The mammalian exercise pressor reflex in health and disease

Smith, Scott A.; Mitchell, Jere H.; Garry, Mary G.

doi:10.1113/expphysiol.2005.032367

Cited by 196 publications

(202 citation statements)

References 82 publications

(131 reference statements)

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“…gastrocnemius) have been used in multiple studies to investigate the exercise pressor reflex (EPR) 13 . Given the interest in studying sensory neurons mediating the EPR, the gastrocnemius muscles were selected for dye injection.…”

Section: Discussionmentioning

confidence: 99%

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Identification of Specific Sensory Neuron Populations for Study of Expressed Ion Channels

Ramachandra

McGrew

Elmslie

2013

JoVE

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Sensory neurons transmit signals from various parts of the body to the central nervous system. The soma for these neurons are located in the dorsal root ganglia that line the spinal column. Understanding the receptors and channels expressed by these sensory afferent neurons could lead to novel therapies for disease. The initial step is to identify the specific subset of sensory neurons of interest. Here we describe a method to identify afferent neurons innervating the muscles by retrograde labeling using a fluorescent dye DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate). Understanding the contribution of ion channels to excitation of muscle afferents could help to better control excessive excitability induced by certain disease states such as peripheral vascular disease or heart failure. We used two approaches to identify the voltage dependent ion channels expressed by these neurons, patch clamp electrophysiology and immunocytochemistry. While electrophysiology plus pharmacological blockers can identify functional ion channel types, we used immunocytochemistry to identify channels for which specific blockers were unavailable and to better understand the ion channel distribution pattern in the cell population. These techniques can be applied to other areas of the nervous system to study specific neuronal groups. Video LinkThe video component of this article can be found at

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Section: Discussionmentioning

confidence: 99%

“…A literature search will provide the information needed to locate the best injection site and the DRGs to be isolated 13,15,16 .…”

Section: Discussionmentioning

confidence: 99%

Identification of Specific Sensory Neuron Populations for Study of Expressed Ion Channels

Ramachandra

McGrew

Elmslie

2013

JoVE

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“…In marine mammals, it has been proposed that depth and exercise may also promote such autonomic conflict, and that behavioral modification of exercise (decreased stroke effort) during dives can minimize the risk of arrhythmias (Williams et al, 2015a,b). andForster, 1996;Mitchell et al, 1983;Smith et al, 2006;Waldrop et al, 1996;Waldrop and Iwamoto, 2006). Of course, the initiation and intensity of exercise are under voluntary control.…”

Section: Neuroregulation Of the Exercise Responsementioning

confidence: 99%

Heart rate regulation in diving sea lions: the vagus nerve rules

Ponganis

McDonald

Tift

et al. 2017

Journal of Experimental Biology

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Recent publications have emphasized the potential generation of morbid cardiac arrhythmias secondary to autonomic conflict in diving marine mammals. Such conflict, as typified by cardiovascular responses to cold water immersion in humans, has been proposed to result from exercise-related activation of cardiac sympathetic fibers to increase heart rate, combined with depth-related changes in parasympathetic tone to decrease heart rate. After reviewing the marine mammal literature and evaluating heart rate profiles of diving California sea lions (Zalophus californianus), we present an alternative interpretation of heart rate regulation that de-emphasizes the concept of autonomic conflict and the risk of morbid arrhythmias in marine mammals. We hypothesize that: (1) both the sympathetic cardiac accelerator fibers and the peripheral sympathetic vasomotor fibers are activated during dives even without exercise, and their activities are elevated at the lowest heart rates in a dive when vasoconstriction is maximal, (2) in diving animals, parasympathetic cardiac tone via the vagus nerve dominates over sympathetic cardiac tone during all phases of the dive, thus producing the bradycardia, (3) adjustment in vagal activity, which may be affected by many inputs, including exercise, is the primary regulator of heart rate and heart rate fluctuations during diving, and (4) heart beat fluctuations (benign arrhythmias) are common in marine mammals. Consistent with the literature and with these hypotheses, we believe that the generation of morbid arrhythmias because of exercise or stress during dives is unlikely in marine mammals.

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“…The Group III (A␦) and IV (C) afferents mediate the exercise pressor reflex that is normally triggered by mechanical and metabotropic signals associated with skeletal muscle contraction (Kaufman and Hayes 2002). This reflex is an important neural mechanism regulating cardiovascular adjustments to exercise (Kaufman and Hayes 2002) and has important clinical implications because inappropriate activation by certain disease states such as peripheral vascular diseases (e.g., claudication) can adversely affect the cardiovascular system (Baccelli et al 1999;Bakke et al 2007;Smith et al 2006). Thus an understanding of the receptors and ion channels that mediate excitability of these muscle afferents could facilitate development of selective treatments to suppress the exercise pressor reflex and normalize cardiovascular function in patients with peripheral vascular disease.…”

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confidence: 99%

Tetrodotoxin-resistant voltage-dependent sodium channels in identified muscle afferent neurons

Ramachandra

McGrew

Baxter

et al. 2012

Journal of Neurophysiology

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(Group III and IV). However, little is known regarding the expressed voltage-dependent ion channels. We identified muscle afferent neurons in dorsal root ganglia (DRGs), using retrograde labeling to examine voltage-dependent sodium (Na V ) channels. In patch-clamp recordings, we found that the dominant Na V current in the majority of identified neurons was insensitive to tetrodotoxin (TTX-R), with Na V current in only a few (14%) neurons showing substantial (Ͼ50%) TTX sensitivity (TTX-S). The TTX-R current was sensitive to a Na V 1.8 channel blocker, A803467. Immunocytochemistry demonstrated labeling of muscle afferent neurons by a Na V 1.8 antibody, which further supported expression of these channels. A portion of the TTX-R Na V current appeared to be noninactivating during our 25-ms voltage steps, which suggested activity of Na V 1.9 channels. The majority of the noninactivating current was insensitive to A803467 but sensitive to extracellular sodium. Immunocytochemistry showed labeling of muscle afferent neurons by a Na V 1.9 channel antibody, which supports expression of these channels. Further examination of the muscle afferent neurons showed that functional TTX-S channels were expressed, but were largely inactivated at physiological membrane potentials. Immunocytochemistry showed expression of the TTX-S

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The mammalian exercise pressor reflex in health and disease

Cited by 196 publications

References 82 publications

Identification of Specific Sensory Neuron Populations for Study of Expressed Ion Channels

Identification of Specific Sensory Neuron Populations for Study of Expressed Ion Channels

Heart rate regulation in diving sea lions: the vagus nerve rules

Tetrodotoxin-resistant voltage-dependent sodium channels in identified muscle afferent neurons

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