Signal transduction in the cardiac k-receptor

Biol Signals. May-Jun 1995;4(3):174-8. doi: 10.1159/000109438.

Abstract

The presence of k-binding sites in the heart suggests a regulatory role of k-receptor in the cardiac functions. Recent studies have provided evidence that activation of cardiac k-receptor elevates intracellular free calcium ([Ca2+]i) by increasing mobilization of calcium from the intracellular store. The mobilization of intracellular calcium results from an increased production of inositol-1,4,5-trisphosphate (IP3). The increase in [Ca2+]i may manifest in cardiac arrhythmias while the depletion of calcium from the intracellular store may reduce the contractility elicited upon depolarization. The responses of IP3/[Ca2+]i are significantly attenuated after development of tolerance to k-opioids due mainly to the impairment of postreceptor events. The attenuated responses of IP3/[Ca2+]i to k-receptor activation may be responsible for the failure of the k-agonists to induce cardiac arrhythmias and to reduce electrically induced calcium transients in the ventricular myocytes.

Publication types

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

MeSH terms

  • Animals
  • Calcium / metabolism
  • Heart / physiology*
  • Humans
  • Inositol 1,4,5-Trisphosphate / metabolism
  • Models, Cardiovascular
  • Myocardial Contraction*
  • Myocardium / metabolism*
  • Receptors, Opioid, kappa / physiology*
  • Signal Transduction*

Substances

  • Receptors, Opioid, kappa
  • Inositol 1,4,5-Trisphosphate
  • Calcium