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Titolo:
Tolerance for ATP-insensitive K-ATP channels in transgenic mice
Autore:
Koster, JC; Knopp, A; Flagg, TP; Markova, KP; Sha, Q; Enkvetchakul, D; Betsuyaku, T; Yamada, KA; Nichols, CG;
Indirizzi:
Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USAWashington Univ St Louis MO USA 63110 l & Physiol, St Louis, MO 63110 USA Univ Jena, Abt Herz Kreislauf Physiol, Inst Physiol, D-6900 Jena, Germany Univ Jena Jena Germany D-6900 hysiol, Inst Physiol, D-6900 Jena, Germany Washington Univ, Sch Med, Dept Med, Div Cardiovasc, St Louis, MO 63110 USAWashington Univ St Louis MO USA 63110 Cardiovasc, St Louis, MO 63110 USA
Titolo Testata:
CIRCULATION RESEARCH
fascicolo: 11, volume: 89, anno: 2001,
pagine: 1022 - 1029
SICI:
0009-7330(20011123)89:11<1022:TFAKCI>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
SENSITIVE POTASSIUM CHANNELS; RAT VENTRICULAR MYOCYTES; ACTION-POTENTIAL DURATION; SULFONYLUREA RECEPTOR; KIR6.2 SUBUNIT; ADENOSINE-TRIPHOSPHATE; NUCLEOTIDE MODULATION; CONTRACTILE FAILURE; INSULIN-SECRETION; STOICHIOMETRY;
Keywords:
K+ current; K-ATP; transgenic; electrocardiogram;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Nichols, CG Washington Univ, Sch Med, Dept Cell Biol & Physiol, 660 S Euclid Ave, St Louis, MO 63110 USA Washington Univ 660 S Euclid Ave St Louis MOUSA 63110 110 USA
Citazione:
J.C. Koster et al., "Tolerance for ATP-insensitive K-ATP channels in transgenic mice", CIRCUL RES, 89(11), 2001, pp. 1022-1029

Abstract

To examine the role of sarcolemmal K-ATP channels in cardiac function, we generated transgenic mice expressing GFP-tagged Kir6.2 subunits with reduced ATP sensitivity under control of the cardiac alpha -myosin heavy chain promoter. Four founder mice were isolated, and both founders and progeny wereall apparently normal and fertile. Electrocardiograms from conscious animals also appeared normal, although mean 24-hour heart rate was approximately10% lower in transgenic animals compared with littermate controls. In excised membrane patches, K-ATP channels were very insensitive to inhibitory ATP: mean K-1/2 ([ATP] causing half-maximal inhibition) was 2.7 mmol/L in high-expressing line 4 myocytes, compared with 51 mu mol/L in littermate control myocytes. Counterintuitively, K-ATP channel density was approximate to4-fold lower in transgenic membrane patches than in control. This reduction of total K-ATP conductance was confirmed in whole-cell voltage-clamp conditions, in which K-ATP was activated by metabolic inhibition. K-ATP conductance was not obvious after break-in of either control or transgenic myocytes, and there was no action potential shortening in transgenic myocytes. In marked contrast to the effects of expression of similar transgenes in pancreatic beta -cells, these experiments demonstrate a profound tolerance for reduced ATP sensitivity of cardiac K-ATP channels and highlight differential effects of channel activity in the electrical activity of the 2 tissues.

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Documento generato il 05/12/20 alle ore 19:52:51