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Titolo:
Activation of alpha(1)-adrenergic receptor during Ca2+ pre-conditioning elicits strong protection against Ca2+ overload injury via protein kinase C signaling pathway
Autore:
Wang, YG; Ashraf, M;
Indirizzi:
Univ Cincinnati, Med Ctr, Dept Pathol & Lab Med, Cincinnati, OH 45267 USA Univ Cincinnati Cincinnati OH USA 45267 Lab Med, Cincinnati, OH 45267 USA
Titolo Testata:
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
fascicolo: 11, volume: 30, anno: 1998,
pagine: 2423 - 2435
SICI:
0022-2828(199811)30:11<2423:AOARDC>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-HEART MYOCYTES; POLYMORPHONUCLEAR NEUTROPHILS; ALPHA-1-ADRENERGIC RECEPTOR; PRECONDITIONING ELICITS; CALCIUM HOMEOSTASIS; MYOCARDIAL-ISCHEMIA; DEPENDENT PROCESSES; TRANSDUCTION; PARADOX; CARDIOMYOCYTES;
Keywords:
alpha(1)-adrenergic receptor; Ca2+ paradox; Ca2+ pre-conditioning; phenylephrine; protein kinase C;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Ashraf, M Univti,ncinnati, Med Ctr, Dept Pathol & Lab Med, 231 Bethesda Ave, Cincinna Univ Cincinnati 231 Bethesda Ave Cincinnati OH USA 45267 incinna
Citazione:
Y.G. Wang e M. Ashraf, "Activation of alpha(1)-adrenergic receptor during Ca2+ pre-conditioning elicits strong protection against Ca2+ overload injury via protein kinase C signaling pathway", J MOL CEL C, 30(11), 1998, pp. 2423-2435

Abstract

The objective was to test the hypothesis that transient activation of the alpha(1)-adrenergic receptor mimics the beneficial effects of Ca2+ preconditioning on the Ca2+ paradox (Ca2+ PD) injury in rat hearts, and that the protection is mediated by protein kinase C (PKC) signaling pathway. Langendorff-perfused rat hearts were subjected to the Ca2+ PD (10 min of Ca2+ depletion followed by 10 min of Ca2+ repletion). The effects of alpha(1)-adrenergic receptor activation and other interventions on functional, biochemical and pathological changes were assessed. In hearts pretreated with 50 mu mol/l phenylephrine, left ventricular end-diastolic pressure and coronary now were significantly preserved after Ca2+ PD; furthermore, peak loss of lactate dehydrogenase was significantly decreased while ATP was significantly preserved. A remarkable preservation of cell structure was observed in phenylephrine-treated hearts in contrast to non-treated Ca2+ PD hearts. However, pre-conditioning elicited by phenylephrine caused only a mild improvement inleft ventricular developed pressure (LVDP) as opposed to its impressive recovery of left ventricular end-diastolic pressure (LVEDP), heart rate (HR),or coronary flow (CF). The salutary effects of phenylephrine on the Ca2+ PD injury were almost similar to those observed in hearts which underwent Ca2+ pre-conditioning (CPC) or were pretreated with 1-stearoyl-2-arachidonoyl-glycerol (SAG), a potent PKC activator. In phenylephrine pretreated hearts, PKC isoform-alpha was localized in the sarcolemma and nucleus, while PKC-delta and PKC-epsilon were localized in the cell membrane, and intercalateddisk respectively. Prazosin, a specific alpha(1)-adrenergic receptor antagonist completely abolished the beneficial effects of phenylephrine on the Ca2+ PD and blocked translocation of PKC isoforms. In addition, prazosin (1 mu mol/l) also reversed salutary effects of CPC. Moreover, the beta-adrenergic antagonist, propranolol, had no effect on the protection provided by phenylephrine against the Ca2+ PD injury. This study suggests that the activation of the alpha(1)-adrenergic receptor confers protection against the lethal injury of the Ca2+ PD via PKC-mediated signaling pathways. The protection is shared by stimuli common with calcium pre-conditioning. (C) 1998 Academic Press.

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Documento generato il 07/04/20 alle ore 01:48:57