Sensitization of group III muscle afferents to static contraction by arachidonic acid

Rotto, D. M.; Schultz, Harold D.; Longhurst, John C.; Kaufman, Marc P.

doi:10.1152/jappl.1990.68.3.861

Cited by 126 publications

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“…Likewise, during contraction it is also plausible that mechanoreceptors are sensitized to mechanical stimulation by alterations in the chemical milieu of the muscle interstitium. 33 In support of this concept, impaired removal of exercise-induced metabolites, which may serve to sensitize these afferent neurons, is likely to occur in heart failure. 5,9 …”

Section: Discussionmentioning

confidence: 99%

“…As stated, it is plausible that initial reductions in peripheral blood flow result in an abnormal accumulation of exercise-induced metabolites in the muscle interstitium. 5,9 As a result, mechanically sensitive neurons may become sensitized to physical distortion, 33 whereas metaboreceptors undergo a period of hyperexcitability. Prolonged exposure to these metabolites may eventually serve to desensitize 22,35 or downregulate metabolically sensitive neurons, culminating in a decrease in their activity.…”

Section: Perspectivesmentioning

confidence: 99%

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Role of the Exercise Pressor Reflex in Rats With Dilated Cardiomyopathy

et al. 2003

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Background-In heart failure, there is a sympathetically mediated hyperkinetic cardiovascular response to exercise that limits tolerance to physical activity. Alterations in skeletal muscle morphology and metabolism have led to the hypothesis that the exercise pressor reflex (EPR) becomes hyperactive after the development of cardiomyopathy and contributes to the exaggerated circulatory response elicited. Methods and Results-To test this hypothesis, Sprague-Dawley rats were divided into the following groups: control, sham, and dilated cardiomyopathy (DCM, induced by ischemic injury). Using transthoracic echocardiography, left ventricular fractional shortening was 47Ϯ2%, 44Ϯ1%, and 24Ϯ2% in control, sham, and DCM rats, respectively. Activation of the EPR by electrically induced static muscle contraction resulted in significantly larger increases in mean arterial pressure and heart rate in DCM animals (32Ϯ2 mm Hg, 13Ϯ1 bpm) compared with control (20Ϯ1 mm Hg, 8Ϯ1 bpm) and sham (20Ϯ2 mm Hg, 8Ϯ1 bpm) rats. Comparable results were obtained with selective stimulation of the mechanically sensitive component of the EPR by passive muscle stretch. The augmentations in EPR and mechanoreflex activity in DCM occurred progressively over a 10-week period, becoming greater as the severity of left ventricular dysfunction increased. Conclusions-In DCM, the potentiated cardiovascular response to static muscle contraction is mediated, in part, by an exaggerated EPR. The muscle mechanoreflex contributes significantly to the EPR dysfunction that develops.

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Section: Discussionmentioning

confidence: 99%

Section: Perspectivesmentioning

confidence: 99%

Role of the Exercise Pressor Reflex in Rats With Dilated Cardiomyopathy

et al. 2003

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“…Mechanoreceptor sensitivity can be altered by a variety of factors, including prostaglandins, bradykinin, and lactic acid (6,27). Arachidonic acid derivatives have been found to selectively excite mechanoreceptors and not metaboreceptors (22,23). Therefore, it is possible that in the heating trials the increased muscle temperature may have altered the chemical milieu of the muscle and increased the concentration of a neurologically active substance that could sensitize the mechanoreceptors.…”

Section: Discussionmentioning

confidence: 99%

Changes in forearm muscle temperature alter renal vascular responses to isometric handgrip

Kuipers

Sauder²,

Kearney³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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The purpose of the present study was to examine the effect of heating and cooling the forearm muscles on renal vascular responses to ischemic isometric handgrip (IHG). It was hypothesized that heating and cooling the forearm would augment and attenuate, respectively, renal vascular responses to IHG. Renal vascular responses to IHG were studied during forearm heating at 39°C ( n = 15, 26 ± 1 yr) and cooling at 26°C ( n = 12, 26 ± 1 yr). For a control trial, subjects performed the experimental protocol while the forearm was normothermic (∼34°C). Muscle temperature (measured by intramuscular probe) was controlled by changing the temperature of water cycling through a water-perfused sleeve. The experimental protocol was as follows: 3 min at baseline, 1 min of ischemia, ischemic IHG to fatigue, and 2 min of postexercise muscle ischemia. At rest, renal artery blood velocity (RBV; Doppler ultrasound) and renal vascular conductance (RVC = RBV/mean arterial blood pressure) were not different between normothermia and the two thermal conditions. During ischemic IHG, there were greater decreases in RBV and RVC in the heating trial. However, RBV and RVC were similar during postexercise muscle ischemia during heating and normothermia. RVC decreased less during cooling than in normothermia while the subjects performed the ischemic IHG protocol. During postexercise muscle ischemia, RVC was greater during cooling than in normothermia. These results indicate that heating augments mechanoreceptor-mediated renal vasoconstriction whereas cooling blunts metaboreceptor-mediated renal vasoconstriction.

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“…This information is projected to the spinal cord and brain stem; eventually, sympathetic outflow increases, mean arterial pressure (MAP) increases, and heart rate (HR) increases (16). Prostanoids are produced during skeletal muscle contraction and subsequently stimulate muscle afferent nerves, thereby contributing to the exercise pressor reflex (32)(33)(34)38). Experiments in cats have demonstrated that intravenous indomethacin (a nonselective inhibitor of cyclooxygenase) attenuates group III and IV afferent nerve responses to dynamic exercise (15).…”

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confidence: 99%

Inhibition of cyclooxygenase attenuates the blood pressure response to plantar flexion exercise in peripheral arterial disease

Müller

Drew

Ross

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Muller MD, Drew RC, Ross AJ, Blaha CA, Cauffman AE, Kaufman MP, Sinoway LI. Inhibition of cyclooxygenase attenuates the blood pressure response to plantar flexion exercise in peripheral arterial disease. Am J Physiol Heart Circ Physiol 309: H523-H528, 2015. First published June 8, 2015 doi:10.1152/ajpheart.00267.2015.-Prostanoids are produced during skeletal muscle contraction and subsequently stimulate muscle afferent nerves, thereby contributing to the exercise pressor reflex. Humans with peripheral arterial disease (PAD) have an augmented exercise pressor reflex, but the metabolite(s) responsible for this augmented response is not known. We tested the hypothesis that intravenous injection of ketorolac, which blocks the activity of cyclooxygenase, would attenuate the rise in mean arterial blood pressure (MAP) and heart rate (HR) evoked by plantar flexion exercise. Seven PAD patients underwent 4 min of single-leg dynamic plantar flexion (30 contractions/min) in the supine posture (workload: 0.5-2.0 kg). MAP and HR were measured on a beat-by-beat basis; changes from baseline in response to exercise were determined. Ketorolac did not affect MAP or HR at rest. During the first 20 s of exercise with the most symptomatic leg, ⌬MAP was significantly attenuated by ketorolac (2 Ϯ 2 mmHg) compared with control (8 Ϯ 2 mmHg, P ϭ 0.005), but ⌬HR was similar (6 Ϯ 2 vs. 5 Ϯ 1 beats/min). Importantly, patients rated the exercise bout as "very light" to "fairly light," and average pain ratings were 1 of 10. Ketorolac had no effect on perceived exertion or pain ratings. Ketorolac also had no effect on MAP or HR in seven age-and sex-matched healthy subjects who performed a similar but longer plantar flexion protocol (workload: 0.5-7.0 kg). These data suggest that prostanoids contribute to the augmented exercise pressor reflex in patients with PAD. PERIPHERAL ARTERIAL DISEASE (PAD) is a form of atherosclerosis that preferentially affects the lower extremity. Because leg blood flow is impaired in PAD, it is not surprising that dynamic exercise, such as walking, provokes pain in the calf, thigh, or buttocks, termed "intermittent claudication." Clinical exercise testing (e.g., the Bruce treadmill protocol) also causes a large increase in blood pressure (BP) in PAD patients, and studies (10, 11) have linked this augmented pressor response to cardiovascular morbidity and mortality. In recent years, our laboratory has focused on BP control in patients with PAD. Specifically, we found that 1) the BP response to single-leg dynamic plantar flexion exercise was augmented in PAD patients compared with healthy control subjects; 2) the pressor response occurred at very low workloads and before the onset of pain; 3) the pressor response correlated with the anklebrachial index (ABI), suggesting that disease severity plays a role; and 4) intravenous infusion of ascorbic acid lowered the pressor response to exercise in PAD (13,28). To date, the mechanisms for these findings are largely unknown. Understanding BP regulation during exercise in PAD ...

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Sensitization of group III muscle afferents to static contraction by arachidonic acid

Cited by 126 publications

References 0 publications

Role of the Exercise Pressor Reflex in Rats With Dilated Cardiomyopathy

Role of the Exercise Pressor Reflex in Rats With Dilated Cardiomyopathy

Changes in forearm muscle temperature alter renal vascular responses to isometric handgrip

Inhibition of cyclooxygenase attenuates the blood pressure response to plantar flexion exercise in peripheral arterial disease

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