VASCULAR ANGIOTENSIN AND THE SYMPATHETIC NERVOUS-SYSTEM - DO THEY INTERACT

We tested the hypothesis that local vascular formation of angiotensin (ANG) II and the sympathetic nervous system potentiate each other. Iso lated rat hindquarters were perfused with an artificial medium, and AN G I and II release was measured by highperformance liquid chromatograp hy and radioimmunoassay. Electrical stimulation of the lumbar sympathe tic chain (0.5, 2, and 8 Hz) did not affect vascular ANG release in Sp rague-Dawley (SD) rats. Hypertensive, ren-2 transgenic (TG+) rat hindq uarters released significantly more ANG I (110 +/- 19 vs. 65 +/- 21 fm ol/30 min in SD rats) and ANG II (235 +/- 22 vs. 140 +/- 30 fmol/30 mi n); however, nerve stimulation did not alter ANG release in TG+ rats. Captopril inhibited vascular ANG II release by 90%, but neither captop ril nor ANG II receptor blockade by losartan affected the presser resp onse to nerve stimulation in SD and TG+ rats. Isoproterenol failed to increase either vascular ANG release or presser response to nerve stim ulation in SD or spontaneously hypertensive rat hindquarters. Exogenou s renin, which increased vascular ANG release approximately 100-fold, prolonged the presser responses to nerve stimulation. We conclude that the vascular renin-ANG system does not interact with the sympathetic nervous system locally. However, high concentrations of ANG II, which can be induced by circulation-derived renin, may prolong the duration of sympathetic nerve-induced vasoconstriction.