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Titolo:
Inhibition of K+ currents by homocysteine in rat ventricular myocytes
Autore:
Shontz, RD; Xu, Z; Patel, KP; Rozanski, GJ;
Indirizzi:
Univ Nebraska, Coll Med, Dept Physiol & Biophys, Med Ctr, Omaha, NE 68198 USA Univ Nebraska Omaha NE USA 68198 & Biophys, Med Ctr, Omaha, NE 68198 USA
Titolo Testata:
JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY
fascicolo: 2, volume: 12, anno: 2001,
pagine: 175 - 182
SICI:
1045-3873(200102)12:2<175:IOKCBH>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
METHYLENETETRAHYDROFOLATE REDUCTASE GENE; PLASMA TOTAL HOMOCYSTEINE; OUTWARD POTASSIUM CURRENT; ENDOTHELIAL DYSFUNCTION; HEART-DISEASE; HYPERHOMOCYST(E)INEMIA;
Keywords:
heart; potassium channels; electrophysiology; patch clamp; cardiomyocytes;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Rozanski, GJ Univ Nebraska, Coll Med, Dept Physiol & Biophys, Med Ctr, 984575 Nebraska Med Ctr, Omaha, NE 68198 USA Univ Nebraska 984575 Nebraska MedCtr Omaha NE USA 68198 USA
Citazione:
R.D. Shontz et al., "Inhibition of K+ currents by homocysteine in rat ventricular myocytes", J CARD ELEC, 12(2), 2001, pp. 175-182

Abstract

Homocysteine Inhibition of K+ Channels in Rat Cardiomyocytes. Introduction: Clinical evidence suggests that increased blood levels of homocysteine may be an independent risk factor for the development of cardiovascular disease, but the functional effects of this sulfhydryl amino acid on the myocardium are poorly understood. The present study was conducted to determine thedirect effects of homocysteine on the electrophysiologic properties of theheart. Methods and Results: Whole-cell voltage-clamp recordings were made in ventricular myocytes isolated from normal rat hearts to analyze the Ca2+-independent, transient outward Kf current (I-to), a major repolarizing current inthese cells. Maximum I-to density (measured at +60 mV) was decreased similar to 47% from baseline in the presence of 500 muM homocysteine (P < 0.05),but the amount of block varied in a frequency- and voltage-dependent manner, Decreased I-to density was not accompanied by significant changes in voltage- or time-dependent properties of the current, nor was it affected by pretreating myocytes with the protein kinase inhibitor staurosporine. Because a portion of total extracellular homocysteine is oxidized, we examined the response to homocystine, the oxidized form of homocysteine. In myocytes superfused with 500 <mu>M homocystine, maximum I-to density was decreased bysimilar to 40% from baseline (P < 0.05). In contrast, the thiolactone formof homocysteine did not alter I-to amplitude. Conclusion: These data suggest that homocysteine and its oxidized form homocystine acutely inhibit I-to channels in ventricular myocytes by mechanisms involving the free thiol or disulfide moieties of these compounds, High homocysteine or homocystine levels may contribute to abnormal repolarizationand arrhythmogenic conditions in the intact heart.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 10:16:36