Augmented input from cardiac sympathetic afferents inhibits baroreflex in rats with heart failure

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Abstract

It has been established that the baroreflex is markedly decreased in chronic heart failure (CHF). Our recent study has indicated that activation of the cardiac sympathetic afferent reflex (CSAR) inhibits the baroreflex in normal rats, and in the rats with CHF the CSAR is significantly enhanced, which is related to augmented central angiotensin II (Ang II) mechanism. Therefore, the hypothesis is that the augmented CSAR in the CHF state tonically inhibits the baroreflex via central AT1 receptor. To test the hypothesis, the rats with myocardial infarction-induced CHF or sham surgery were anesthetized with α-chloralose and urethane, vagotomized, and recordings were made of the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). We found: (1) left ventricular epicardial application of capsaicin or electrical stimulation of the central end of the left cardiac sympathetic nerve blunted the baroreflex in both sham and CHF rats; (2) left ventricular epicardial application of lidocaine had no significant effects on the baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope, 1.7±0.3 to 2.9±0.2%/mm Hg; P<0.01); and (3) intracerebral ventricular injection of losartan had no significant effect on baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope 1.9±0.2 to 3.1±0.2%/mm Hg; P<0.01). These results suggest that tonic cardiac sympathetic afferent input plays an important role in the blunted baroreflex associated with CHF, which is mediated by central AT1 receptors.

Original languageEnglish (US)
Pages (from-to)1173-1181
Number of pages9
JournalHypertension
Volume45
Issue number6
DOIs
StatePublished - Jun 1 2005

Fingerprint

Baroreflex
Heart Failure
Reflex
Chloralose
Losartan
Capsaicin
Urethane
Lidocaine
Angiotensin II
Electric Stimulation
Arterial Pressure
Myocardial Infarction
Kidney
Injections

Keywords

  • Baroreflex
  • Cardiac function
  • Heart failure
  • Reflex
  • Renal nerves
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Internal Medicine

Cite this

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title = "Augmented input from cardiac sympathetic afferents inhibits baroreflex in rats with heart failure",
abstract = "It has been established that the baroreflex is markedly decreased in chronic heart failure (CHF). Our recent study has indicated that activation of the cardiac sympathetic afferent reflex (CSAR) inhibits the baroreflex in normal rats, and in the rats with CHF the CSAR is significantly enhanced, which is related to augmented central angiotensin II (Ang II) mechanism. Therefore, the hypothesis is that the augmented CSAR in the CHF state tonically inhibits the baroreflex via central AT1 receptor. To test the hypothesis, the rats with myocardial infarction-induced CHF or sham surgery were anesthetized with α-chloralose and urethane, vagotomized, and recordings were made of the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). We found: (1) left ventricular epicardial application of capsaicin or electrical stimulation of the central end of the left cardiac sympathetic nerve blunted the baroreflex in both sham and CHF rats; (2) left ventricular epicardial application of lidocaine had no significant effects on the baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope, 1.7±0.3 to 2.9±0.2{\%}/mm Hg; P<0.01); and (3) intracerebral ventricular injection of losartan had no significant effect on baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope 1.9±0.2 to 3.1±0.2{\%}/mm Hg; P<0.01). These results suggest that tonic cardiac sympathetic afferent input plays an important role in the blunted baroreflex associated with CHF, which is mediated by central AT1 receptors.",
keywords = "Baroreflex, Cardiac function, Heart failure, Reflex, Renal nerves, Sympathetic nervous system",
author = "Lie Gao and Schultz, {Harold D} and Patel, {Kaushik P} and Zucker, {Irving H} and Wei Wang",
year = "2005",
month = "6",
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doi = "10.1161/01.HYP.0000168056.66981.c2",
language = "English (US)",
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T1 - Augmented input from cardiac sympathetic afferents inhibits baroreflex in rats with heart failure

AU - Gao, Lie

AU - Schultz, Harold D

AU - Patel, Kaushik P

AU - Zucker, Irving H

AU - Wang, Wei

PY - 2005/6/1

Y1 - 2005/6/1

N2 - It has been established that the baroreflex is markedly decreased in chronic heart failure (CHF). Our recent study has indicated that activation of the cardiac sympathetic afferent reflex (CSAR) inhibits the baroreflex in normal rats, and in the rats with CHF the CSAR is significantly enhanced, which is related to augmented central angiotensin II (Ang II) mechanism. Therefore, the hypothesis is that the augmented CSAR in the CHF state tonically inhibits the baroreflex via central AT1 receptor. To test the hypothesis, the rats with myocardial infarction-induced CHF or sham surgery were anesthetized with α-chloralose and urethane, vagotomized, and recordings were made of the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). We found: (1) left ventricular epicardial application of capsaicin or electrical stimulation of the central end of the left cardiac sympathetic nerve blunted the baroreflex in both sham and CHF rats; (2) left ventricular epicardial application of lidocaine had no significant effects on the baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope, 1.7±0.3 to 2.9±0.2%/mm Hg; P<0.01); and (3) intracerebral ventricular injection of losartan had no significant effect on baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope 1.9±0.2 to 3.1±0.2%/mm Hg; P<0.01). These results suggest that tonic cardiac sympathetic afferent input plays an important role in the blunted baroreflex associated with CHF, which is mediated by central AT1 receptors.

AB - It has been established that the baroreflex is markedly decreased in chronic heart failure (CHF). Our recent study has indicated that activation of the cardiac sympathetic afferent reflex (CSAR) inhibits the baroreflex in normal rats, and in the rats with CHF the CSAR is significantly enhanced, which is related to augmented central angiotensin II (Ang II) mechanism. Therefore, the hypothesis is that the augmented CSAR in the CHF state tonically inhibits the baroreflex via central AT1 receptor. To test the hypothesis, the rats with myocardial infarction-induced CHF or sham surgery were anesthetized with α-chloralose and urethane, vagotomized, and recordings were made of the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). We found: (1) left ventricular epicardial application of capsaicin or electrical stimulation of the central end of the left cardiac sympathetic nerve blunted the baroreflex in both sham and CHF rats; (2) left ventricular epicardial application of lidocaine had no significant effects on the baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope, 1.7±0.3 to 2.9±0.2%/mm Hg; P<0.01); and (3) intracerebral ventricular injection of losartan had no significant effect on baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope 1.9±0.2 to 3.1±0.2%/mm Hg; P<0.01). These results suggest that tonic cardiac sympathetic afferent input plays an important role in the blunted baroreflex associated with CHF, which is mediated by central AT1 receptors.

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KW - Cardiac function

KW - Heart failure

KW - Reflex

KW - Renal nerves

KW - Sympathetic nervous system

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