increased renal, but not mesenteric, vascular resistance; and intra mesenteric artery infusions of angiotensin II increased mesenteric, but not renal, vascular resistance. Infusions of angiotensin II into the hindquart er and carotid vascular beds caused little change in hindquarter and caroti d 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 p rimarily the renal vascular bed and to a lesser extent the gut circulation, and those tissues that are most responsive to angiotensin II also metaboli ze angiotensin II better than tissues that are less responsive to angiotens in II.