Postexercise alpha-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide.

Abstract

We tested the hypothesis that a single bout of dynamic exercise produces a postexercise hypotension (PEH) and alpha(1)-adrenergic receptor hyporesponsiveness in spontaneously hypertensive rats (SHR). The postexercise alpha(1)-adrenergic receptor hyporesponsiveness is due to an enhanced buffering of vasoconstriction by nitric oxide. Male (n = 8) and female (n = 5) SHR were instrumented with a Doppler ultrasonic flow probe around the femoral artery. Distal to the flow probe, a microrenathane catheter was inserted into a branch of the femoral artery for the infusion of the alpha(1)-adrenergic receptor agonist phenylephrine (PE). A microrenathane catheter was inserted into the descending aorta via the left common carotid artery for measurements of arterial pressure (AP) and heart rate. Dose-response curves to PE (3.8 x 10(-3) - 1.98 x 10(-2)microg/kHz) were generated before and after a single bout of dynamic exercise. Postexercise AP was reduced in male (13 +/- 3 mmHg) and female SHR (18 +/- 7 mmHg). Postexercise vasoconstrictor responses to PE were reduced in males due to an enhanced influence of nitric oxide. However, in females, postexercise vasoconstrictor responses to PE were not altered. Results suggest that nitric oxide- mediated alpha(1)-adrenergic receptor hyporesponsiveness contributes to PEH in male but not female SHR.