Effects of ATP antagonists on purinoceptor-operated inward currents in rat phaeochromocytoma cells

Ken Nakazawa, Kazuhide Inoue, Kannosuke Fujimori, Akira Takanaka

Research output: Contribution to journalArticlepeer-review

56 Citations (Scopus)

Abstract

The effects of suramin, reactive blue 2 (RB2) and d-tubocurarine (d-TC) were investigated electrophysiologically to elucidate the mechanisms underlying their antagonism of P2 purinoceptor-mediated responses. All three compounds inhibited an adenosine triphosphate (ATP)-activated inward current in rat phaeochromocytoma PC12 cells in a concentration-dependent manner. The order of potency was RB2 > suramin > d-TC. The inhibition induced by suramin or RB2 was reversible, whereas that induced by d-TC was not reversed after a 5-min rinse. The inactivation of the ATP-activated current was accelerated by d-TC but not by suramin or RB2. RB2 administered simultaneously with ATP exerted much weaker inhibition compared to that induced by prior administration, suggesting that RB2 is a slowly acting antagonist. This was not observed for suramin or d-TC. Suramin and RB2 caused a parallel shift in the concentration/response curve for the ATP-activated current. With d-TC the maximal response of ATP was decreased but the concentration producing half-maximal response was unchanged. The voltage dependency of the ATP-activated current showed less inward rectification in the presence of d-TC. Suramin or RB2 did not affect the voltage dependency. These results suggest that suramin and RB2 reversibly block binding of ATP to receptors, whereas d-TC blocks ion permeability through the ATP-activated channel.

Original languageEnglish
Pages (from-to)214-219
Number of pages6
JournalPflügers Archiv European Journal of Physiology
Volume418
Issue number3
DOIs
Publication statusPublished - Apr 1 1991
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

Fingerprint

Dive into the research topics of 'Effects of ATP antagonists on purinoceptor-operated inward currents in rat phaeochromocytoma cells'. Together they form a unique fingerprint.

Cite this