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Oxytocin-induced changes in single cell K⁺ currents and smooth muscle contraction of guinea-pig gastric antrum

To study the effects of oxytocin on both spontaneous phasic contractions and K⁺ outward currents (I_K) of the so-called 'non-target' smooth muscle cells, physiological concentrations of oxytocin ranging between 10^–12 mol/l and 10^–8 mol/l were applied to smooth muscle preparations and single voltage-clamped cells isolated from the circular layer of the guinea-pig gastric antrum. Oxytocin (10^–12mol/l to 10^–8 mol/l) suppressed, in a dose-dependent manner, the tetrodotoxin- and atropine-resistant spontaneous phasic contractions and shifted rightward the dose–response curves of 10^–7 mol/l charybdotoxin and 10^–3mol/l BaCl₂. In cells with preloaded intracellular Ca²⁺ stores, oxytocin (10^–12 mol/l to 10^–9 mol/l) caused a dose-dependent activation of the charybdotoxin-blockable non-inactivating component of I_K (I_K(s1)) of single voltage-clamped cells, which was accompanied by hyperpolarization of the cell membranes. ⁸Lys-vasopressin and ⁸arg-vasopressin failed to mimic the effects of oxytocin on both contraction and K⁺ currents. Further, the oxytocin-induced activation of I_K(s1) was effectively antagonized by 5x 10^–8 mol/l U-73122 or 5x 10^–6 mol/l 2-nitro-4-carboxyphenyl N,N-diphenylcarbamate (inhibitors of the cell membrane phospholipase C), as well as by intracellularly applied heparin (selective inhibitor of inositol-1,4,5-trisphosphate (IP₃)-induced Ca²⁺ release channels). In cells incubated in the absence of Ca²⁺ entry throughout the study, oxytocin (10^–9 mol/l) caused a slight and transient increase of I_K(s1) amplitudes. Neither ryanodine (10^–6 mol/l nor cyclopiazonic acid (10^–6 mol/l) were able to restore the I_K-activating effect of oxytocin in these cells.

The data obtained suggest (i) that selective oxytocin receptors are present on the membranes of guinea-pig antral smooth muscle cells, (ii) that the oxytocin-related relaxation may result from the activation of Ca²⁺-sensitive K⁺ conductivity via activation of IP₃-induced release of C^a from the submembrane located cisternae of the sarcoplasmic reticulum Ca²⁺ stores and (iii) in turn, this evokes a non-inactivating component of I_K, hyperpolarizing the cell membrane.

European Journal of Endocrinology 136 531–538