Potentiation by adrenaline of thrombin-induced elevation of pHi is not essential for synergistic activation of human platelets.
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.
Steen
V M
VM
Department of Biochemistry, University of Bergen, Norway.
Cook
C A
CA
Tysnes
O B
OB
Holmsen
H
H
D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects*; D002352:Carrier Proteins / Q000037:antagonists & inhibitors; D004357:Drug Synergism; D004837:Epinephrine / Q000494:pharmacology*; D005453:Fluorescence; D006801:Humans; D006863:Hydrogen-Ion Concentration; D017923:Sodium-Hydrogen Exchangers; D013917:Thrombin / Q000494:pharmacology*
D002352:Carrier Proteins; D017923:Sodium-Hydrogen Exchangers; D000584:Amiloride; D013917:Thrombin; C039614:ethylisopropylamiloride; D004837:Epinephrine