Abstract
Nonadrenergic inhibitory and excitatory junction potentials (IJP and EJP) in the intestinal smooth muscle cells are of a complex transmitter and ion nature. The IJP consist of two components; the initial, fast, component is of a purinergic nature. Low-conductance Ca2+-dependent potassium channels (SK(Ca)) are involved in generation of the initial component of IJP because this component can be specifically and reversibly blocked by apamin. Probably, local Ca2+ release from the InsP3-sensitive store can be a link between the P2Y receptors and activation of the SK(Ca) channels because inhibition of the activity of phospholipase C (PLC) decreases IJP. The second, slow, component of IJP is nitric oxide-dependent. Such a component of IJP develops due to activation of high-conductance Ca2+-dependent potassium channels (BK(Ca)) because this component can be blocked by TEA and charybdotoxin. The release of Ca2+ from the ryanodine-sensitive store is responsible for activation of the BK(Ca) channels and generation of the second component of IJP. Thus, it appears that Ca2+ released from one of the intracellular stores can activate only a certain type of the Ca2+-dependent K+ channels involved in the generation of IJP.
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