[Ca2+]i-dependent membrane currents in guinea-pig ventricular cells in the absence of Na/Ca exchange

Pflugers Arch. 1995 Sep;430(5):871-8. doi: 10.1007/BF00386189.

Abstract

Transient inward currents (Iti) during oscillations of intracellular [Ca2+] ([Ca2+]i) in ventricular myocytes have been ascribed to Na/Ca exchange. We have investigated whether other Ca2+-dependent membrane currents contribute to Iti in single guinea-pig ventricular myocytes, by examining membrane currents during [Ca2+]i oscillations and during caffeine-induced Ca2+ release from the sarcoplasmic reticulum in the absence of Na+. Membrane currents were recorded during whole-cell voltage clamp and [Ca2+]i measured simultaneously with fura-2. In the absence of Na/Ca exchange, i.e., with Li+, Cs+ or N-methyl-D-glucamine (NMDG+) substituted for Na+, the cell could be loaded with Ca2+ by repetitive depolarizations to +10 mV, resulting in spontaneous [Ca2+]i oscillations. During these oscillations, no inward currents were seen, but instead spontaneous Ca2+ release was accompanied by a shift of the membrane current in the outward direction at potentials between -40 mV and +60 mV. This [Ca2+]i-dependent outward current shift was not abolished when NMDG+ was substituted for internal monovalent cations, nor was it sensitive to substitution of external Cl-. It was however, sensitive to the blockade of ICa by verapamil. These results suggest that the transient outward current shift observed during spontaneous Ca2+ release represents [Ca2+]i-dependent transient inhibition of ICa. Similarly, during the [Ca2+]i transients induced by brief caffeine (10 mM) applications, we could not detect membrane currents attributable to a Ca2+-activated nonselective cation channel, or to a Ca2+-activated Cl- channel; however, transient Ca2+-dependent inhibition of ICa was again observed. We conclude that neither the Ca2+-activated nonselective cation channel nor the Ca2+-activated Cl- channel contribute significantly to the membrane currents during spontaneous [Ca2+]i oscillations in guinea-pig ventricular myocytes. However, in the voltage range between -40 mV and +60 mV Ca2+-dependent transient inhibition of ICa will contribute to the oscillations of the membrane current.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caffeine / pharmacology
  • Calcium / metabolism
  • Calcium / physiology
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels / drug effects
  • Calcium Channels / metabolism*
  • Carrier Proteins / metabolism*
  • Cations / pharmacology
  • Cell Membrane / drug effects
  • Cell Membrane / metabolism
  • Chloride Channels / metabolism
  • Guinea Pigs
  • Heart / drug effects
  • Heart Ventricles / drug effects
  • Heart Ventricles / metabolism
  • In Vitro Techniques
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Myocardial Contraction / physiology
  • Myocardium / cytology
  • Myocardium / metabolism*
  • Patch-Clamp Techniques
  • Sodium / pharmacology
  • Sodium-Calcium Exchanger
  • Verapamil / pharmacology

Substances

  • Calcium Channel Blockers
  • Calcium Channels
  • Carrier Proteins
  • Cations
  • Chloride Channels
  • Sodium-Calcium Exchanger
  • Caffeine
  • Sodium
  • Verapamil
  • Calcium