In permeabilised endothelial cells IP3-induced Ca2+ release is dependent on the cytoplasmic concentration of monovalent cations

doi:10.1016/S0008-6363(97)00207-1

Cardiovascular Research 1998 37(1):263-270; doi:10.1016/S0008-6363(97)00207-1
© 1998 by European Society of Cardiology

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In permeabilised endothelial cells IP₃-induced Ca²⁺ release is dependent on the cytoplasmic concentration of monovalent cations

Peter G Wood and James I Gillespie^*

The Department of Physiological Sciences, The Medical School, Newcastle University, Newcastle upon Tyne NE2 4HH, UK

^* Corresponding author. Tel. +44 191 2226988; Fax +44 191 2226988; E-mail: J.I.Gillespie@newcastle.ac.uk

Objective: IP₃-induced Ca²⁺ release from the intracellular storesplays a role in the production of vasoactive substances in theendothelium. In many cells, Ca²⁺ release is accompanied by aninward movement of K⁺ whose function may be to dissipate thepotential difference created by the loss of positive chargefrom the internal stores. The existence of such a mechanismin endothelial cells was investigated. Methods: Using saponin-permeabilisedbovine aortic endothelial (BAE) cells, the effects of K⁺ onthe IP₃-induced ⁴⁵Ca²⁺ release were investigated. Results: Replacementof K⁺ with NMG inhibited IP₃ (3 µM)-induced ⁴⁵Ca²⁺ releaseby 55%. The ability of other ions to allow IP₃-induced ⁴⁵Ca²⁺release was found to be K⁺=Na⁺>Cs⁺>Rb⁺>>Co²⁺. TheK⁺ channel blockers TEA, 4AP and 3,4-DAP were found to significantlyinhibit IP₃-induced ⁴⁵Ca²⁺ release by 16%, 36% and 27%, respectively.Conclusions: The data suggest that Ca²⁺ release from intracellularstores is partly dependent on a movement of K⁺ through K⁺ channelsin the store membranes. In contrast, 9AA (400 µM) andsubstitution with Co²⁺ abolished the response. Therefore, K⁺is important for IP₃-induced ⁴⁵Ca²⁺ release, but other ionsare also likely to act as counter-ions. 9AA and Co²⁺ probablyact on sites other than those involving ER monovalent cationchannels. The possibility that a counter-ion system plays arole in the activation of endothelial cells is discussed.

KEYWORDS IP₃, inositol 1,4,5-trisphosphate; BAE, bovine aortic endothelial; NMG, N-methyl-D-glucamine; TEA, tetraethyl ammonium; 4AP, 4-aminopyridine; 3,4-DAP, 3,4-diaminopyridine; 9AA, 9-aminoacridine; CICR, Ca²⁺-induced-Ca²⁺ release; ER, endoplasmic reticulum; SR, sarcoplasmic reticulum; DMEM, Dulbecco's modified Eagle's medium; SDS, sodium dodecyl sulfate; cpm, counts per minute; Tris, (hydroxymethyl)-methylamine; choline, [2-hydroxyethyl]trimethyl-ammonium; SERCA, sarco/endoplasmic reticulum ATPase; NO, nitric oxide

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