Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
MECHANISMS OF ALTERATIONS IN CARDIAC MEMBRANE CA2+ TRANSPORT DUE TO EXCESS CATECHOLAMINES
Autore:
DHALLA KS; RUPP H; BEAMISH RE; DHALLA NS;
Indirizzi:
ST BONIFACE GEN HOSP,RES CTR,DIV CARDIOVASC SCI,351 TACHE AVE WINNIPEG MB R2H 2A6 CANADA ST BONIFACE GEN HOSP,RES CTR,DIV CARDIOVASC SCI WINNIPEG MB R2H 2A6 CANADA UNIV MANITOBA,FAC MED,DEPT PHYSIOL WINNIPEG MB CANADA
Titolo Testata:
Cardiovascular drugs and therapy
, volume: 10, anno: 1996, supplemento:, 1
pagine: 231 - 238
SICI:
0920-3206(1996)10:<231:MOAICM>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED CARDIOMYOPATHY; MOXONIDINE; HYPERTENSION;
Keywords:
CATECHOLAMINE-INDUCED CARDIOTOXICITY; CARDIAC CA2+ TRANSPORT; OXIDATIVE STRESS; CARDIAC MEMBRANES; INTRACELLULAR CA2+ OVERLOAD;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
24
Recensione:
Indirizzi per estratti:
Citazione:
K.S. Dhalla et al., "MECHANISMS OF ALTERATIONS IN CARDIAC MEMBRANE CA2+ TRANSPORT DUE TO EXCESS CATECHOLAMINES", Cardiovascular drugs and therapy, 10, 1996, pp. 231-238

Abstract

The occurrence of excessive catecholamine release is often associatedwith stress due to the lifestyle of Western societies. Contrary to the general thinking that excess catecholamines produce cardiotoxicity mainly via binding to adrenoceptors, there is increasing evidence that catecholamine-induced deleterious actions may also occur through oxidative mechanisms. In this overview it is shown that a high dose of isoproterenol induces a biphasic change in cardiac Ca2+ transport in the sarcolemma and in sarcoplasmic reticulum. Both sarcolemmal and sarcoplasmic reticular Ca2+-transport activities are initially increased to maintain Ca2+ homeostasis and then are impaired, which may be associatedwith the occurrence of intracellular Ca2+ overload. On the other hand, mitochondrial Ca2+-transport activities exhibited a delayed increase. Pretreatment with vitamin E partially prevented the deleterious changes in cardiac membranes as well as the depressed energetic status of the heart muscle cell. It is concluded that excess catecholamines affect Ca2+-transport mechanisms primarily via oxidation reactions involving free radical-mediated damage. Thus drug approaches that reduce circulating catecholamines and/or prevent their oxidation should prove beneficial. A combination therapy involving inhibitors of catecholamine release, blockers of adrenoceptors, and antioxidants may be indicated for stress-induced heart disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 23:16:36