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

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Abdala, AP; McBryde, FD; Marina, N; Hendy, EB; Engelman, ZJ; Fudim, M; Sobotka, PA; Gourine, AV; Paton, JFR

Published Date

  • September 1, 2012

Published In

Volume / Issue

  • 590 / 17

Start / End Page

  • 4269 - 4277

PubMed ID

  • 22687617

Pubmed Central ID

  • PMC3473284

Electronic International Standard Serial Number (EISSN)

  • 1469-7793

Digital Object Identifier (DOI)

  • 10.1113/jphysiol.2012.237800


  • eng

Conference Location

  • England