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001-es BibID:BIBFORM030336
035-os BibID:PMID: 15320833
Első szerző:Mohácsi Attila (orvos)
Cím:Effects of endothelins on cardiac and vascular cells : new therapeutic target for the future? / Attila Mohácsi, János Magyar, Tamás Bányász, Péter P. Nánási
Dátum:2004
ISSN:1570-1611 (Linking)
Megjegyzések:The predominant isoform of the endothelin peptide family. endothelin-1 (ET-1)exerts various biological effects. These include effects on arterial smoothmuscle cells causing intense vasoconstriction and stimulation of cardiac cells.ET-1 promotes changes in cardiomyocytes that are consistent with electricalremodelling such as changes in ionic current density and inhomogeneousprolongation of action potential duration resulting in increased dispersion. Asfor the underlying mechanisms, ET-1 was shown to suppress several cAMP-dependentionic currents, such as ICa, IK and ICl in various mammalian cardiac preparationsincluding human myocytes; however, the degree of suppression of these currents isdifferent and highly dependent on experimental conditions. The proposedarrhythmogenic effects of ET-1 may also involve enhancement of Ca2+ release fromintracellular stores, generation of IP3, and acidosis due to stimulation of theNa+/H+ exchange. Furthermore, ET-1 acts as the natural counterpart toendothelium-derived nitric oxide, which exerts vasodilator, antithrombotic andantiproliferative effects, and inhibits leukocyte adhesion to the vascular wall.Effects of ET-1 are mediated through interaction with two major types of cellsurface receptors. ETA receptors have been associated with electricalremodelling, vasoconstriction and cell growth, while ETB receptors are involvedin the clearance of ET-1, inhibition of endothelial apoptosis, release of NO andprostacyclins, and inhibition of the expression of ET-1 converting enzyme. Thederangement of endothelial function in various cardiovascular diseases, such ascardiomyopathies, hypertension or arteriosclerosis, is a crucial element of thepathomechanism, thus ET receptors are considered as important therapeutictargets. Indeed, ET receptor antagonists may be able to preserve or restoreendothelial integrity and may have antiarrhythmic properties; therefore, they arepromising tools in cardiovascular medicine.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
0 (Endothelin-1)
0 (Endothelins)
0 (Protein Isoforms)
0 (Receptors, Endothelin)
7440-70-2 (Calcium)
Animals
Calcium/*metabolism
Electric Stimulation
Endothelin-1/adverse effects/metabolism/physiology
Endothelins/antagonists & inhibitors/biosynthesis/physiology
Humans
Muscle, Smooth, Vascular/drug effects/metabolism/physiology
Myocardial Contraction/drug effects/physiology
Myocytes, Cardiac/drug effects/metabolism
Protein Isoforms
Receptors, Endothelin/antagonists & inhibitors
Signal Transduction/drug effects
Vasoconstriction/drug effects/physiology
Ventricular Fibrillation/drug therapy
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current vascular pharmacology. - 2 : 1 (2004), p. 53-63. -
További szerzők:Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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