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Inhibition of K ATP channel activity augments baroreflex‐mediated vasoconstriction in exercising human skeletal muscle
Author(s) -
Keller David Melvin,
Ogoh Shigehiko,
Greene Shane,
OlivenciaYurvati A.,
Raven Peter B.
Publication year - 2004
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.2004.071993
Subject(s) - vasoconstriction , baroreflex , mean arterial pressure , blood pressure , medicine , cardiology , vasodilation , ingestion , heart rate , anesthesia , endocrinology
In the present investigation we examined the role of ATP‐sensitive potassium (K ATP ) channel activity in modulating carotid baroreflex (CBR)‐induced vasoconstriction in the vasculature of the leg. The CBR control of mean arterial pressure (MAP) and leg vascular conductance (LVC) was determined in seven subjects (25 ± 1 years, mean ± s.e.m. ) using the variable‐pressure neck collar technique at rest and during one‐legged knee extension exercise. The oral ingestion of glyburide (5 mg) did not change mean arterial pressure (MAP) at rest (86 versus 89 mmHg, P > 0.05), but did appear to increase MAP during exercise (87 versus 92 mmHg, P = 0.053). However, the CBR–MAP function curves were similar at rest before and after glyburide ingestion. The CBR‐mediated decrease in LVC observed at rest (∼39%) was attenuated during exercise in the exercising leg (∼15%, P < 0.05). Oral glyburide ingestion partially restored CBR‐mediated vasoconstriction in the exercising leg (∼40% restoration, P < 0.05) compared to control exercise. These findings indicate that K ATP channel activity modulates sympathetic vasoconstriction in humans and may prove to be an important mechanism by which functional sympatholysis operates in humans during exercise.