title: Acute exercise enhances nitric oxide modulation of vascular response to phenylephrine.
abstract: 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.
authors.affiliation: Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown 44272.
authors.forename: R D
authors.initials: RD
authors.lastname: Patil
authors.forename: S E
authors.initials: SE
authors.lastname: DiCarlo
authors.forename: H L
authors.initials: HL
authors.lastname: Collins
mesh_terms: D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000187:drug effects; D001808:Blood Vessels / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D007083:Iliac Artery / Q000187:drug effects / Q000502:physiology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology*; D010656:Phenylephrine / Q000494:pharmacology*; D005082:Physical Exertion; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology
chemical_list: D010656:Phenylephrine; D009569:Nitric Oxide; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester