ACUTE EXERCISE ENHANCES NITRIC-OXIDE MODULATION OF VASCULAR-RESPONSE TO PHENYLEPHRINE

The influence of the release of endothelium-derived nitric oxide (NO) on the vaso-constrictor response to phenylephrine (PE) was evaluated b efore and after a single bout of dynamic exercise. Each rat ran on a m otor-driven treadmill at 12-18 m/min, 10-18% grade until exhaustion (a vg time 45 min). Sprague-Dawley rats (n = 6) were instrumented with a Doppler ultrasonic flow probe-around the right common iliac artery. Ju st distal to the flow probe, a catheter was placed into the right ilia c artery for local infusions. A Teflon catheter was placed in the desc ending aorta to measure mean arterial blood pressure (MAP) and heart r ate (HR). PE (0.005-0.075 mug/kg) and NO inhibitor N(omega)-nitro-L-ar ginine methyl ester hydrochloride (L-NAME, 0.2-0.25 mg/kg) were inject ed into the functionally isolated hindlimb. HR and MAP were not altere d by any of the injections because we selected doses below those which elicited systemic responses. Dose-response curves to PE were generate d in the control and postexercise condition, with and without the NO s ynthase inhibitor L-NAME. Exercise significantly attenuated the maxima l vaso-constrictor response to PE (45.6 +/- 1.6%). L-NAME enhanced the maximal vasoconstrictor response to PE 49.8 +/- 4.5% in the control c ondition and 121.4 +/- 5.9% in the postexercise conditions. Thus, alth ough NO inhibition enhanced the vasoconstrictor response to PE in the control and postexercise conditions, the enhanced vasoconstrictor resp onse to PE after L-NAME was significantly greater in the postexercise condition. Results suggest that NO contributes to the exercise induced attenuation of alpha1-adrenergic receptor stimulation.