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Titolo:
HYPOXIA-INDUCED ACTIVATION OF K-ATP CHANNELS LIMITS ENERGY DEPLETION IN THE GUINEA-PIG HEART
Autore:
DECKING UKM; REFFELMANN T; SCHRADER J; KAMMERMEIER H;
Indirizzi:
UNIV DUSSELDORF,INST HERZ & KREISLAUFPHYSIOL D-40225 DUSSELDORF GERMANY RHEIN WESTFAL TH AACHEN,INST PHYSIOL D-52057 AACHEN GERMANY
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 2, volume: 38, anno: 1995,
pagine: 734 - 742
SICI:
0363-6135(1995)38:2<734:HAOKCL>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
SENSITIVE POTASSIUM CHANNELS; CARDIAC-MUSCLE; RAT-HEART; METABOLIC INHIBITION; CONTRACTILE FAILURE; ADENOSINE FORMATION; ISCHEMIA; MYOCYTES; SULFONYLUREA; REDUCTION;
Keywords:
CARDIAC FUNCTION; ENERGY METABOLISM; ADENOSINE 5'-TRIPHOSPHATE FREE ENERGY;
Tipo documento:
Note
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
U.K.M. Decking et al., "HYPOXIA-INDUCED ACTIVATION OF K-ATP CHANNELS LIMITS ENERGY DEPLETION IN THE GUINEA-PIG HEART", American journal of physiology. Heart and circulatory physiology, 38(2), 1995, pp. 734-742

Abstract

The functional role of ATP-dependent potassium channels (K-ATP) in hypoxic cardiac failure was investigated in isolated guinea pig hearts with glibenclamide and rimalkalim as inhibitor and activator, respectively. Monophasic action potential duration at 90% of repolarization (MAP(90)), left ventricular function, and cardiac energy status ((31)Pp nuclear magnetic resonance spectroscopy) were measured during normoxic (95% O-2) and hypoxic (20% O-2) perfusion. In normoxic hearts, 1 mu M glibenclamide did not affect MAP(90), left ventricular function, and coronary flow (n = 4). In contrast, rimalkalim rapidly shortened MAP(90) and left ventricular pressure (LVP) in a dose-dependent fashion (e.g., by 60.2 +/- 3.5 and 80.8 +/- 8.2%, respectively, with 0.6 mu M rimalkalim). This latter effect was reversed by 1 mu M glibenclamide (n = 4). With hypoxic perfusion, a reduction in LVP was observed, along with a shortening of the action potential (MAPS,; 202 +/- 13 vs. 164 +/ 9ms) and an increase in coronary flow. Glibenclamide (1 mu M) reversedthe MAP(90) shortening and the increase in coronary flow. In addition, glibenclamide increased LVP transiently (n = 4). When coronary flow of hypoxic hearts was kept constant, however, glibenclamide elicited asustained positive inotropic effect (n = 7). After glibenclamide, an increase in LVP from 54 +/- 4 to 64 +/- 3 mmHg was observed, along with a reduction in the free energy change of ATP hydrolysis from -54.5 +/- 1.9 to -52.9 +/- 0.2 kJ/mol and a further increase in the coronary venous adenosine from 269 +/- 48 to 1,680 +/- 670 nmol/l. In contrast,0.1 mu M rimalkalim further shortened the action potential of hypoxichearts and caused a major reduction of systolic force. This was accompanied by a partial restoration of the free energy change of ATP hydrolysis (-55.8 +/- 0.7 kJ/ mel) and a decrease in venous adenosine (157 27 nmol/l). Our results suggest that K-ATP channels are activated during hypoxia when there are only small changes in cytosolic ATP. This channel activation contributes to the downregulation of contractile force. These findings are consistent with the hypothesis that hypoxia-induced activation of K-ATP channels constitutes a protective mechanism that conserves the cardiac energy status under conditions of insufficient O-2 supply.

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Documento generato il 01/12/20 alle ore 10:46:56