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Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat.

Publication ,  Journal Article
Abdala, AP; McBryde, FD; Marina, N; Hendy, EB; Engelman, ZJ; Fudim, M; Sobotka, PA; Gourine, AV; Paton, JFR
Published in: J Physiol
September 1, 2012

The peripheral chemoreflex is known to be enhanced in individuals with hypertension. In pre-hypertensive (PH) and adult spontaneously hypertensive rats (SHRs) carotid body type I (glomus) cells exhibit hypersensitivity to chemosensory stimuli and elevated sympathoexcitatory responses to peripheral chemoreceptor stimulation. Herein, we eliminated carotid body inputs in both PH-SHRs and SHRs to test the hypothesis that heightened peripheral chemoreceptor activity contributes to both the development and maintenance of hypertension. The carotid sinus nerves were surgically denervated under general anaesthesia in 4- and 12-week-old SHRs. Control groups comprised sham-operated SHRs and aged-matched sham-operated and carotid sinus nerve denervated Wistar rats. Arterial blood pressure was recorded chronically in conscious, freely moving animals. Successful carotid sinus nerve denervation (CSD) was confirmed by testing respiratory responses to hypoxia (10% O(2)) or cardiovascular responses to i.v. injection of sodium cyanide. In the SHR, CSD reduced both the development of hypertension and its maintenance (P<0.05) and was associated with a reduction in sympathetic vasomotor tone (as revealed by frequency domain analysis and reduced arterial pressure responses to administration of hexamethonium; P<0.05 vs. sham-operated SHR) and an improvement in baroreflex sensitivity. No effect on blood pressure was observed in sham-operated SHRs or Wistar rats. In conclusion, carotid sinus nerve inputs from the carotid body are, in part, responsible for elevated sympathetic tone and critical for the genesis of hypertension in the developing SHR and its maintenance in later life.

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Published In

J Physiol

DOI

EISSN

1469-7793

Publication Date

September 1, 2012

Volume

590

Issue

17

Start / End Page

4269 / 4277

Location

England

Related Subject Headings

  • Treatment Outcome
  • Rats, Wistar
  • Rats, Inbred SHR
  • Rats
  • Prehypertension
  • Physiology
  • Hypertension
  • Humans
  • Heart Rate
  • Disease Models, Animal
 

Citation

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Abdala, A. P., McBryde, F. D., Marina, N., Hendy, E. B., Engelman, Z. J., Fudim, M., … Paton, J. F. R. (2012). Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat. J Physiol, 590(17), 4269–4277. https://doi.org/10.1113/jphysiol.2012.237800
Abdala, Ana P., Fiona D. McBryde, Nephtali Marina, Emma B. Hendy, Zoar J. Engelman, Marat Fudim, Paul A. Sobotka, Alexander V. Gourine, and Julian F. R. Paton. “Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat.J Physiol 590, no. 17 (September 1, 2012): 4269–77. https://doi.org/10.1113/jphysiol.2012.237800.
Abdala AP, McBryde FD, Marina N, Hendy EB, Engelman ZJ, Fudim M, et al. Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat. J Physiol. 2012 Sep 1;590(17):4269–77.
Abdala, Ana P., et al. “Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat.J Physiol, vol. 590, no. 17, Sept. 2012, pp. 4269–77. Pubmed, doi:10.1113/jphysiol.2012.237800.
Abdala AP, McBryde FD, Marina N, Hendy EB, Engelman ZJ, Fudim M, Sobotka PA, Gourine AV, Paton JFR. Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat. J Physiol. 2012 Sep 1;590(17):4269–4277.
Journal cover image

Published In

J Physiol

DOI

EISSN

1469-7793

Publication Date

September 1, 2012

Volume

590

Issue

17

Start / End Page

4269 / 4277

Location

England

Related Subject Headings

  • Treatment Outcome
  • Rats, Wistar
  • Rats, Inbred SHR
  • Rats
  • Prehypertension
  • Physiology
  • Hypertension
  • Humans
  • Heart Rate
  • Disease Models, Animal