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J Physiol Volume 561, Number 1, 273-282, November 15, 2004 DOI: 10.1113/jphysiol.2004.071993
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Inhibition of KATP channel activity augments baroreflex-mediated vasoconstriction in exercising human skeletal muscle

David Melvin Keller1, Shigehiko Ogoh1, Shane Greene1, A Olivencia-Yurvati1 and Peter B Raven1

1 University of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA

In the present investigation we examined the role of ATP-sensitive potassium (KATP) 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 KATP channel activity modulates sympathetic vasoconstriction in humans and may prove to be an important mechanism by which functional sympatholysis operates in humans during exercise.

(Received 15 July 2004; accepted after revision 31 August 2004; first published online 2 September 2004)
Corresponding author D. M. Keller: Institute for Exercise and Environmental Medicine, 7232 Greenville Ave, Dallas, TX 75231, USA. Email: davidkeller{at}texashealth.org




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