Exaggerated muscle mechanoreflex control of reflex renal vasoconstriction in heart failure

Middlekauff, Holly R.; Nitzsche, Egbert U.; Hoh, Carl K.; Hamilton, Michèle A.; Fonarow, Gregg C.; Hage, A.; Moriguchi, J.

doi:10.1152/jappl.2001.90.5.1714

Cited by 100 publications

(122 citation statements)

References 19 publications

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“…Similar findings have been reported in humans, as low levels of involuntary biceps contraction, a strategy used to selectively engage the mechanoreflex, has been shown to enhance renal vasoconstriction in CHF patients. 11 Taken together, these findings suggest that the EPR dysfunction observed in cardiomyopathy is mediated, in part, by the muscle mechanoreflex. The mechanisms by which the mechanoreflex causes augmentations in EPR function remain obscure.…”

Section: Discussionmentioning

confidence: 91%

“…[1][2][3][4][5][6] In addition, cardiovascular regulation during physical activity is clearly altered with CHF, because studies using dynamic and static forms of exercise have demonstrated augmentations in sympathetic nerve activity, vascular resistance, heart rate (HR), and blood pressure. [7][8][9][10][11][12][13][14][15] Two distinct neural control mechanisms are activated by exercise: central command and the exercise pressor reflex (EPR). Central command is a mechanism whereby signals from a central site responsible for recruiting motor units activate cardiovascular control areas in the brain stem.…”

mentioning

confidence: 99%

“…21 Because the metabolic component of the reflex may be blunted in CHF, 10,22 it has been hypothesized that the mechanical component of the reflex preferentially drives the EPR hyperactivity that develops. 11,23 The contribution of neurally mediated peripheral mechanisms to the evolution of reduced exercise capacity in heart failure is poorly understood. The purpose of this investigation was to use a novel rat model 24 to determine whether EPRmediated changes in circulatory hemodynamics are altered with dilated cardiomyopathy (DCM) in the absence of central command.…”

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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: 91%

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confidence: 99%

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confidence: 99%

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Role of the Exercise Pressor Reflex in Rats With Dilated Cardiomyopathy

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“…Specifically, sympathetic tone to muscle is elevated (24,29,36,42), renal vasoconstriction is enhanced (13,30,31,34), and the rise in muscle blood flow is attenuated in heart failure (13,25,35,41). The reduced blood supply to the kidney leads to excessive stimulation of renin secretion and inappropriate salt and water retention (6, 13), whereas the reduced skeletal muscle blood flow is an important contributor to exercise intolerance (51) in these patients.…”

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Sympathetic responses to exercise in myocardial infarction rats: a role of central command

Koba¹,

Gao²,

Xing³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Koba, Satoshi, Zhaohui Gao, Jihong Xing, Lawrence I Sinoway, and Jianhua Li. Sympathetic responses to exercise in myocardial infarction rats: a role of central command. Am J Physiol Heart Circ Physiol 291: H2735-H2742, 2006. First published July 14, 2006 doi:10.1152/ajpheart.00522.2006.-In congestive heart failure (CHF), exaggerated sympathetic activation is observed during exercise, which elicits excess peripheral vasoconstriction. The mechanisms causing this abnormality are not fully understood. Central command is a central neural process that induces parallel activation of motor and cardiovascular systems. This study was undertaken to determine whether central command serves as a mechanism that contributes to the exaggerated sympathetic response to exercise in CHF. In decerebrated rats, renal and lumbar sympathetic nerve responses (RSNA and LSNA, respectively) to 30 s of fictive locomotion were examined. The fictive locomotion was induced by electrical stimulation of the mesencephalic locomotor region (MLR). The study was performed in control animals (fractional shortening Ͼ 40%) and animals with myocardial infarctions (MI; fractional shortening Ͻ 30%). With low stimulation of the MLR (current intensity ϭ 20 A), the sympathetic responses were not significantly different in the control (RSNA: ϩ18 Ϯ 4%; LSNA: ϩ3 Ϯ 2%) and MI rats (RSNA: ϩ16 Ϯ 5%; LSNA: ϩ8 Ϯ 3%). With intense stimulation of the MLR (50 A), the responses were significantly greater in MI rats (RSNA: ϩ127 Ϯ 15%; LSNA: ϩ57 Ϯ 10%) than in the control rats (RSNA: ϩ62 Ϯ 5%; LSNA: ϩ21 Ϯ 6%). In this study, the data demonstrate that RSNA and LSNA responses to intense stimulation of the MLR are exaggerated in MI rats. We suggest that intense activation of central command may play a role in evoking exaggerated sympathetic activation and inducing excessive peripheral vasoconstriction during exercise in CHF.congestive heart failure; mesencephalic locomotor region; renal sympathetic nerve activity; lumbar sympathetic nerve activity EXERCISE ACTIVATES THE SYMPATHETIC nervous system, increases blood pressure, and leads to an increase in blood flow to exercising skeletal muscle. This increase in muscle blood flow is associated with reduced renal blood flow (23). Two principal neural mechanisms are proposed to increase sympathetic nerve activity (SNA) and regulate the cardiovascular system during exercise. These are termed the exercise pressor reflex and central command. The exercise pressor reflex is a neural reflex that arises from receptors sensitive to mechanical and metabolic stimuli in exercising skeletal muscles and stimulates the medulla through the muscle thin afferent fibers (18). Central command is a feed-forward neural mechanism that induces parallel activation of motor and cardiovascular systems (9, 50). The brain sites that generate motor signals also send descending projections to sympathetic neurons (19,20,22).Congestive heart failure (CHF) includes abnormal cardiovascular regulation in exercise. Specifically, sympathetic tone to muscle is elevat...

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“…These observations suggest that the muscle metaboreflex is attenuated in HF. By contrast, the muscle mechanoreflex activation due to passive stretch of skeletal muscles evoked a significant elevation of muscle SNA 67) and enhanced renal vasoconstriction 68) in HF patients. These findings suggest that the muscle mechanoreflex is enhanced in HF.…”

Section: Contribution Of Rat Studies To Understanding Mechanisms Undementioning

confidence: 80%

Exercise pressor reflex in health and diseases: Animal studies

Koba

2015

JPFSM

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A reflex originating in exercising skeletal muscle contributes to sympathoexcitation during exercise. This muscle-based reflex is termed the exercise pressor reflex (EPR). In this review, mechanisms underlying activation of the EPR are examined based on findings mainly obtained from cat studies. Specifically, roles played by chemical and mechanical stimuli due to contraction in increasing discharges of muscle afferent fibers are discussed. Roles metabolic byproducts play in stimulating and sensitizing muscle afferents are also examined. Central cardiovascular sites involved in activation of the EPR are investigated. In this review, moreover, mechanisms by which the EPR function becomes abnormal in heart failure and hypertension are discussed on the basis of experimental data mainly provided by rat studies. In heart failure, the muscle metaboreflex is attenuated while the mechanoreflex is enhanced. In hypertension, both the muscle metabo-and mechano-reflexes are enhanced. Peripheral factors leading to EPR dysfunction in these pathological conditions are examined.

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Exaggerated muscle mechanoreflex control of reflex renal vasoconstriction in heart failure

Cited by 100 publications

References 19 publications

Role of the Exercise Pressor Reflex in Rats With Dilated Cardiomyopathy

Role of the Exercise Pressor Reflex in Rats With Dilated Cardiomyopathy

Sympathetic responses to exercise in myocardial infarction rats: a role of central command

Exercise pressor reflex in health and diseases: Animal studies

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