Document Detail

Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat.
MedLine Citation:
PMID:  22687617     Owner:  NLM     Status:  MEDLINE    
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.
Ana P Abdala; Fiona D McBryde; Nephtali Marina; Emma B Hendy; Zoar J Engelman; Marat Fudim; Paul A Sobotka; Alexander V Gourine; Julian F R Paton
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-06-11
Journal Detail:
Title:  The Journal of physiology     Volume:  590     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-10     Completed Date:  2013-02-11     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  4269-77     Citation Subset:  IM    
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MeSH Terms
Arterial Pressure / physiology
Baroreflex / physiology
Carotid Body / physiopathology*
Chemoreceptor Cells / physiology
Disease Models, Animal
Heart Rate / physiology
Hypertension / etiology,  physiopathology*,  therapy
Prehypertension / etiology,  physiopathology,  therapy
Rats, Inbred SHR
Rats, Wistar
Treatment Outcome
Grant Support
095064//Wellcome Trust; FS/12/1/29080//British Heart Foundation; R01 NS069220/NS/NINDS NIH HHS; RG/07/006/23634//British Heart Foundation; //British Heart Foundation; //Wellcome Trust
Comment In:
J Physiol. 2012 Sep 1;590(Pt 17):4123   [PMID:  22962032 ]

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