Nerve Growth Factor Decreases in Sympathetic and Sensory Nerves of Rats with Chronic Heart Failure

Xing, Jihong; Lu, Jinling; Li, Jianhua

doi:10.1007/s11064-014-1348-5

Cited by 10 publications

(7 citation statements)

References 49 publications

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“…Our prior study demonstrated that the levels of NGF in sympathetic neurons and DRG neurons of rats are impaired after heart failure induced by ligation of the coronary artery [41]. NGF can affect the response of TRPV1 in DRG neurons [42].…”

Section: Discussionmentioning

confidence: 99%

The Role Played by Adenosine in Modulating Reflex Sympathetic and Pressor Responses Evoked by Stimulation of TRPV1 in Muscle Afferents

Xing

2016

Cell Physiol Biochem

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Background/Aims: Activation of metabolite-sensitive transient receptor potential vanilloid type 1 (TRPV1) receptors (capsaicin receptors) in afferent nerves of the hindlimb muscles of rats increases renal sympathetic nerve activity (RSNA) and blood pressure (BP) via a reflex mechanism. The purpose of this study was to examine the role of adenosine in modulating the reflex RSNA and BP responses to stimulation of TRPV1. Methods: RSNA and BP responses were recorded in rats. Immunofluorescence and patch-clamp methods were employed to examine the receptor mechanisms responsible for the effects of adenosine. Results: Adenosine, in the concentration of 100 µM, injected into the femoral artery had an inhibitory effect on the reflex RSNA and BP responses induced by capsaicin. Likewise, arterial injection of adenosine analogue CGS21680 (A_2A subtype receptor agonist, 10 µM and100 µM) also attenuated the reflex responses. In addition, co-existence of A_2A and TRPV1 was observed in the dorsal root ganglion neurons. The prior application of adenosine or CGS21680 inhibited the magnitude of capsaicin-induced currents in muscle sensory neurons. Conclusion: Adenosine contributes to muscle afferent TRPV1-engaged reflex sympathetic and pressor responses. It is likely that TRPV1 response is impaired as the levels of adenosine are increased in the hindlimb muscles under diseased conditions.

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Section: Discussionmentioning

confidence: 99%

The Role Played by Adenosine in Modulating Reflex Sympathetic and Pressor Responses Evoked by Stimulation of TRPV1 in Muscle Afferents

Xing

2016

Cell Physiol Biochem

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“…These studies were conducted in healthy, normotensive young animals and it is possible that age, hypertension, and other comorbidities alter the rate of nerve regrowth. 30 Finally, whether our findings in normotensive sheep can be directly translated into the human situation remains unclear, but because we denervated with the same catheter and algorithm used in patients it is likely that this model has some clinical relevance. In fact, estimates of efferent RDN based on renal norepinephrine spillover in patients 5 suggest …”

Section: Strengths and Limitationsmentioning

confidence: 99%

Reinnervation of Renal Afferent and Efferent Nerves at 5.5 and 11 Months After Catheter-Based Radiofrequency Renal Denervation In Sheep

et al. 2015

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T here is extensive evidence that renal afferent and efferent nerves play a critical role in the control of renal function and in setting the level of arterial blood pressure.1 This includes the findings that in experimental and human hypertension there are increases in renal sympathetic nerve activity (RSNA) and renal norepinephrine spillover, respectively. In addition, surgical renal denervation (RDN) reduces blood pressure in hypertensive animals and patients, 1-4 although in patients this was associated with several side effects. 4 The development of catheter-based radiofrequency RDN has resulted in a resurgence of interest in RDN as a treatment for resistant hypertensive patients. Initial trials demonstrated reductions in office systolic blood pressure 5,6 and in the 36-month follow-up from the first trial 93% of patients showed reductions in office systolic blood pressure of ≥10 mm Hg after RDN. 7 In contrast, the recent Symplicity HTN-3 trial did not demonstrate reductions in systolic blood pressure beyond that observed in sham control patients 6 months after RDN, 8 although there is still debate on factors that may have led to the lack of effect, such as procedural and population variability.It would be expected that destruction of the renal nerves reduces blood pressure because the efferent renal nerves play a major role in stimulating renin release, causing renal vasoconstriction and inducing sodium retention.1 It is also plausible that in hypertension, increased afferent renal nerve activity may cause a reflex increase in sympathetic outflow and worsening hypertension.9,10 Such actions are supported by findings that in some hypertensive patients, catheter-based RDN reduced the level of muscle SNA 11,12 and plasma norepinephrine. 13 Despite these proposed mechanisms, it is unknown how Abstract-Previous studies indicate that catheter-based renal denervation reduces blood pressure and renal norepinephrine spillover in human resistant hypertension. The effects of this procedure on afferent sensory and efferent sympathetic renal nerves, and the subsequent degree of reinnervation, have not been investigated. We therefore examined the level of functional and anatomic reinnervation at 5.5 and 11 months after renal denervation using the Symplicity Flex catheter. In normotensive anesthetized sheep (n=6), electric stimulation of intact renal nerves increased arterial pressure from 99±3 to 107±3 mm Hg (afferent response) and reduced renal blood flow from 198±16 to 85±20 mL/min (efferent response). In a further group (n=6), immediately after denervation, renal sympathetic nerve activity was absent and the responses to electric stimulation were abolished. At 11 months after denervation (n=5), renal sympathetic nerve activity and the responses to electric stimulation were at normal levels. Immunohistochemical staining for renal efferent (tyrosine hydroxylase) and renal afferent nerves (calcitonin gene-related peptide), as well as renal norepinephrine levels, was normal 11 months after denervation. Findings at 5.5...

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“…It is also of interest to determine if NGF is involved in the sensitivity of the EPR in the CHF state. However, the studies by Garry et al [33,34] and Xing et al [35] excluded this possibility because they reported that NGF concentration in lumbar DRGs was decreased in the CHF state. Given that NGF is produced by peripheral tissues such as skin and skeletal muscle and retrogradely transported to DRG soma via axonal flow, this observation suggests a low capacity of peripheral tissues to produce NGF.…”

Section: Discussionmentioning

confidence: 99%

Increased Brain-Derived Neurotrophic Factor in Lumbar Dorsal Root Ganglia Contributes to the Enhanced Exercise Pressor Reflex in Heart Failure

Schiller

Hong

Xia

et al. 2019

IJMS

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An exaggerated exercise pressor reflex (EPR) is associated with excessive sympatho-excitation and exercise intolerance in the chronic heart failure (CHF) state. We hypothesized that brain-derived neurotrophic factor (BDNF) causes the exaggerated EPR via sensitizing muscle mechanosensitive afferents in CHF. Increased BDNF expression was observed in lumbar dorsal root ganglia (DRGs) from CHF rats compared to sham rats. Immunofluorescence data showed a greater increase in the number of BDNF-positive neurons in medium and large-sized DRG subpopulations from CHF rats. Patch clamp data showed that incubation with BDNF for 4–6 h, significantly decreased the current threshold-inducing action potential (AP), threshold potential and the number of APs during current injection in Dil-labeled isolectin B4 (IB4)-negative medium-sized DRG neurons (mainly mechano-sensitive) from sham rats. Compared to sham rats, CHF rats exhibited an increased number of APs during current injection in the same DRG subpopulation, which was significantly attenuated by 4-h incubation with anti-BDNF. Finally, chronic epidural delivery of anti-BDNF attenuated the exaggerated pressor response to either static contraction or passive stretch in CHF rats whereas this intervention had no effect on the pressor response to hindlimb arterial injection of capsaicin. These data suggest that increased BDNF in lumbar DRGs contributes to the exaggerated EPR in CHF.

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Nerve Growth Factor Decreases in Sympathetic and Sensory Nerves of Rats with Chronic Heart Failure

Cited by 10 publications

References 49 publications

The Role Played by Adenosine in Modulating Reflex Sympathetic and Pressor Responses Evoked by Stimulation of TRPV1 in Muscle Afferents

The Role Played by Adenosine in Modulating Reflex Sympathetic and Pressor Responses Evoked by Stimulation of TRPV1 in Muscle Afferents

Reinnervation of Renal Afferent and Efferent Nerves at 5.5 and 11 Months After Catheter-Based Radiofrequency Renal Denervation In Sheep

Increased Brain-Derived Neurotrophic Factor in Lumbar Dorsal Root Ganglia Contributes to the Enhanced Exercise Pressor Reflex in Heart Failure

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