On the mechanism of histamine induced enhancement of the cardiac Ca2+ current

Pflugers Arch. 1987 Sep;410(1-2):23-9. doi: 10.1007/BF00581891.

Abstract

In guinea pig ventricular myocytes, the effect of histamine on the slow Ca2+ current (ICa) was studied and the following results were obtained: (1) Superfusion of cells with histamine resulted in a dose-dependent enhancement of the amplitude of ICa. The threshold concentration of histamine was 10(-8) M, half maximal increase occurred at 3 X 10(-7) M and maximal enhancement (about 3-4-fold) at 5 X 10(-6) M. (2) The histamine effect was greatly reduced by the H2 antagonist cimetidine (10(-5) M) but only slightly by the H1 antagonist diphenhydramine (10(-5) M). (3) Effects of isoprenaline (ISP) and histamine at maximal effective concentrations on ICa were not additive, suggesting that both agents use the same intracellular pathway. Intracellular infusion of a blocker of the cAMP-dependent protein kinase, Rp-cAMPS (10(-4) M), prevented the histamine effect. (4) The involvement of GTP-dependent transducer proteins was studied by cell dialysis with several GTP derivatives. Intracellular application of the stable GDP-analogue, GDP-beta-S, reduced the histamine effect on ICa, whereas the stable GTP analogue, GTP-gamma-S, mimicked the histamine effect.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Cyclic AMP / physiology
  • Female
  • Guanosine Triphosphate / physiology
  • Guinea Pigs
  • Heart / physiology*
  • Heart Ventricles / cytology
  • Histamine / pharmacology*
  • Histamine Antagonists / pharmacology
  • In Vitro Techniques
  • Ion Channels / drug effects*
  • Male

Substances

  • Histamine Antagonists
  • Ion Channels
  • Histamine
  • Guanosine Triphosphate
  • Cyclic AMP
  • Calcium