Acute exercise enhances nitric oxide modulation of vascular response to phenylephrine

R. D. Patil, S. E. DiCarlo and H. L. Collins Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown 44272. The influence of the release of endothelium-derived nitric oxide (NO) on the vasoconstrictor response to phenylephrine (PE) was evaluated before and after a single bout of dynamic exercise. Each rat ran on a motor-driven treadmill at 12-18 m/min, 10-18% grade until exhaustion (avg time 45 min). Sprague-Dawley rats (n = 6) were instrumented with a Doppler ultrasonic flow probe around the right common iliac artery. Just distal to the flow probe, a catheter was placed into the right iliac artery for local infusions. A Teflon catheter was placed in the descending aorta to measure mean arterial blood pressure (MAP) and heart rate (HR). PE (0.005-0.075 microgram/kg) and NO inhibitor N omega-nitro-L-arginine methyl ester hydrochloride (L-NAME, 0.2-0.25 mg/kg) were injected into the functionally isolated hindlimb. HR and MAP were not altered by any of the injections because we selected doses below those which elicited systemic responses. Dose-response curves to PE were generated in the control and postexercise condition, with and without the NO synthase inhibitor L-NAME. Exercise significantly attenuated the maximal vasoconstrictor response to PE (45.6 +/- 1.6%). L-NAME enhanced the maximal vasoconstrictor response to PE 49.8 +/- 4.5% in the control condition and 121.4 +/- 5.9% in the postexercise conditions. Thus, although NO inhibition enhanced the vasoconstrictor response to PE in the control and postexercise conditions, the enhanced vasoconstrictor response to PE after L-NAME was significantly greater in the postexercise condition. Results suggest that NO contributes to the exercise induced attenuation of alpha 1-adrenergic receptor stimulation.