Abstract
The purpose of this study was to determine the effects of one-time acute heat treatment (HT) on the exaggerated exercise pressor reflex in a model of peripheral arterial insufficiency induced by ligation of the femoral artery and was to further examine the underlying mechanism of ATP-P2X3 signal activity during this process. The blood pressure (BP) response to static muscle contraction and muscle tendon stretch was recorded to determine the exercise pressor reflex. Also, αβ-methylene ATP (αβ-me ATP) was injected into the arterial blood supply of the hindlimb muscles to stimulate P2X3 receptors in the muscle afferent nerves. To process one-time acute HT, a heating pad was placed locally on the hindlimb and the muscle temperature (Tm) was increased by ~1.5°C and maintained for 5 min. Compared with control rats, a greater mean arterial pressure (MAP) response to muscle contraction was observed in rats with femoral occlusion in a pre-heat control session (28 ± 2 mmHg in occluded rats/n = 12 vs. 18 ± 2 mmHg in control rats/n = 9; p < 0.05). The one-time acute HT attenuated the amplification of the BP response in rats with femoral artery occlusion (MAP response: 19 ± 8 mmHg in occluded rats + HT/n = 11; p < 0.05 vs. occluded rats). In contrast, HT did not significantly attenuate amplification of MAP response to muscle stretch and αβ-me ATP injection in rats with femoral artery occlusion and controls (all p > 0.05). Our data suggest that one-time acute HT selectively attenuates the amplified pressor response induced by activation of the metabolic and mechanical components of the reflex in rats after femoral artery occlusion. The suppressing effects of acute HT on the exaggerated exercise pressor reflex are likely mediated through a reduction in metabolites (e.g., ATP) stimulating the muscle afferent nerves in contracting muscle, but unlikely through direct alteration of P2X receptors per se.
Highlights
On a global scale, peripheral artery disease (PAD) is one of the major cardiovascular concerns and affects more than 200 million individuals (Song et al, 2019)
A greater mean arterial pressure (MAP) response following static muscle contraction was observed in PAD rats (26 ± 8 mmHg in PAD rats/n = 11 vs. 18 ± 5 mmHg in control rats/n = 10; p < 0.05) during the pre-heat CON session
In post-heat REC session (20 min after the heat treatment (HT)), a greater MAP response during static muscle contraction was regained in PAD rats (27 ± 3 mmHg in PAD rats/n = 10 vs. 20 ± 4 mmHg in control rats/n = 8; p < 0.05)
Summary
Peripheral artery disease (PAD) is one of the major cardiovascular concerns and affects more than 200 million individuals (Song et al, 2019). A risk of cardiovascular events should be considered for the patients during the exercise activity (Collins and Billman, 1989). In the process of exercise, the mechanical stimuli and the metabolic products (e.g., lactate, ATP, and protons) generated in the contracting muscles activate the receptors in the Group III and IV muscle afferents (Li and Xing, 2012). The peripheral mechanism leading to increases in blood pressure (BP) and heart rate (HR) responses to muscle contraction during exercise was termed as the “exercise pressor reflex (EPR)” (Coote et al, 1971; McCloskey and Mitchell, 1972; Victor et al, 1988; Sinoway et al, 1989). The SNA reduces muscle metabolite-mediated vasodilation (Shoemaker et al, 1999; Hammond et al, 2001), and limits the blood flow directed to the exercising muscles.
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