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Lack of Sympathetic‐mediated Restraint of Hypoxic Vasodilation
Author(s) -
Naik Jay S,
Hester Robert L
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a278-d
Subject(s) - vasodilation , prazosin , yohimbine , vasoconstriction , phenylephrine , endocrinology , medicine , chemistry , adrenergic antagonist , antagonist , pharmacology , blood pressure , receptor
Systemic hypoxia (SH) causes increases in sympathetic nerve activity (SNA) as well as vasodilation in the skeletal muscle vasculature. Whether the increase in SNA in response to SH restrains the vasodilatory response to hypoxia in order to maintain blood pressure or if it is overridden (i.e., sympatholysis) to facilitate the vasodilation remains controversial. We hypothesized that increased SNA attenuates the magnitude of the vasodilation in response to SH. Male golden hamsters were anesthetized with pentobarbital sodium, and the cremaster muscle was prepared for in vivo microscopy. Animals spontaneously breathed either a gas mixture containing 30%‐O 2 or 8%‐O 2 (3 min.). Experiments were performed in the presence of vehicle or either prazosin (10 −7 M; α 1 ‐antagonist) or yohimbine (10 −5 M; α 2 ‐antagonist) Effectiveness of receptor blockade was verified by examining vasoconstriction to phenylephrine (α 1 ) or clonidine (α 2 ) in the presence of the inhibitor (30 min pretreatment). Maximal vasodilation was measured by administering 10μM Acetylcholine. Control baseline diameter was 9.4 ± 0.6 μm. Neither prazosin nor yohimbine affected baseline diameter. SH produced a vasodilation in cremasteric arterioles (Δ= 12.8 ± 1 μm). Pre‐treating arterioles with either inhibitor had no effect on the hypoxia‐induced vasodilation (Δ= 14.4 ± 3 μm and 9.6 ± 4 μm for prazosin and yohimbine, respectively). Acetylcholine‐induced vasodilation was significantly larger than that caused by SH (Δ= 19.8 ±2 μm). These results suggest that sympathetic‐mediated vasoconstriction is overridden, maximizing the vasodilatory response to SH. This work was supported by NIH F32HL082438 and NIH HL‐51971 and HL 63958.