ArticleBritish journal of pharmacology1993
Membrane current responses to externally-applied ATP in the longitudinal muscle of the chicken rectum.
Article in British journal of pharmacology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
1. Membrane current responses to ATP in enzymically-dispersed single smooth muscle cells from the chicken rectum were investigated by the whole-cell voltage clamp technique. 2. In cells dialysed with a KCl-rich solution under voltage clamp at a holding potential of -40 mV, ATP (10 microM) produced an inward current followed by an outward current. When the holding potential was changed to 0 mV and -80 mV, the biphasic current response to ATP was converted to an outward current alone and an inward current alone, respectively. 3. External application of tetraethylammonium (TEA, 5 mM), intracellular dialysis with a CsCl-rich solution, or inclusion of EGTA (10 mM) in the pipette abolished the outward current response to ATP. 4. Neither depletion of Ca2+ store with caffeine (10 mM) nor block of voltage-gated Ca2+ channels with nifedipine (10 microM) affected the biphasic current response to ATP. After removal of the extracellular Ca2+ the outward current response to ATP was abolished. 5. alpha,beta-methylene ATP (100 microM) elicited a current similar to the ATP-induced current. In the presence of alpha,beta-methylene ATP (100 microM), application of ATP (100 microM) was without effect. 6. In CsCl-filled cells, ATP analogues elicited an inward current and the order of potency was ATP not equal to alpha, beta-methylene ATP > ADP >> AMP. 7. Inclusion of GTP gamma S (0.2 mM) or GDP beta S (2 mM) in the pipette did not affect the ATP-induced inward current in CsCl-filled cells. The reversal potential of the ATP-induced inward current was about 0 mV and was completely inhibited after replacement of the cations in the bath solution by Tris. The reversal potential remained almost unchanged after replacement of Na+ in the bath solution with 1 10 mM Ca2+, but shifted in the negative direction after replacement of Na+ or both Na+ and Ca2+ with glucosamine.8. The results suggest that ATP acts on P2 purinoceptors to cause activation of cation channels with selectivity for Ca2+ over Na+. Moreover, it appears that no G-protein-mediated mechanism is involved and increased Ca2+ entry through the cation channels causes activation of Ca2+-activated K+ channels.
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