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H 1 receptor‐mediated vasodilatation contributes to postexercise hypotension
Author(s) -
Lockwood Jennifer M.,
Wilkins Brad W.,
Halliwill John R.
Publication year - 2005
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2004.080325
Subject(s) - medicine , vasodilation , blood pressure , supine position , mean arterial pressure , femoral artery , vascular resistance , anesthesia , endocrinology , heart rate
In normally active individuals, postexercise hypotension after a single bout of aerobic exercise is due to an unexplained peripheral vasodilatation. Histamine has been shown to be released during exercise and could contribute to postexercise vasodilatation via H 1 receptors in the peripheral vasculature. The purpose of this study was to determine the potential contribution of an H 1 receptor‐mediated vasodilatation to postexercise hypotension. We studied 14 healthy normotensive men and women (ages 21.9 ± 2.1 years) before and through to 90 min after a 60 min bout of cycling at 60% on randomized control and H 1 receptor antagonist days (540 mg oral fexofenadine hydrochloride; Allegra). Arterial blood pressure (automated auscultation) and femoral blood flow (Doppler ultrasound) were measured in the supine position. Femoral vascular conductance was calculated as flow/pressure. Fexofenadine had no effect on pre‐exercise femoral vascular conductance or mean arterial pressure ( P > 0.5). At 30 min postexercise on the control day, femoral vascular conductance was increased (Δ+33.7 ± 7.8%; P < 0.05 versus pre‐exercise) while mean arterial pressure was reduced (Δ−6.5 ± 1.6 mmHg; P < 0.05 versus pre‐exercise). In contrast, at 30 min postexercise on the fexofenadine day, femoral vascular conductance was not elevated (Δ+10.7 ± 9.8%; P = 0.7 versus pre‐exercise) and mean arterial pressure was not reduced (Δ−1.7 ± 1.2 mmHg; P = 0.2 versus pre‐exercise). Thus, ingestion of an H 1 receptor antagonist markedly reduces vasodilatation after exercise and blunts postexercise hypotension. These data suggest H 1 receptor‐mediated vasodilatation contributes to postexercise hypotension.