Cardiac sympathetic afferent reflex control of cardiac function in normal and chronic heart failure states

Wang, Han Jun; Rozanski, George J.; Zucker, Irving H.

doi:10.1113/jp273764

Cited by 55 publications

(74 citation statements)

References 33 publications

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“…These findings in the control state should be considered in the context of what is known in disease states, including chronic CHF, where the CSAR is significantly enhanced (41,43) and contributes to the pathophysiology of CHF, including adverse remodeling of both the cardiac nervous system and heart (46). VR1 depletion in the setting for chronic myocardial infarction diminished adverse cardiac remodeling and improved cardiovascular function (39,40). Chronic cardiac dysfunction causes adverse remodeling both in the heart and within its neural hierarchy (1-3, 24, 31, 35).…”

Section: H962 Trpv1 Depletion and Cardiac Stressmentioning

confidence: 80%

Cardiac vanilloid receptor-1 afferent depletion enhances stellate ganglion neuronal activity and efferent sympathetic response to cardiac stress

Yoshie

Rajendran

Massoud

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

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Afferent fibers expressing the vanilloid receptor 1 (VR1) channel have been implicated in cardiac nociception; however, their role in modulating reflex responses to cardiac stress is not well understood. We evaluated this role in Yorkshire pigs by percutaneous epicardial application of resiniferatoxin (RTX), a toxic activator of the VR1 channel, resulting in the depletion of cardiac VR1-expressing afferents. Hemodynamics, epicardial activation recovery intervals, and in vivo activity of stellate ganglion neurons (SGNs) were recorded in control and RTX-treated animals. Stressors included inferior vena cava or aortic occlusion and rapid right ventricular pacing (RVP) to induce dyssynchrony and ischemia. In the epicardium, stellate ganglia, and dorsal root ganglia, immunostaining for the VR1 channel, calcitonin gene-related peptide, and substance P was significantly diminished by RTX. RTX-treated animals exhibited higher basal systolic blood pressures and contractility than control animals. Reflex responses to epicardial bradykinin and capsaicin were mitigated by RTX. Cardiovascular reflex function, as assessed by inferior vena cava or aortic occlusion, was similar in RTX-treated versus control animals. RTX-treated animals exhibited resistance to hemodynamic collapse induced by RVP. Activation recovery interval shortening during RVP, a marker of cardiac sympathetic outflow, was greater in RTX-treated animals and exhibited significant delay in returning to baseline values after cessation of RVP. The basal firing rate of SGNs and firing rates in response to RVP were also greater in RTX-treated animals, as was the SGN network activity in response to cardiac stressors. These data suggest that elimination of cardiac nociceptive afferents reorganizes the central-peripheral nervous system interaction to enhance cardiac sympathetic outflow. NEW & NOTEWORTHY Our work demonstrates a role for cardiac vanilloid receptor-1-expressing afferents in reflex processing of cardiovascular stress. Current understanding suggests that elimination of vanilloid receptor-1 afferents would decrease reflex cardiac sympathetic outflow. We found, paradoxically, that sympathetic outflow to the heart is instead enhanced at baseline and during cardiac stress.

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Section: H962 Trpv1 Depletion and Cardiac Stressmentioning

confidence: 80%

Cardiac vanilloid receptor-1 afferent depletion enhances stellate ganglion neuronal activity and efferent sympathetic response to cardiac stress

Yoshie

Rajendran

Massoud

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

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“…RTX has been shown to ablate the TRPV1‐positive spinal afferent nerve endings on the heart (Wang et al. , ). RTX (1 mg; Sigma‐Aldrich) was dissolved in a 1:1:8 mixture of ethanol, Tween‐80 (Sigma‐Aldrich), and isotonic saline.…”

Section: Methodsmentioning

confidence: 99%

“…The upper thoracic sympathetic afferent ganglia were ablated by injecting resiniferatoxin (RTX; Sigma-Aldrich), an ultrapotent agonist of the TRPV1 receptor into the subarachnoid space via the catheter. RTX has been shown to ablate the TRPV1-positive spinal afferent nerve endings on the heart (Wang et al 2014(Wang et al , 2017. RTX (1 mg; Sigma-Aldrich) was dissolved in a 1:1:8 mixture of ethanol, Tween-80 (Sigma-Aldrich), and isotonic saline.…”

Section: Upper Thoracic Spinal Sympathetic Afferent Denervationmentioning

confidence: 99%

Sympatho-excitatory response to pulmonary chemosensitive spinal afferent activation in anesthetized, vagotomized rats

et al. 2018

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The sensory innervation of the lung is well known to be innervated by nerve fibers of both vagal and sympathetic origin. Although the vagal afferent innervation of the lung has been well characterized, less is known about physiological effects mediated by spinal sympathetic afferent fibers. We hypothesized that activation of sympathetic spinal afferent nerve fibers of the lung would result in an excitatory pressor reflex, similar to that previously characterized in the heart. In this study, we evaluated changes in renal sympathetic nerve activity (RSNA) and hemodynamics in response to activation of TRPV1‐sensitive pulmonary spinal sensory fibers by agonist application to the visceral pleura of the lung and by administration into the primary bronchus in anesthetized, bilaterally vagotomized, adult Sprague‐Dawley rats. Application of bradykinin (BK) to the visceral pleura of the lung produced an increase in mean arterial pressure (MAP), heart rate (HR), and RSNA. This response was significantly greater when BK was applied to the ventral surface of the left lung compared to the dorsal surface. Conversely, topical application of capsaicin (Cap) onto the visceral pleura of the lung, produced a biphasic reflex change in MAP, coupled with increases in HR and RSNA which was very similar to the hemodynamic response to epicardial application of Cap. This reflex was also evoked in animals with intact pulmonary vagal innervation and when BK was applied to the distal airways of the lung via the left primary bronchus. In order to further confirm the origin of this reflex, epidural application of a selective afferent neurotoxin (resiniferatoxin, RTX) was used to chronically ablate thoracic TRPV1‐expressing afferent soma at the level of T1–T4 dorsal root ganglia pleura. This treatment abolished all sympatho‐excitatory responses to both cardiac and pulmonary application of BK and Cap in vagotomized rats 9–10 weeks post‐RTX. These data suggest the presence of an excitatory pulmonary chemosensitive sympathetic afferent reflex. This finding may have important clinical implications in pulmonary conditions inducing sensory nerve activation such as pulmonary inflammation and inhalation of chemical stimuli.

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“…In a comparative analytical study between the HF and non-HF animal groups, the renal sympathetic nerve activity exhibits augmented response and proportionately direct correlation with the cohort of animals suffering from the HF [11]. As shows in (Figure 4) the same outcomes for capsaicin.…”

Section: Figurementioning

confidence: 63%

“…As it shows, unlike, bradykinin rises three important characteristics of the heart, lidocaine falls in these activities by comparing the changes in both groups of control and CHF. [11].…”

Section: Figurementioning

confidence: 99%

How Abnormal Sympatho-Activation Can Potentially Develop Heart Failure: A Mini Review

Patrikios¹,

Badri²

2020

JICOA

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Cardiac sympathetic afferent that signal the sensation of cardiac pain, ostensibly, has more underlying mechanisms than what scientists have ever been led to believe. Cardiac sympathetic afferent reflex, also known as (CSAR), has been shown to be responsive to a variety of stimuli. Many of which scientists observed in increased levels during ischemia hydrogen ion, oxygen radicals, potassium, lactate, ATP, prostaglandins bradykinin, substance p and, finally and most importantly, endogenous substances (neurohormones) such as norepinephrine (NE). In the outset of chronic heart failure (HF), it has been known for a long time, that there are abnormalities in arterial baroreceptor input which depress its sensitivity, and arterial chemoreceptors seem augmented. Therefore, they tend to not only initiate sympathetic outflow but also to sensitise cardiac afferents which are appearing to do the same thing where there are abnormalities in vagus mechano-reflexes as well. Some of these receptors are in the spinal reticulate tract and interestingly these a third pathways give off neurons to the brainstem some in the hypothalamus and trance translate through the thalamus and then ultimately up into the cortex where we have sensation of pain. Here in this essay, we aim to discuss important aspects of cardiac failure in relation to abnormal sympatho-activators through evaluation of different available studies and animal models.

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Cardiac sympathetic afferent reflex control of cardiac function in normal and chronic heart failure states

Cited by 55 publications

References 33 publications

Cardiac vanilloid receptor-1 afferent depletion enhances stellate ganglion neuronal activity and efferent sympathetic response to cardiac stress

Cardiac vanilloid receptor-1 afferent depletion enhances stellate ganglion neuronal activity and efferent sympathetic response to cardiac stress

Sympatho-excitatory response to pulmonary chemosensitive spinal afferent activation in anesthetized, vagotomized rats

How Abnormal Sympatho-Activation Can Potentially Develop Heart Failure: A Mini Review

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