Effect of angiotensin II on plasma adenosine concentrations in the rat

Our previous studies indicate that angiotensin II may stimulate release of adenosine from rat lungs, leading to an increase in plasma adenosine concentrations in renovascular hypertensive rats. Such an increase in plasma adenosine levels might be of physiological importance since this nucleoside is a known inhibitor of renin release and could therefore participate in a negative feedback loop whereby angiotensin II could limit its own biosynthesis. However, our previous studies examining angiotensin II-induced adenosine release were performed under nonphysiological conditions involving, in one case, perfusion of rat lungs with a salt solution and, in another case, collection of plasma adenosine samples from anesthetized, laparotomized rats. In the present study, we have addressed the hypothesis that angiotensin II stimulates an increase in plasma adenosine concentrations under more physiological conditions. Using microbore high-performance liquid chromatography, we determined the concentrations of adenosine in plasma samples collected from (a) the left ventricle and jugular vein of anesthetized rats during acute intravenous infusions of angiotensin II (1, 10, and 100 ng/min) and (b) the carotid artery of conscious, unrestrained rats exposed to chronic elevations of either exogenous angiotensin II (intraperitoneal infusion of angiotensin II, 125 ng/min) or endogenous angiotensin II (induction of renovascular hypertension by clipping the left renal artery or by ligating the suprarenal aorta). Both ventricular and venous plasma levels of adenosine were significantly elevated in anesthetized rats during acute infusions of angiotensin II at 10 ng/min but not at the higher and lower infusion rates.(ABSTRACT TRUNCATED AT 250 WORDS)