Effects of ATP on specific [3H](+)-isradipine binding in rat ventricular cardiomyocytes

Eur J Pharmacol. 1996 May 6;303(1-2):115-22. doi: 10.1016/0014-2999(96)00071-4.

Abstract

In heart membranes, specific [3H](+)-isradipine binding is reduced in membranes from ischemic hearts and by adding 1 mM ATP at low Ca2+ concentrations (1 microM). We investigated if ATP affected specific [3H](+)-isradipine binding in intact rat ventricular cardiomyocytes. Reducing intracellular ATP by 2 h hypoxia (N2 gas) and glucose-free buffer with 1 mM CN-, did not affect density or dissociation constant of [3H](+)-isradipine binding in cardiomyocytes at extracellular 30 mM K+. Extracellular 10 mM ATP inhibited binding in cardiomyocytes by 90% and 50%, respectively, in 30 mM and 120 mM K+ buffer with Ca2+ and Mg2+. Omitting Ca2+ and Mg2+ from the buffer had no effect on the binding inhibition of ATP. Hence, in cardiomyocytes, reducing intracellular ATP has no effect on specific [3H](+)-isradipine binding, whereas high extracellular ATP in the presence of Ca2+ and Mg2+ inhibits binding. Apparently, ATP effects on binding differ in cardiomyocytes and membranes.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Adenosine Triphosphate / pharmacology*
  • Animals
  • Calcium Channels / drug effects*
  • Calcium Channels / metabolism*
  • Cell Hypoxia / physiology
  • Heart / drug effects*
  • Heart Ventricles / drug effects
  • Heart Ventricles / metabolism
  • Isradipine / metabolism*
  • Magnesium / metabolism
  • Male
  • Myocardium / metabolism*
  • Rats
  • Rats, Wistar

Substances

  • Calcium Channels
  • Adenosine Triphosphate
  • Magnesium
  • Isradipine