Possible relationship between the release of calcium ions and inactivation of the potassium conductance induced by noradrenaline in smooth muscle of the Guinea-pig vas deferens.

Abstract

In order to examine whether any change in cytoplasmic Ca2+ concentration occurs during the noradrenaline (NA)-induced change in the membrane potential, the isometric tension of smooth muscle of the guinea-pig vas deferens was recorded together with membrane potentials using the sucrose-gap method. NA induced a depolarization and an increase in cytoplasmic Ca2+ comprising two (initial and second) phases. In time courses, the depolarization and the second phase of the increase in cytoplasmic Ca2+ were similar. Only at the phase around the onset of the depolarization, the membrane conductance was increased but then, it was decreased. Lowering the external Ca2+ concentration and application of D600 suppressed all of the NA-induced responses. In addition, D600 diminished the size of the NA-induced decrement in the membrane conductance. The present results suggest that the initial phase of the increase in the cytoplasmic Ca2+ is due to the influx of Ca2+ and the second phase, probably to the release of Ca2+ from some intracellular stores. It was discussed that the release of Ca2+ might occur at the internal surface of the membrane, and the membrane might be left less permeable to K+ as a result.noradrenaline ; D600; Ca release ; K inactivation ; guinea-pig vas deferensIn previous reports (Wakui and Inomata 1985; Wakui and Fukushi 1986), we suggested that through a-adrenergic receptor activation, noradrenaline (NA) reduced the K+ conductance and consequently induced the membrane depolarization in smooth muscle of the guinea-pig vas deferens. This hypothesis has been supported by the following evidence in the experiments using the double sucrosegap method : 1) The NA-induced depolarization is associated with a reduction in the membrane conductance. 2) The reversal potential of the NA-induced depolarization is negative to the resting membrane potential. 3) The reversal

Evidence for suppression of potassium conductance by noradrenaline in smooth muscle of guinea-pig vas deferens.

“…Though further investigations seem to be required to explain the above problem, one possible explanation is that by an employment of such a very large membrane depolarization preceding the NA application, some factor, which seems to be indispensable for the process of a reduction in the K conductance by NA, may be inactivated. This speculation is based on the findings that for the generation of the NA-induced depolarization, not only an existence of Ca ions in the external solution (Magaribuchi et al 1971;Wakui and Inomata 1984), but also a movement of the Ca ions into the cytoplasm (Wakui and Fukushi 1986) are essential. A large membrane depolarization may reduce the amount of the influx of Ca ions by diminishing the electrical gradient across the membrane.…”

Two α‐adrenergic contractions with different Ca2+ activation mechanisms in response to field nerve stimulation in the circular smooth muscle of guinea‐pig vas deferens

“…However, in our previous study (Fukushi & Wakui, 1986a) nicotinic receptor antagonists, such as d-tubocurarine, did not reduce the after-response. This suggests little involvement of a cholinergic-noradrenergic mechanism in this tissue, because the cholinergic-noradrenergic mechanism in other tissues (rabbit heart; Lindmar, Loffelholz & Muscholl, 1968;pulmonary artery;Su & Bevan, 1970;guinea-pig heart;Westfall & Brasted, 1972;rat brain slices;Westfall, 1974) including the longitudinal smooth muscle of the guinea-pig vas deferens (Wakui & Fukushi, 1986a;Fukushi & Wakui, 1986b, 1987 is known to work through nicotinic acetylcholine receptors at the noradrenergic nerve terminals.…”

“…On the other hand, less susceptibility of the second component to the drug indicates that the component is due to pharmacomechanical coupling (Somlyo & Somlyo, 1968), caused by Ca2+ entering through a voltageinsensitive pathway, i.e. receptor operated channels of the cell membrane (Bolton, 1975) and/or releasing from the intracellular stores via receptor activation (Swedin, 197 1;Wakui & Fukushi, 1986b). This is also similar to the event observed in the longitudinal smooth muscle of guinea-pig vas deferens (Blakeley et al, 1981).…”