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Glibenclamide prevents the attenuation of the exercise pressor reflex by tempol in the ligated rats
Author(s) -
Yamauchi Katsuya,
Leal Anna K.,
Stone Audrey J.,
Kaufman Marc P.
Publication year - 2012
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.26.1_supplement.1078.38
Subject(s) - reflex , glibenclamide , femoral artery , chemistry , medicine , endocrinology , anesthesia , superoxide , pharmacology , biochemistry , enzyme , diabetes mellitus
In decerebrated rats, ligation of a femoral artery has been shown to exaggerate the exercise pressor reflex, an effect which is attenuated by tempol. The action of tempol has been attributed to its ability to scavenge superoxide radicals. Tempol, in addition, opens ATP sensitive potassium channels, an effect which could also explain its ability to attenuate the exercise pressor reflex in rats with ligated femoral arteries. To test this alternative explanation, we measured the effect of femoral arterial injection of glibenclamide (0.1 mg/kg), which blocks ATP sensitive potassium channels, on the tempol‐induced attenuation of the exercise pressor reflex in decerebrated rats whose femoral arteries had been occluded 72 hours before the start of the experiment. In the first group of rats (n=6), which were not given glibenclamide, tempol attenuated the exercise pressor reflex from 36 ± 5 to 15 ± 2 mmHg (P< 0.05). In the second group of rats (n=8), which were given glibenclamide just before tempol, the superoxide scavenger had no effect on the exercise pressor reflex, which averaged 28 ± 2 mmHg before tempol and 26 ± 2 mmHg afterwards (P> 0.05). We conclude that tempol attenuated the exercise pressor reflex by opening ATP sensitive potassium channels on the endings of group III and IV muscle afferents. Tempol does not appear to attenuate the exaggerated exercise pressor reflex by scavenging superoxide radicals.