Abstract
We reported previously that tempol attenuated the exercise pressor and muscle mechanoreceptor reflexes in rats whose femoral arteries were ligated, whereas tempol did not attenuate these reflexes in rats whose femoral arteries were freely perfused. Although the mechanism whereby tempol attenuated these reflexes in rats whose femoral artery was ligated was independent of its ability to scavenge reactive oxygen species, its nature remains unclear. An alternative explanation for the tempol-induced attenuation of these reflexes involves ATP-sensitive potassium channels (K Atp) and calcium-activated potassium channels (BK Ca), both of which are opened by tempol. We tested the likelihood of this explanation by measuring the effects of either glibenclamide (0.1 mg/kg), which blocks K Atp channels, or iberiotoxin (20 or 40 (μg/kg), which blocks BK Ca channels, on the tempol-induced attenuation of the exercise pressor and muscle mechanoreceptor reflexes in decerebrated rats whose femoral arteries were ligated. We found that glibenclamide prevented the tempol-induced attenuation of both reflexes, whereas iberiotoxin did not. We also found that the amount of protein comprising the pore of the K Atp channel in the dorsal root ganglia innervating hindlimbs whose femoral artery was ligated was significantly greater than that in the dorsal root ganglia innervating hindlimbs whose femoral arteries were freely perfused. In contrast, the amounts of protein comprising the BK Ca channel in the dorsal root ganglia innervating the ligated and freely perfused hindlimbs were not different. We conclude that tempol attenuated both reflexes by opening K Atp channels, an effect that hyperpolarized muscle afferents stimulated by static contraction or tendon stretch.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 332-340 |
| Number of pages | 9 |
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 303 |
| Issue number | 3 |
| State | Published - Aug 1 2012 |
| Externally published | Yes |
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Keywords
- Adenosine 5'-triphosphate
- Calcium-activated potassium channels
- Peripheral artery disease
- Static contraction
- Tendon stretch
- Thin fiber muscle afferents
ASJC Scopus subject areas
- Physiology
- Physiology (medical)
- Cardiology and Cardiovascular Medicine
Cite this
Blockade of ATP-sensitive potassium channels prevents the attenuation of the exercise pressor reflex by tempol in rats with ligated femoral arteries. / Yamauchi, Katsuya; Stone, Audrey J.; Stocker, Sean D.; Kaufman, Marc P.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 303, No. 3, 01.08.2012, p. 332-340.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Blockade of ATP-sensitive potassium channels prevents the attenuation of the exercise pressor reflex by tempol in rats with ligated femoral arteries
AU - Yamauchi, Katsuya
AU - Stone, Audrey J.
AU - Stocker, Sean D.
AU - Kaufman, Marc P
PY - 2012/8/1
Y1 - 2012/8/1
N2 - We reported previously that tempol attenuated the exercise pressor and muscle mechanoreceptor reflexes in rats whose femoral arteries were ligated, whereas tempol did not attenuate these reflexes in rats whose femoral arteries were freely perfused. Although the mechanism whereby tempol attenuated these reflexes in rats whose femoral artery was ligated was independent of its ability to scavenge reactive oxygen species, its nature remains unclear. An alternative explanation for the tempol-induced attenuation of these reflexes involves ATP-sensitive potassium channels (K Atp) and calcium-activated potassium channels (BK Ca), both of which are opened by tempol. We tested the likelihood of this explanation by measuring the effects of either glibenclamide (0.1 mg/kg), which blocks K Atp channels, or iberiotoxin (20 or 40 (μg/kg), which blocks BK Ca channels, on the tempol-induced attenuation of the exercise pressor and muscle mechanoreceptor reflexes in decerebrated rats whose femoral arteries were ligated. We found that glibenclamide prevented the tempol-induced attenuation of both reflexes, whereas iberiotoxin did not. We also found that the amount of protein comprising the pore of the K Atp channel in the dorsal root ganglia innervating hindlimbs whose femoral artery was ligated was significantly greater than that in the dorsal root ganglia innervating hindlimbs whose femoral arteries were freely perfused. In contrast, the amounts of protein comprising the BK Ca channel in the dorsal root ganglia innervating the ligated and freely perfused hindlimbs were not different. We conclude that tempol attenuated both reflexes by opening K Atp channels, an effect that hyperpolarized muscle afferents stimulated by static contraction or tendon stretch.
AB - We reported previously that tempol attenuated the exercise pressor and muscle mechanoreceptor reflexes in rats whose femoral arteries were ligated, whereas tempol did not attenuate these reflexes in rats whose femoral arteries were freely perfused. Although the mechanism whereby tempol attenuated these reflexes in rats whose femoral artery was ligated was independent of its ability to scavenge reactive oxygen species, its nature remains unclear. An alternative explanation for the tempol-induced attenuation of these reflexes involves ATP-sensitive potassium channels (K Atp) and calcium-activated potassium channels (BK Ca), both of which are opened by tempol. We tested the likelihood of this explanation by measuring the effects of either glibenclamide (0.1 mg/kg), which blocks K Atp channels, or iberiotoxin (20 or 40 (μg/kg), which blocks BK Ca channels, on the tempol-induced attenuation of the exercise pressor and muscle mechanoreceptor reflexes in decerebrated rats whose femoral arteries were ligated. We found that glibenclamide prevented the tempol-induced attenuation of both reflexes, whereas iberiotoxin did not. We also found that the amount of protein comprising the pore of the K Atp channel in the dorsal root ganglia innervating hindlimbs whose femoral artery was ligated was significantly greater than that in the dorsal root ganglia innervating hindlimbs whose femoral arteries were freely perfused. In contrast, the amounts of protein comprising the BK Ca channel in the dorsal root ganglia innervating the ligated and freely perfused hindlimbs were not different. We conclude that tempol attenuated both reflexes by opening K Atp channels, an effect that hyperpolarized muscle afferents stimulated by static contraction or tendon stretch.
KW - Adenosine 5'-triphosphate
KW - Calcium-activated potassium channels
KW - Peripheral artery disease
KW - Static contraction
KW - Tendon stretch
KW - Thin fiber muscle afferents
UR - http://www.scopus.com/inward/record.url?scp=84864557866&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84864557866&partnerID=8YFLogxK
M3 - Article
C2 - 22636679
AN - SCOPUS:84864557866
VL - 303
SP - 332
EP - 340
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6135
IS - 3
ER -