A novel receptor-operated Ca2+-permeable channel activated by ATP in smooth muscle.
Receptor-operated Ca2+ entry has been proposed as a signalling mechanism in many cells. Receptor-operated Ca2+ channels (ROCs) were first postulated in smooth muscle by Bolton, van Breemen and Somlyo and Somlyo, but recordings of directly ligand-gated Ca2+ current are lacking. Here we describe receptor-operated Ca2+ current evoked in arterial smooth muscle cells by ATP, a sympathetic neurotransmitter. ATP activates channels with approximately 3:1 selectivity for Ca2+ over Na+ at near-physiological concentrations and with a unitary conductance of approximately 5 pS in 110 mM Ca2+ or Ba2+. The channels can be opened even at very negative potentials and resist inhibition by cadmium or nifedipine, unlike voltage-gated Ca2+ channels; they are not blocked by Mg2+, unlike NMDA (N-methyl-D-aspartate)-activated channels; they are directly activated by ligand, without involvement of readily diffusible second messengers, unlike cation channels in neutrophils and T lymphocytes. Thus, the ATP-activated channels provide a distinct mechanism for excitatory synaptic current and Ca2+ entry in smooth muscle.
D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D004553:Electric Conductivity; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D011817:Rabbits; D011956:Receptors, Cell Surface / Q000502:physiology*; D013569:Synapses / Q000502:physiology
D007473:Ion Channels; D011956:Receptors, Cell Surface; D002104:Cadmium; D000255:Adenosine Triphosphate; D009543:Nifedipine; D002118:Calcium