Role of endothelin in α-adrenoceptor coronary vasoconstriction
| Autor: | Eric O. Feigl, Keith Neu Richmond, Mark W. Gorman, Martin Farias, Johnathan D. Tune |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Male
medicine.medical_specialty Pyridines Physiology Vasodilator Agents Physical Exertion Tetrazoles Hemodynamics Norepinephrine (medication) Phenylephrine Dogs Oxygen Consumption Tezosentan Coronary Circulation Physiology (medical) Internal medicine medicine Animals Myocyte biology business.industry Endothelins Fissipedia Receptors Adrenergic alpha biology.organism_classification Endocrinology Vasoconstriction Circulatory system medicine.symptom Cardiology and Cardiovascular Medicine Endothelin receptor business Adrenergic alpha-Agonists medicine.drug |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 288:H1937-H1942 |
| ISSN: | 1522-1539 0363-6135 |
| DOI: | 10.1152/ajpheart.01076.2004 |
| Popis: | It has been proposed that α-adrenoceptor vasoconstriction in coronary resistance vessels results not from α-adrenoceptors on coronary smooth muscle but from α-adrenoceptors on cardiac myocytes that stimulate endothelin (ET) release. The present experiments tested the hypothesis that the α-adrenoceptor-mediated coronary vasoconstriction that normally occurs during exercise is due to endothelin. In conscious dogs ( n = 10), the endothelin ETA/ETBreceptor antagonist tezosentan (1 mg/kg iv) increased coronary venous oxygen tension at rest but not during treadmill exercise. This result indicates that basal endothelin levels produce a coronary vasoconstriction at rest that is not observed during the coronary vasodilation during exercise. In contrast, the α-adrenoceptor antagonist phentolamine increased coronary venous oxygen tension during exercise but not at rest. The difference between the endothelin blockade and α-adrenoceptor blockade results indicates that α-adrenoceptor coronary vasoconstriction during exercise is not due to endothelin. However, in anesthetized dogs, bolus intracoronary injections of the α-adrenoceptor agonist phenylephrine produced reductions in coronary blood flow that were partially antagonized by endothelin receptor blockade with tezosentan. These results are best explained if α-adrenoceptor-induced endothelin release requires high pharmacological concentrations of catecholamines that are not reached during exercise. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|