A delayed ATP-elicited K+ current in freshly isolated smooth muscle cells from mouse aorta.
Adenosine 5'-triphosphate (ATP) activated two sequential responses in freshly isolated mouse aortic smooth muscle cells. In the first phase, ATP activated Ca(2+)-dependent K(+) or Cl(-) currents and the second phase was the activation of a delayed outward current with a reversal potential of -75.9 +/- 1.4 mV. A high concentration of extracellular K(+) (130 mM) shifted the reversal potential of the delayed ATP-elicited current to -3.5 +/- 1.3 mV. The known K(+)-channel blockers, iberiotoxin, charybdotoxin, glibenclamide, apamin, 4-aminopyridine, Ba(2+) and tetraethylammonium chloride all failed to inhibit the delayed ATP-elicited K(+) current. Removal of ATP did not decrease the amplitude of the ATP-elicited current back to the control values. The simultaneous recording of cytosolic free Ca(2+) and membrane currents revealed that the first phase of the ATP-elicited response is associated with an increase in intracellular Ca(2+), while the second delayed phase develops after the return of cytosolic free Ca(2+) to control levels.ATP did not activate Ca(2+)-dependent K(+) currents, but did elicit Ca(2+)-independent K(+) currents, in cells dialyzed with ethylene glycol-bis (2-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA). The delay of activation of Ca(2+)-independent currents decreased from 10.5 + 3.4 to 1.27 +/- 0.33 min in the cells dialyzed with 2 mM EGTA. Adenosine alone failed to elicit a Ca(2+)-independent K(+) current but simultaneous application of ATP and adenosine activated the delayed K(+) current. Intracellular dialysis of cells with guanosine 5'-O-(2-thiodiphosphate) transformed the Ca(2+)-independent ATP-elicited response from a sustained to a transient one. A phospholipase C inhibitor, U73122 (1 microM), was shown to abolish the delayed ATP-elicited response. These results indicate that the second phase of the ATP-elicited response was a delayed Ca(2+)-independent K(+) current activated by exogenous ATP. This phase might represent a new vasoregulatory pathway in vascular smooth muscle cells.
Serir
Karima
K
Department of Zoology and Animal Biology, University of Geneva, Sciences III, 30 Quai Ernest Ansermet, CH-1211 Geneva 4, Switzerland.
Hayoz
Sebastien
S
Fanchaouy
Mohammed
M
Bény
Jean-Louis
JL
Bychkov
Rostislav
R
D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D001011:Aorta / Q000166:cytology / Q000378:metabolism*; D002478:Cells, Cultured; D051379:Mice; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D014664:Vasodilation / Q000502:physiology
D000255:Adenosine Triphosphate; D011188:Potassium