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Articles in PresS, published online ahead of print November 29, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00490.2001
Submitted on August 14, 2001
Accepted on November 16, 2001
1 Physiology, Wayne State University School of Medcine, Detroit, Michigan, USA
* To whom correspondence should be addressed. E-mail: sdicarlo{at}med.wayne.edu.
We tested the hypothesis that a single bout of dynamic exercise produces a post-exercise hypotension (PEH) and
1-adrenergic receptor hypo-responsiveness in spontaneously hypertensive rats (SHR). Furthermore, the post-exercise
1-adrenergic receptor hypo-responsiveness 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 micro-renathane catheter was inserted into a branch of the femoral artery for the infusion of the
1-adrenergic receptor agonist phenylephrine (PE). A micro-renathane catheter was inserted into the descending aorta via the left common carotid artery for measurements of arterial pressure (AP) and heart rate (HR). Dose response curves to PE (3.8 x 10 -3 µg/kHz - 1.98 x 10 -2 µg/kHz) were generated before and after a single bout of dynamic exercise. Post-exercise AP was reduced in male (13 ± 3 mmHg) and female SHR (18 ± 7 mmHg). Post-exercise vasoconstrictor responses to PE were reduced in males due to an enhanced influence of nitric oxide. However in females, post-exercise vasoconstrictor responses to PE were not altered. Results suggest that nitric oxide mediated
1-adrenergic receptor hypo-responsiveness contributes to PEH in male but not female SHR.
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