| Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat. | |
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MedLine Citation:
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PMID: 22687617 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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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:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2012-06-11 |
Journal Detail:
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Title: The Journal of physiology Volume: 590 ISSN: 1469-7793 ISO Abbreviation: J. Physiol. (Lond.) Publication Date: 2012 Sep |
Date Detail:
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Created Date: 2012-09-10 Completed Date: 2013-02-11 Revised Date: 2013-06-05 |
Medline Journal Info:
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Nlm Unique ID: 0266262 Medline TA: J Physiol Country: England |
Other Details:
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Languages: eng Pagination: 4269-77 Citation Subset: IM |
Affiliation:
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School of Physiology & Pharmacology, Bristol Heart Institute, Medical Science Building, University of Bristol, Bristol BS8 1TD, UK. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arterial Pressure / physiology Baroreflex / physiology Carotid Body / physiopathology* Chemoreceptor Cells / physiology Denervation Disease Models, Animal Heart Rate / physiology Humans Hypertension / etiology, physiopathology*, therapy Prehypertension / etiology, physiopathology, therapy Rats Rats, Inbred SHR Rats, Wistar Treatment Outcome |
| Grant Support | |
ID/Acronym/Agency:
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095064//Wellcome Trust; R01 NS069220/NS/NINDS NIH HHS; //British Heart Foundation; //Wellcome Trust |
| Comments/Corrections | |
Comment In:
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J Physiol. 2012 Sep 1;590(Pt 17):4123
[PMID:
22962032
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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