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Tetraethylammonium potentiates the activity of muscarinic potassium channels in guinea-pig atrial myocytes

Desuo Wang and David L. Armstrong

1. The modulation of native muscarinic potassium channels (K_ACh) by tetraethylammonium (TEA) was studied at 35^oC in cell-free patches from acutely dissociated guinea-pig atrial myocytes. The channels were identified unambiguously by their conductance, inward rectification, rapid gating kinetics and pharmacological responses to muscarinic agonists and GTPS.

2. Addition of 5 mM TEA to the cytoplasmic side of the patches almost doubled the open probability of K_ACh channels that had been activated maximally by GTPS. In contrast even 30 mM TEA did not significantly potentiate the response to carbachol in whole-cell recordings.

3. Unlike GTPS, TEA alone did not activate K_ACh channels de novo, but in patches that showed spontaneous K_ACh activity, 5 mM TEA increased channel open probability fourfold in the absence of added sodium, ATP or guanine nucleotides. Furthermore, the effect of TEA was not blocked by 10 M atropine or by 1 mM GDPS, and subsequent addition of 0.1 mM GTPS did not stimulate channel activity further in the presence of TEA.

4. Phosphatidylinositol 4,5-bisphosphate (PIP₂) also stimulates K_ACh channels under these conditions, but the kinetics of gating differ from channels stimulated by either TEA or GTP, which are very similar to one another.

5. The effects of TEA were not mimicked by tetramethyl- or tetrapentylammonium or by sodium or spermine, and TEA did not potentiate the activity of other inwardly rectifying potassium (K_ATP) channels in patches from cardiac myocytes.

6. We consider the possibility that TEA is mimicking the effect of an unidentified cellular factor, not sodium or PIP₂, which normally occupies the TEA site on K_ACh channel proteins but which diffuses away when the patch is excised.