Direct measurement of cardiac sympathetic efferent  nerve activity during dynamic exercise

Tsuchimochi, Hirotsugu; Matsukawa, Kanji; Komine, Hidehiko; Murata, Jun

doi:10.1152/ajpheart.00112.2002

Cited by 55 publications

(72 citation statements)

References 44 publications

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“…Although these limitations must be taken into account, the present finding that gadolinium did not at all alter the time course and magnitude of the cardiovascular responses at the onset of voluntary static exercise in conscious cats suggests a role of central command in producing the initial cardiovascular adaptation at least in the presence of gadolinium. The central command hypothesis is supported by previous findings from Matsukawa and colleagues (24,25,43) demonstrating that cardiac and renal sympathetic efferent nerve activities start to increase immediately before or at the onset of static and dynamic exercise, which in turn contributes to tachycardia and pressor response in several seconds. The rapid sympathetic nerve responses are hardly explained by the muscle mechanoreflex.…”

Section: Central Command But Not the Muscle Mechanoreflex Is Responmentioning

confidence: 62%

Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

Matsukawa¹,

Nakamoto²,

Inomoto³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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The cardiovascular adaptation at the onset of voluntary static exercise is controlled by the autonomic nervous system. Two neural mechanisms are responsible for the cardiovascular adaptation: one is central command descending from higher brain centers, and the other is a muscle mechanosensitive reflex from activation of mechanoreceptors in the contracting muscles. To examine which mechanism played a major role in producing the initial cardiovascular adaptation during static exercise, we studied the effect of intravenous administration of gadolinium (55 mol/kg), a blocker of stretch-activated ion channels, on the increases in heart rate (HR) and mean arterial blood pressure (MAP) at the onset of voluntary static exercise (pressing a bar with a forelimb) in conscious cats. HR increased by 31 Ϯ 5 beats/min and MAP increased by 15 Ϯ 1 mmHg at the onset of voluntary static exercise. Gadolinium affected neither the baseline values nor the initial increases of HR and MAP at the onset of exercise, although the peak force applied to the bar tended to decrease to 65% of the control value before gadolinium. Furthermore, we examined the effect of gadolinium on the reflex responses in HR and MAP (18 Ϯ 7 beats/min and 30 Ϯ 6 mmHg, respectively) during passive mechanical stretch of a forelimb or hindlimb in anesthetized cats. Gadolinium significantly blunted the passive stretch-induced increases in HR and MAP, suggesting that gadolinium blocks the stretch-activated ion channels and thereby attenuates the reflex cardiovascular responses to passive mechanical stretch of a limb. We conclude that the initial cardiovascular adaptation at the onset of voluntary static exercise is predominantly induced by feedforward control of central command descending from higher brain centers but not by a muscle mechanoreflex. muscle mechanosensitive receptors; stretch-activated ion channels; mechanical stretch of skeletal muscle; exercise pressor reflex; conscious cats

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Section: Central Command But Not the Muscle Mechanoreflex Is Responmentioning

confidence: 62%

Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

Matsukawa¹,

Nakamoto²,

Inomoto³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…This is the first demonstration of a requirement for PKC⑀ signaling in cardioprotection mediated by ␣ 1 -adrenergic receptors. Our findings suggest that PKC⑀ KO mice will be useful for future investigation of exercise-induced protection, a strategy that reduces ischemia-reperfusion injury in association with norepinephrine release (43).…”

Section: Discussionmentioning

confidence: 84%

Preservation of Base-line Hemodynamic Function and Loss of Inducible Cardioprotection in Adult Mice Lacking Protein Kinase Cϵ

Gray

Zhou

Schafhalter-Zoppoth

et al. 2004

Journal of Biological Chemistry

104

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Signaling pathways involving protein kinase C isozymes are modulators of cardiovascular development and response to injury. Protein kinase C⑀ activation in cardiac myocytes reduces necrosis caused by coronary artery disease. However, it is unclear whether protein kinase C⑀ function is required for normal cardiac development or inducible protection against oxidative stress. Protein kinase C␦ activation is also observed during cardiac preconditioning. However, its role as a promoter or inhibitor of injury is controversial. We examined hearts from protein kinase C⑀ knock-out mice under physiological conditions and during acute ischemia reperfusion. Null-mutant and wild-type mice displayed equivalent base-line morphology and hemodynamic function. Targeted disruption of the protein kinase C⑀ gene blocked cardioprotection caused by ischemic preconditioning and ␣ 1 -adrenergic receptor stimulation. Protein kinase C␦ activation increased in protein kinase C⑀ knock-out myocytes without altering resistance to injury. These observations support protein kinase C⑀ activation as an essential component of cardioprotective signaling. Our results favor protein kinase C␦ activation as a mediator of normal growth. This study advances the understanding of cellular mechanisms responsible for preservation of myocardial integrity as potential targets for prevention and treatment of ischemic heart disease.Coronary artery disease and chronic heart failure are important causes of death worldwide. Cellular signaling pathways that regulate cardiovascular development and responses to injury, particularly those involving protein kinase C (PKC) 1 isozymes, are under intense investigation. For example, MochlyRosen et al. (1) found that activation of PKC⑀ translocation in transgenic mouse hearts caused physiological hypertrophy and reduced the size of individual myocytes. In contrast, postnatal inhibition of PKC⑀ translocation produced lethal dilated cardiomyopathy and increased cardiac myocyte volumes (1). Wu et al. (2) later observed that activation of PKC⑀ translocation in G␣ q transgenic hearts improved contractile function. Conversely, inhibition of PKC⑀ translocation converted the G␣ q hypertrophic phenotype to a dilated cardiomyopathy (2). However, no previous investigations established whether PKC⑀ activation was an absolute requirement for normal cardiac growth or whether compensatory changes in the expression of other myocardial proteins developed in the absence of PKC⑀-mediated signaling.Two lines of evidence support the hypothesis that PKC⑀ activation promotes myocardial resistance to injury during periods of oxidative stress. First, both ischemic preconditioning and pharmacological approaches that induce cardioprotection increase PKC⑀ immunoreactivity and kinase function in cell particulate fractions (3). Second, transgenic expression of a constitutively active PKC⑀ (4) or a peptide agonist of PKC⑀ translocation (5) reduces cardiac myocyte necrosis during ischemia reperfusion. However, it is unclear whether PKC⑀ activation represe...

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“…Moreover, this anticipation might have augmented feedforward cardiovascular regulation, termed central command, which represents descending signals arising from higher brain centers (15). Central command is likely to cause sympathoexcitation, which contributes to the rapid cardiovascular adaptation observed during exercise (16,20). The responses in HR, AP, and blood flow of the hand to Braille reading observed in this study might have been strongly affected by central command.…”

Section: Discussionmentioning

confidence: 69%

Modulation of radial blood flow during Braille character discrimination task

Murata¹,

Matsukawa²,

Komine³

et al. 2012

Acta Physiologica Hungarica

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Purpose: Human hands are excellent in performing sensory and motor function. We hypothesized that blood flow of the hand are dynamically regulated by sympathetic outflow during concentrated finger perception. To identify this hypothesis, we measured radial blood flow (RBF), radial vascular conductance (RVC), heart rate (HR), and arterial blood pressure (AP) during Braille reading performed under the blind condition in nine healthy subjects. The subjects were instructed to read a flat plate with raised letters (Braille reading) for 30 s by the forefinger, and to touch a blank plate as control for the Braille discrimination procedure.Results: HR and AP slightly increased during Braille reading but remained unchanged during the touching of the blank plate. RBF and RVC were reduced during the Braille character discrimination task (decreased by -46% and -49%, respectively).Furthermore, the changes in RBF and RVC were much greater during the Braille character discrimination task than during the touching of the blank plate (decreased by -20% and -20%, respectively). Conclusions:These results suggested that the distribution of blood flow to the hand is modulated via sympathetic nerve activity during concentrated finger perception.

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Direct measurement of cardiac sympathetic efferent nerve activity during dynamic exercise

Cited by 55 publications

References 44 publications

Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

Preservation of Base-line Hemodynamic Function and Loss of Inducible Cardioprotection in Adult Mice Lacking Protein Kinase Cϵ

Modulation of radial blood flow during Braille character discrimination task

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