Discharge properties of cardiac and renal sympathetic nerves and their impaired responses to changes in blood volume in heart failure

Ramchandra, Rohit; Hood, Sally G.; Frithiof, Robert; May, Clive N.

doi:10.1152/ajpregu.00191.2009

Cited by 44 publications

(39 citation statements)

References 42 publications

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“…Briefly, each animal underwent two surgical procedures under general anesthesia before experimentation (30). Anesthesia was induced with 5% Pentothal Sodium (0.4 mg/kg iv) and maintained with a 2% isoflurane-air-O 2 mixture.…”

Section: Methodsmentioning

confidence: 99%

Role of endothelin-1 in mediating changes in cardiac sympathetic nerve activity in heart failure

Abukar

May

Ramchandra

2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Heart failure (HF) is associated with increased sympathetic nerve activity to the heart (CSNA), which is directly linked to mortality in HF patients. Previous studies indicate that HF is associated with high levels of plasma endothelin-1 (ET-1), which correlates with the severity of the disease. We hypothesized that blockade of endothelin receptors would decrease CSNA. The effects of intravenous tezosentan (a nonselective ETA and ETB receptor antagonist) (8 mg·kg−1·h−1) on resting levels of CSNA, arterial pressure, and heart rate were determined in conscious normal sheep ( n = 6) and sheep with pacing-induced HF ( n = 7). HF was associated with a significant decrease in ejection fraction (from 74 ± 2% to 38 ± 1%, P < 0.001) and a significant increase in resting levels of CSNA burst incidence (from 56 ± 11 to 87 ± 2 bursts/100 heartbeats, P < 0.01). Infusion of tezosentan for 60 min significantly decreased resting mean aterial pressure (MAP) in both normal and HF sheep (−8 ± 4 mmHg and −4 ± 3 mmHg, respectively; P < 0.05). This was associated with a significant decrease in CSNA (by 25 ± 26% of control) in normal sheep, but there was no change in CSNA in HF sheep. Calculation of spontaneous baroreflex gain indicated significant impairment of the baroreflex control of HR after intravenous tezosentan infusion in normal animals but no change in HF animals. These data suggest that endogenous levels of ET-1 contribute to the baseline levels of CSNA in normal animals, but this effect is absent in HF.

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Section: Methodsmentioning

confidence: 99%

Role of endothelin-1 in mediating changes in cardiac sympathetic nerve activity in heart failure

Abukar

May

Ramchandra

2016

American Journal of Physiology-Regulatory, Integrative and Comp

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“…26,27 Intrapelvic infusion of capsaicin (1 µg/1 mL for 1 minute) had no significant effects on MAP, HR or RSNA, with a trend toward a small increase in RBF (−6±3 mL/min; P<0.09). In view of this lack of treatment effect this was not repeated in the other groups.…”

Section: Physiological Datamentioning

confidence: 97%

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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“…Failure to match cardiac output to increased preload leads to high renal sympathetic nerve activity (RSNA) and its modulation in response to altered circulating blood volume is blunted or abolished (52). Normally sympathetic nerve-derived norepinephrine causes afferent arteriolar contraction and reduces renal blood flow (11).…”

Section: Sympathetic Nervesmentioning

confidence: 99%

Renal neurohormonal regulation in heart failure decompensation

Jönsson

Becirovic‐Agic

Narfström

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Discharge properties of cardiac and renal sympathetic nerves and their impaired responses to changes in blood volume in heart failure

Cited by 44 publications

References 42 publications

Role of endothelin-1 in mediating changes in cardiac sympathetic nerve activity in heart failure

Role of endothelin-1 in mediating changes in cardiac sympathetic nerve activity in heart failure

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

Renal neurohormonal regulation in heart failure decompensation

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