Article
Temperature modulates P2X receptor-mediated cardiovascular responses to muscle afferent activation.
Heart and Vascular Institute, Division of Cardiology, Department of Medicine, H047, Penn State College of Medicine, Milton S. Hershey Medical Center, 500 University Dr., Hershey, PA 17033, USA.
AJP Heart and Circulatory Physiology (impact factor:
3.71).
10/2006;
291(3):H1255-61.
DOI:10.1152/ajpheart.01303.2005
Source: PubMed
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Citations (0)
- Cited In (2)
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Article: Interstitial adenosine triphosphate modulates muscle afferent nerve-mediated pressor reflex.
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ABSTRACT: Previous work has shown that muscle contraction elevates interstitial adenosine triphosphate concentration ([ATP]i), which is likely due to the release of ATP from active skeletal muscle. ATP activation of purinergic receptors P2X on thin muscle afferent fibers further enhances cardiovascular responses to contraction. Thus, the purposes of this study were: (1) to examine the mechanisms by which ATP is released from muscle in response to mechanical stimulation; and (2) to study the effects of interstitial ATP concentrations on modulating pressor response to muscle contraction. Static contraction of the triceps surae muscle was evoked by electrical stimulation (at 5 HZ and 2.5 times motor threshold) of the tibial nerve in 9 anesthetized cats. Muscle interstitial ATP samples were collected from microdialysis probes inserted into the muscles. Dialysate ATP concentrations were determined using the luciferin-luciferase assay. In a control experiment, contraction was induced after 0.5 ml of saline was injected into the arterial blood supply of the hindlimb muscles. This increased [ATP]i by 220% (P < 0.05 vs. baseline). After gadolinium (1 mM), a blocker of mechanically sensitive channels, was injected into the muscles, contraction increased [ATP]i by 112% (P < 0.05 vs. control). In contrast, glibenclamide (an inhibitor of the ATP-binding cassette protein), monensin, and brefeldin A, which interfere with vesicular formation (or trafficking) and inhibit exocytosis, did not significantly affect ATP release by muscle contraction. In addition, a regression analysis showed that [ATP]i was linearly related to the pressor response to muscle contraction. The data suggest that ATP release from skeletal muscle is mediated via involvement of mechanosensitive channels. These findings further support a physiological role for release of ATP in modulating cardiovascular responses during static muscle contraction.Muscle & Nerve 07/2008; 38(2):972-7. · 2.37 Impact Factor -
Article: Exaggerated Pressor Response in Relation to Attenuated Muscle Temperature Response during Contraction in Ischemic Heart Failure.
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ABSTRACT: It is known that muscle temperature (T(m)) increases with exercise. The purpose of this study was to examine if contraction-induced increase in T(m) was altered in rats with heart failure (HF) induced by chronic myocardial infraction (MI) as compared with healthy control animals. A temperature probe was inserted in the triceps surae muscle to continuously measure T(m) throughout experiments. Static muscle contraction was induced by electrical stimulation of the sciatic nerve for 1 min. As baseline T(m) was 34°C, contraction increased temperature by 1.6 ± 0.18°C in nine health control rats and by 1.0 ± 0.15°C in 10 MI rats (P < 0.05 vs. control). Note that there were no differences in developed muscle tension and muscle weight between the two groups. In addition, muscle contraction increased mean arterial pressure by 23 ± 3 mmHg in control rats and by 31 ± 3 mmHg in MI rats (P < 0.05 vs. control). A regression analysis further shows that there is an inverse liner relationship between the pressor response and static contraction-induced increase in T(m). Our data suggest that T(m) increase evoked by contraction is impaired in MI rats. The abnormal alteration in T(m) likely modifies the reflex cardiovascular responses in MI via mechanisms of temperature-sensitive receptors on muscle afferent nerves.Frontiers in physiology. 01/2012; 3:443.
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Keywords
35 degrees
35 degrees C
39 degrees C
5 min
arterial blood supply
arterial pressure
enhances cardiovascular responses induced
hindlimb muscle
increases blood pressure
MAP response
muscle interstitial space
muscle mechanoreceptors
Muscle stretch
muscle temperature
P2X receptor
purinergic P2X receptors
reflex muscle response
static muscle contraction
stimulate P2X receptors
stretch-evoked response