Document Detail


SITES OF ACTION OF GHRELIN RECEPTOR LIGANDS IN CARDIOVASCULAR CONTROL.
MedLine Citation:
PMID:  22886413     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Circulating ghrelin reduces blood pressure but the mechanism for this action is unknown. This study investigated whether ghrelin has direct vasodilator effects mediated through the growth hormone secretagogue receptor 1a (GHSR1a) and whether ghrelin reduces sympathetic nerve activity. Mice expressing enhanced green fluorescent protein under control of the promoter for GHSR and RT-PCR were used to locate sites of receptor expression. Effects of ghrelin and the non-peptide GHSR1a agonist, capromorelin, on rat arteries and on transmission in sympathetic ganglia were measured in vitro. In addition, rat blood pressure and sympathetic nerve activity responses to ghrelin were determined in vivo. In reporter mice, expression of GHSR was revealed at sites where it has been previously demonstrated (hypothalamic neurons, renal tubules, sympathetic preganglionic neurons) but not in any artery studied, including mesenteric, cerebral and coronary arteries. In rat, RT-PCR detected GHSR1a mRNA expression in spinal cord and kidney but not in the aorta or in mesenteric arteries. Moreover, the aorta and mesenteric arteries from rats were not dilated by ghrelin or capromorelin at concentrations >100 times their EC(50) determined in cells transfected with human or rat GHSR1a. These agonists did not affect transmission from preganglionic sympathetic neurons that express GHSR1a. Intravenous application of ghrelin lowered blood pressure and decreased splanchnic nerve activity. It is concluded that the blood pressure reduction to ghrelin occurs concomitantly with a decrease in sympathetic nerve activity and is not caused by direct actions on blood vessels or by inhibition of transmission in sympathetic ganglia.
Authors:
Brid Callaghan; Billie Hunne; Haruko Hirayama; Daniela M Sartor; Trung V Nguyen; Fe C Abogafie; Dorota M Ferens; Peter McIntyre; Kung Ban; Jonathan Baell; John B Furness; James A Brock
Related Documents :
8824693 - Effects of acute and chronic angiotensin converting enzyme inhibition by spirapril on c...
12539133 - Neurocardiological basis for intraindividual ecg variability.
8017663 - Effects of pressure-controlled with different i:e ratios versus volume-controlled venti...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-8-10
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  -     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-8-13     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
1University of Melbourne.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  PACAP causes PAC1/VPAC2 receptor mediated hypertension and sympathoexcitation in normal and hyperten...
Next Document:  Microparticle release in remote ischemic conditioning mechanism.