Electrical stimulation of the aortic depressor nerve in conscious rats overcomes the attenuation of the baroreflex in chronic heart failure

Tomás O.C. Teixeira Pinto, Renata M. Lataro, Jaci A. Castania, Marina T. Durand, Carlos A.A. Silva, Kaushik P. Patel, Rubens Fazan, Helio C. Salgado

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Chronic heart failure (CHF) is characterized by autonomic dysfunction combined with baroreflex attenuation. The hypotensive and bradycardic responses produced by electrical stimulation of the aortic depressor nerve (ADN) were examined in conscious CHF and control male Wistar rats (12–13 wk old). Furthermore, the role of parasympathetic and sympathetic nervous system in mediating the cardiovascular responses to baroreflex activation was evaluated by selective β1-adrenergic and muscarinic receptor antagonists. CHF was induced by myocardial infarction. After 6 wk, the subjects were implanted with electrodes for ADN stimulation. Twenty-four hours later, electrical stimulation of the ADN was applied for 20 s using five different frequencies (5, 15, 30, 60, and 90 Hz), while the arterial pressure was recorded by a catheter implanted into the femoral artery. Electrical stimulation of the ADN elicited progressive and similar hypotensive and bradycardic responses in control (n = 12) and CHF (n = 11) rats, while the hypotensive response was not affected by methylatropine. Nevertheless, the reflex bradycardia was attenuated by methylatropine in control, but not in CHF rats. Atenolol did not affect the hypotensive or bradycardic response in either group. The ADN function was examined under anesthesia through electroneurographic recordings. The arterial pressure-ADN activity relationship was attenuated in CHF rats. In conclusion, despite the attenuation of baroreceptor function in CHF rats, the electrical stimulation of the ADN elicited a stimulus-dependent hypotension and bradycardia of similar magnitude as observed in control rats. Therefore, electrical activation of the aortic baroreflex overcomes both the attenuation of parasympathetic function and the sympathetic overdrive.

Original languageEnglish (US)
Pages (from-to)R612-R618
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume310
Issue number7
DOIs
StatePublished - Apr 2016

Fingerprint

Baroreflex
Electric Stimulation
Heart Failure
Bradycardia
Arterial Pressure
Parasympathetic Nervous System
Implanted Electrodes
Pressoreceptors
Muscarinic Antagonists
Adrenergic Antagonists
Atenolol
Sympathetic Nervous System
Muscarinic Receptors
Femoral Artery
Hypotension
Reflex
Wistar Rats
Catheters
Anesthesia
Myocardial Infarction

Keywords

  • Aortic depressor nerve
  • Baroreflex activation
  • Electric stimulation
  • Heart failure

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Electrical stimulation of the aortic depressor nerve in conscious rats overcomes the attenuation of the baroreflex in chronic heart failure. / Teixeira Pinto, Tomás O.C.; Lataro, Renata M.; Castania, Jaci A.; Durand, Marina T.; Silva, Carlos A.A.; Patel, Kaushik P.; Fazan, Rubens; Salgado, Helio C.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 310, No. 7, 04.2016, p. R612-R618.

Research output: Contribution to journalArticle

Teixeira Pinto, Tomás O.C. ; Lataro, Renata M. ; Castania, Jaci A. ; Durand, Marina T. ; Silva, Carlos A.A. ; Patel, Kaushik P. ; Fazan, Rubens ; Salgado, Helio C. / Electrical stimulation of the aortic depressor nerve in conscious rats overcomes the attenuation of the baroreflex in chronic heart failure. In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 2016 ; Vol. 310, No. 7. pp. R612-R618.
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AU - Teixeira Pinto, Tomás O.C.

AU - Lataro, Renata M.

AU - Castania, Jaci A.

AU - Durand, Marina T.

AU - Silva, Carlos A.A.

AU - Patel, Kaushik P.

AU - Fazan, Rubens

AU - Salgado, Helio C.

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AB - Chronic heart failure (CHF) is characterized by autonomic dysfunction combined with baroreflex attenuation. The hypotensive and bradycardic responses produced by electrical stimulation of the aortic depressor nerve (ADN) were examined in conscious CHF and control male Wistar rats (12–13 wk old). Furthermore, the role of parasympathetic and sympathetic nervous system in mediating the cardiovascular responses to baroreflex activation was evaluated by selective β1-adrenergic and muscarinic receptor antagonists. CHF was induced by myocardial infarction. After 6 wk, the subjects were implanted with electrodes for ADN stimulation. Twenty-four hours later, electrical stimulation of the ADN was applied for 20 s using five different frequencies (5, 15, 30, 60, and 90 Hz), while the arterial pressure was recorded by a catheter implanted into the femoral artery. Electrical stimulation of the ADN elicited progressive and similar hypotensive and bradycardic responses in control (n = 12) and CHF (n = 11) rats, while the hypotensive response was not affected by methylatropine. Nevertheless, the reflex bradycardia was attenuated by methylatropine in control, but not in CHF rats. Atenolol did not affect the hypotensive or bradycardic response in either group. The ADN function was examined under anesthesia through electroneurographic recordings. The arterial pressure-ADN activity relationship was attenuated in CHF rats. In conclusion, despite the attenuation of baroreceptor function in CHF rats, the electrical stimulation of the ADN elicited a stimulus-dependent hypotension and bradycardia of similar magnitude as observed in control rats. Therefore, electrical activation of the aortic baroreflex overcomes both the attenuation of parasympathetic function and the sympathetic overdrive.

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