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Circulation. 1998;98:969-976

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(Circulation. 1998;98:969-976.)
© 1998 American Heart Association, Inc.

Clinical Investigation and Reports

Increased Availability and Open Probability of Single L-Type Calcium Channels From Failing Compared With Nonfailing Human Ventricle

Frank Schröder, MD; Renate Handrock, PhD; Dirk J. Beuckelmann, MD; Stephan Hirt, MD; Roger Hullin, MD; Leo Priebe, MD; Robert H. G. Schwinger, MD; Joachim Weil, MD; ; Stefan Herzig, MD

From the Departments of Pharmacology (F.S., R.H., S. Herzig) and Cardiology (D.J.B., L.P., R.H.G.S.), University of Cologne; the Department of Cardiothoracic Surgery, University of Kiel (S. Hirt); the Department of Cardiology, Ludwig-Maximilians-University, Munich (R.H.); and the Department of Pharmacology, University of Hamburg (J.W.), Germany.

Correspondence to Stefan Herzig, MD, Department of Pharmacology, University of Cologne, Gleueler Straße 24, 50931 Cologne, Germany. E-mail stefan.herzig{at}uni-koeln.de

Background—The role of the L-type calcium channel in human heart failure is unclear, on the basis of previous whole-cell recordings.

Methods and Results—We investigated the properties of L-type calcium channels in left ventricular myocytes isolated from nonfailing donor hearts (n=16 cells) or failing hearts of transplant recipients with dilated (n=9) or ischemic (n=7) cardiomyopathy. The single-channel recording technique was used (70 mmol/L Ba2+). Peak average currents were significantly enhanced in heart failure (38.2±9.3 fA) versus nonfailing control hearts (13.2±4.5 fA, P=0.02) because of an elevation of channel availability (55.9±6.7% versus 26.4±5.3%, P=0.001) and open probability within active sweeps (7.36±1.51% versus 3.18±1.33%, P=0.04). These differences closely resembled the effects of a cAMP-dependent stimulation with 8-Br-cAMP (n=11). Kinetic analysis of the slow gating shows that channels from failing hearts remain available for a longer time, suggesting a defect in the dephosphorylation. Indeed, the phosphatase inhibitor okadaic acid was unable to stimulate channel activity in myocytes from failing hearts (n=5). Expression of calcium channel subunits was measured by Northern blot analysis. Expression of {alpha}1C- and ß-subunits was unaltered. Whole-cell current measurements did not reveal an increase of current density in heart failure.

Conclusions—Individual L-type calcium channels are fundamentally affected in severe human heart failure. This is probably important for the impairment of cardiac excitation-contraction coupling.


Key Words: calcium channels • heart failure • myocytes




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