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Decreased density of mesenteric arteries but not of myocardial endothelin receptors and function in rats with chronic ischemic heart failure.

Artikel i vetenskaplig tidskrift
Författare Michael Fu
Xiang-Ying Sun
Thomas Hedner
Qing-Ping Feng
Qi-Ming Liang
Johan Hoebeke
Åke Hjalmarson
Publicerad i Journal of cardiovascular pharmacology
Volym 22
Nummer/häfte 2
Sidor 177-82
ISSN 0160-2446
Publiceringsår 1993
Publicerad vid Wallenberglaboratoriet
Institutionen för invärtesmedicin, Avdelningen för klinisk farmakologi
Sidor 177-82
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord 5'-Nucleotidase, metabolism, Animals, Blood Pressure, drug effects, Chronic Disease, Decerebrate State, physiopathology, Down-Regulation, drug effects, physiology, Iodine Radioisotopes, diagnostic use, Male, Mesenteric Arteries, physiology, Myocardial Ischemia, metabolism, Myocardium, metabolism, Rats, Rats, Sprague-Dawley, Receptors, Endothelin, metabolism, Vasodilator Agents, pharmacology
Ämneskategorier Fysiologi

Sammanfattning

Mesenteric artery and cardiac ventricular endothelin receptors and endothelin-1-induced pressor responses were studied in normal rats and rats with chronic congestive heart failure induced by myocardial ischemia (4 weeks after coronary artery ligation). In mesenteric arteries of rats with chronic ischemic heart failure, endothelin receptor density was significantly decreased by 59%, whereas the dissociation constant was increased 2.8-fold, as compared with controls. There were, however, no changes in endothelin-receptor density or the dissociation constant in cardiac ventricular membrane preparations from rats with congestive heart failure as compared with controls. In pithed rats with congestive heart failure there was a reduced pressor response to a bolus injection of endothelin-1 (800 pmole/kg body weight), while the vasodilatory response was unaltered as compared with sham-operated controls. These results demonstrate that there is a decreased vascular endothelin-receptor function due to a down-regulated endothelin receptor. The in vivo data indicate that this is due to impaired endothelin A but not endothelin B receptor function. Thus, there is an impaired arterial but not cardiac ventricular endothelin receptor-mediated signalling system in the rat with chronic ischemic heart failure.

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