Journal of Applied Physiology
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J Appl Physiol (September 1, 2005). doi:10.1152/japplphysiol.00959.2005
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Submitted on August 5, 2005
Accepted on August 25, 2005

H2-Receptor Mediated Vasodilation Contributes to Postexercise Hypotension

Jennifer L McCord1, Julie M Beasley1, and John R Halliwill1*

1 Department of Human Physiology, University of Oregon, Eugene, OR, USA

* To whom correspondence should be addressed. E-mail: halliwil{at}uoregon.edu.

The early (~30 min) postexercise hypotension response after a session of aerobic exercise is due in part to H1-receptor mediated vasodilation. The purpose of this study was to determine the potential contribution of H2-receptor mediated vasodilation to postexercise hypotension. We studied ten healthy normotensive men and women (ages 23.7 ± 3.4 yr) before and through 90 min after a 60 min bout of cycling at 60% VO2peak on randomized control and H2-receptor antagonist days (300 mg oral ranitidine). Arterial pressure (automated auscultation), cardiac output (acetylene-washin) and femoral blood flow (Doppler ultrasound) were measured. Vascular conductance was calculated as flow/mean arterial pressure. Sixty min postexercise on the control day, femoral ({Delta} 62.3 ± 15.6%; P < 0.01) and systemic ({Delta} 13.8 ± 5.3%; P = 0.01) vascular conductances were increased while mean arterial pressure was reduced ({Delta} -6.7 ± 1.1 mmHg; P < 0.01). Conversely, 60 min postexercise with ranitidine, femoral ({Delta} 9.4 ± 9.2%; P = 0.34) and systemic ({Delta} -2.8 ± 4.8%; P = 0.35) vascular conductances were not elevated and mean arterial pressure was not reduced ({Delta} -2.2 ± 1.3 mmHg; P = 0.12). Furthermore, postexercise femoral and systemic vascular conductances were lower (P < 0.05) and mean arterial pressure was higher (P = 0.01) on the ranitidine day compared to control. Ingestion of ranitidine markedly reduces vasodilation after exercise and blunts postexercise hypotension, suggesting H2-receptor mediated vasodilation contributes to postexercise hypotension.




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