VR-1 receptor blockade attenuates the pressor response to capsaicin but has no effect on the pressor response to contraction in cats

Kindig, Angela E.; Heller, Todd B.; Kaufman, Marc P.

doi:10.1152/ajpheart.00735.2004

Cited by 36 publications

(35 citation statements)

References 41 publications

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“…The responses to capsaicin are mediated through activation of the transient receptor potential vanilloid 1 channel. This receptor has recently been shown to be activated during muscle contraction in rats (45), although data from cats suggest that this receptor may not be involved in EPR responses (25). Nevertheless, the greater capsaicin-induced increase in MAP in spontaneously HTN rats (45), over a range of doses, provides some evidence that the metabolic component of the EPR is exaggerated in hypertension.…”

Section: Discussionmentioning

confidence: 98%

Exaggerated sympathetic and pressor responses to handgrip exercise in older hypertensive humans: role of the muscle metaboreflex

Delaney

Greaney

Edwards

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

164

194

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Recent animal studies have reported that exercise pressor reflex (EPR)-mediated increases in blood pressure are exaggerated in hypertensive (HTN) rodents. Whether these findings can be extended to human hypertension remains unclear. Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and venous metabolites were measured in normotensive (NTN; n = 23; 60 ± 1 yr) and HTN (n = 15; 63 ± 1 yr) subjects at baseline, and during static handgrip at 30 and 40% maximal voluntary contraction (MVC) followed by a period of postexercise ischemia (PEI) to isolate the metabolic component of the EPR. Changes in MAP from baseline were augmented in HTN subjects during both 30 and 40% MVC handgrip (P < 0.05 for both), and these group differences were maintained during PEI (30% PEI trial: Δ15 ± 2 NTN vs. Δ19 ± 2 HTN mmHg; 40% PEI trial: Δ16 ± 1 NTN vs. Δ23 ± 2 HTN mmHg; P < 0.05 for both). Similarly, in HTN subjects, MSNA burst frequency was greater during 30 and 40% MVC handgrip (P < 0.05 for both), and these differences were maintained during PEI [30% PEI trial: 35 ± 2 (NTN) vs. 44 ± 2 (HTN) bursts/min; 40% PEI trial: 36 ± 2 (NTN) vs. 48 ± 2 (HTN) bursts/min; P < 0.05 for both]. No group differences in metabolites were observed. MAP and MSNA responses to a cold pressor test were not different between groups, suggesting no group differences in generalized sympathetic responsiveness. In summary, compared with NTN subjects, HTN adults exhibit exaggerated sympathetic and pressor responses to handgrip exercise that are maintained during PEI, indicating that activation of the metabolic component of the EPR is augmented in older HTN humans.

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Section: Discussionmentioning

confidence: 98%

Exaggerated sympathetic and pressor responses to handgrip exercise in older hypertensive humans: role of the muscle metaboreflex

Delaney

Greaney

Edwards

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

164

194

View full text Add to dashboard Cite

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“…However, the TRPV1 receptor appears to play little role in stimulating thin fiber afferents in cats during static contraction of freely perfused muscles (21). Protons (lower pH) in the muscle interstitium may be required in mediating the reflex responses with activation of TRPV1 because TRPV1 response is sensitive to pH.…”

Section: Discussionmentioning

confidence: 99%

Contribution of nerve growth factor to augmented TRPV1 responses of muscle sensory neurons by femoral artery occlusion

Xing¹,

Lu²,

Li³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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In rats, hindlimb muscle ischemia induced by femoral artery occlusion augments the sympathetic nervous response to stimulation of transient receptor potential vanilloid type 1 (TRPV1) by injection of capsaicin into the arterial blood supply of the hindlimb muscles. The enhanced sympathetic response is due to alterations in TRPV1 receptor expression and its responsiveness in sensory neurons. The underlying mechanism by which TRPV1 receptor responses are increased after muscle vascular insufficiency/ischemia is unclear. In this report we tested the hypothesis that muscle ischemia elevates nerve growth factor (NGF) levels in primary afferent neurons, thereby increasing TRPV1 responsiveness. Muscle vascular insufficiency induced by the femoral artery ligation significantly increased NGF in the dorsal root ganglion (DRG) compared with sham controls. Furthermore, when NGF was infused in the hindlimb muscles of healthy rats (72 h using an osmotic minipump), the magnitude of the DRG neuron response to capsaicin was augmented (5.4 +/- 0.54 nA with NGF infusion vs. 3.0 +/- 0.17 nA in control; P < 0.05). With the addition of NGF in the culture dish containing the DRG neurons, the magnitude of the DRG neuron response to capsaicin was greater (6.4 +/- 0.27 nA; P < 0.05 vs. control) than that seen in control (2.9 +/- 0.16 nA). Note that this NGF effect was seen in isolectin B(4)-negative DRG neurons, a group of thin fiber nerves that contain neuropeptides and depend on NGF for survival. These data suggest that NGF affects a selective subpopulation of the afferent neurons in mediating augmented TRPV1 responses after femoral artery occlusion.

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“…These potential activators of the TRPV1 receptor are present during exercise. An earlier study by Kindig et al (2005) demonstrated that TRPV1 blockade failed to prevent the pressor response to static contraction in decerebrated cats, indicating that TRPV1 plays little role in evoking the EPR. On the contrary, Smith et al (2010) recently reported that TRPV1 blockade attenuated the pressor response to static contraction in decerebrate rats, indicating that TRPV1 plays an important role in evoking the EPR.…”

Section: Mechanisms Underlying the Beneficial Effect Of Ext On The Exmentioning

confidence: 98%

Muscle reflex in heart failure: the role of exercise training

Wang¹,

Zucker²,

Wang³

2012

Front. Physio.

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Exercise evokes sympathetic activation and increases blood pressure and heart rate (HR). Two neural mechanisms that cause the exercise-induced increase in sympathetic discharge are central command and the exercise pressor reflex (EPR). The former suggests that a volitional signal emanating from central motor areas leads to increased sympathetic activation during exercise. The latter is a reflex originating in skeletal muscle which contributes significantly to the regulation of the cardiovascular and respiratory systems during exercise. The afferent arm of this reflex is composed of metabolically sensitive (predominantly group IV, C-fibers) and mechanically sensitive (predominately group III, A-delta fibers) afferent fibers. Activation of these receptors and their associated afferent fibers reflexively adjusts sympathetic and parasympathetic nerve activity during exercise. In heart failure, the sympathetic activation during exercise is exaggerated, which potentially increases cardiovascular risk and contributes to exercise intolerance during physical activity in chronic heart failure (CHF) patients. A therapeutic strategy for preventing or slowing the progression of the exaggerated EPR may be of benefit in CHF patients. Long-term exercise training (ExT), as a non-pharmacological treatment for CHF increases exercise capacity, reduces sympatho-excitation and improves cardiovascular function in CHF animals and patients. In this review, we will discuss the effects of ExT and the mechanisms that contribute to the exaggerated EPR in the CHF state.

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VR-1 receptor blockade attenuates the pressor response to capsaicin but has no effect on the pressor response to contraction in cats

Cited by 36 publications

References 41 publications

Exaggerated sympathetic and pressor responses to handgrip exercise in older hypertensive humans: role of the muscle metaboreflex

Exaggerated sympathetic and pressor responses to handgrip exercise in older hypertensive humans: role of the muscle metaboreflex

Contribution of nerve growth factor to augmented TRPV1 responses of muscle sensory neurons by femoral artery occlusion

Muscle reflex in heart failure: the role of exercise training

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