Potentiation by adrenaline of thrombin-induced elevation of pHi is not essential for synergistic activation of human platelets

FEBS Lett. 1989 Jul 3;250(2):211-4. doi: 10.1016/0014-5793(89)80722-7.

Abstract

Gel-filtrated human platelets were stimulated with thrombin in the absence and presence of adrenaline. Adrenaline markedly enhanced the thrombin-induced increase in cytoplasmic pH (pHi) in BCECF-loaded platelets. This rise in pHi was strongly inhibited by the Na+/H+ exchange blocker EIPA. The potentiation by adrenaline of thrombin-induced PLC activation measured as [32P]PA formation and final platelet responses was, however, not blocked by EIPA, even at low concentrations of thrombin. These results indicate that the enhancement by adrenaline of thrombin-induced cytoplasmic alkalinization may be a secondary effect which is not essential for the potentiation by adrenaline of platelet activation by thrombin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amiloride / analogs & derivatives
  • Amiloride / pharmacology
  • Blood Platelets / drug effects*
  • Carrier Proteins / antagonists & inhibitors
  • Drug Synergism
  • Epinephrine / pharmacology*
  • Fluorescence
  • Humans
  • Hydrogen-Ion Concentration
  • Sodium-Hydrogen Exchangers
  • Thrombin / pharmacology*

Substances

  • Carrier Proteins
  • Sodium-Hydrogen Exchangers
  • Amiloride
  • Thrombin
  • ethylisopropylamiloride
  • Epinephrine