Interactions between angiotensin II and nitric oxide during exercise in normal and heart failure rats

1 Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California 95616; and 2 Departments of Kinesiology and of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506 We hypothesized that nitric oxide (NO) opposes ANG II-induced increases in arterial pressure and reductions in renal, splanchnic, and skeletal muscle vascular conductance during dynamic exercise in normal and heart failure rats. Regional blood flow and vascular conductance were measured during treadmill running before (unblocked exercise) and after 1 ) ANG II AT 1 -receptor blockade (losartan, 20 mg/kg ia), 2 ) NO synthase (NOS) inhibition [ N G -nitro- L -arginine methyl ester ( L -NAME); 10 mg/kg ia], or 3 ) ANG II AT 1 -receptor blockade + NOS inhibition (combined blockade). Renal conductance during unblocked exercise (4.79 ± 0.31 ml · 100 g 1 · min 1 · mmHg 1 ) was increased after ANG II AT 1 -receptor blockade (6.53 ± 0.51 ml · 100 g 1 · min 1 · mmHg 1 ) and decreased by NOS inhibition (2.12 ± 0.20 ml · 100 g 1 · min 1 · mmHg 1 ) and combined inhibition (3.96 ± 0.57 ml · 100 g 1 · min 1 · mmHg 1 ;all P