FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Previous Volume 328:1244-1251 April 29, 1993 Number 17 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

	Full Text Purchase this article Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

The movement of ions across cardiac cell membranes generates the electrical potentials that activate the heart. Today's molecular biology is providing breathtaking new insights into the regulation of this electrical activity, which is the basis of electrocardiography. Whereas only a few years ago depolarization and repolarization of heart cells were attributed to changing membrane resistance, cardiac action potentials are now understood in terms of structural changes in the proteins that control ion fluxes across the plasma membrane.

Ions cross hydrophobic lipid membranes by passing through regulated pores formed by members of an extended family of ion-channel proteins. The opening and . . . [Full Text of this Article]

Ions as Charge Carriers during the Action Potential

General Features of Plasma-Membrane Ionic Currents

Gating of Ion Channels

Structure of Plasma-Membrane Ion Channels

The Channel Subunits

The Channel Domains

Diversity and Evolution of Channel Structure

Sodium and Calcium Channels

The Family of Potassium Channels

Rectifying Currents

Cardiac Potassium Currents

Clinical Implications of the Structure and Function of Ion Channels

Antiarrhythmic Drugs

Prevention of Sudden Cardiac Death

Repolarization Abnormalities

Conclusions

Source Information

From the Cardiology Division, Department of Medicine, University of Connecticut, 263 Farmington Ave., Farmington, CT 06030-1305, where reprint requests should be addressed to Dr. Katz.

References

This article has been cited by other articles:

• Levy, J. H., Tanaka, K. A., Bailey, J. M. (2008). Cardiac Surgical Pharmacology. Card Surg Adult 3: 77-110 [Full Text]  
• Zerumsky, K., McBride, B. F. (2006). Ranolazine in the management of chronic stable angina. Am J Health Syst Pharm 63: 2331-2338 [Abstract] [Full Text]  
• Harris, N. S. (2006). Case 24-2006 -- A 40-Year-Old Woman with Hypotension after an Overdose of Amlodipine. NEJM 355: 602-611 [Full Text]  
• Smetana, P., Batchvarov, V. N., Hnatkova, K., Camm, A. J., Malik, M. (2004). Ventricular gradient and nondipolar repolarization components increase at higher heart rate. Am. J. Physiol. Heart Circ. Physiol. 286: H131-H136 [Abstract] [Full Text]  
• Smetana, P., Batchvarov, V., Hnatkova, K., John Camm, A, Malik, M. (2003). Sex differences in the rate dependence of the T wave descending limb. Cardiovasc Res 58: 549-554 [Abstract] [Full Text]  
• Erxleben, C., Gomez-Alegria, C., Darden, T., Mori, Y., Birnbaumer, L., Armstrong, D. L. (2003). Modulation of cardiac CaV1.2 channels by dihydropyridine and phosphatase inhibitor requires Ser-1142 in the domain III pore loop. Proc. Natl. Acad. Sci. USA 100: 2929-2934 [Abstract] [Full Text]  
• Bailey, J. M., Tanaka, K. A., Levy, J. H. (2003). Cardiac Surgical Pharmacology. Card Surg Adult 2: 85-118 [Full Text]  
• Phillippe, M., Basa, A. (1997). Effects of Sodium and Calcium Channel Blockade on Cytosolic Calcium Oscillations and Phasic Contractions of Myometrial Tissue. Reproductive Sciences 4: 72-77 [Abstract]  
• Ishikawa, Y., Homcy, C. J. (1997). The Adenylyl Cyclases as Integrators of Transmembrane Signal Transduction. Circ. Res. 80: 297-304 [Full Text]  
• Knight, C. J., Panesar, M., Wilson, D. J., Chronos, N. A.F., Patel, D., Fox, K., Goodall, A. H. (1997). Different Effects of Calcium Antagonists, Nitrates, and ß-Blockers on Platelet Function: Possible Importance for the Treatment of Unstable Angina. Circulation 95: 125-132 [Abstract] [Full Text]  
• Drici, M. D., Burklow, T. R., Haridasse, V., Glazer, R. I., Woosley, R. L. (1996). Sex Hormones Prolong the QT Interval and Downregulate Potassium Channel Expression in the Rabbit Heart. Circulation 94: 1471-1474 [Abstract] [Full Text]  
• Seisenberger, C., Specht, V., Welling, A., Platzer, J., Pfeifer, A., Kuhbandner, S., Striessnig, J., Klugbauer, N., Feil, R., Hofmann, F. (2000). Functional Embryonic Cardiomyocytes after Disruption of the L-type alpha 1C (Cav1.2) Calcium Channel Gene in the Mouse. J. Biol. Chem. 275: 39193-39199 [Abstract] [Full Text]