The effect of noradrenaline on the permeability of depolarized intestinal smooth muscle to inorganic ions

Jenkinson, D. H.; Morton, Ian K. M.

doi:10.1113/jphysiol.1967.sp008144

Cited by 56 publications

(28 citation statements)

References 36 publications

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“…This implies that Ca maintaining the persistent responsiveness was not in the general extracellular space or in any structure accessible to this space by diffusion. Accordingly noradrenaline does not seem to have caused the contractions in EDTA by increasing the permeability of the cell membrane and allowing general extracellular Ca to enter in the way that acetylcholine appears to contact intestinal smooth muscle in Ca-containing K-rich solutions (Evans, Schild & Thesleff, 1958;Durbin & Jenkinson, 1961 a, b; Jenkinson & Morton, 1967). Noradrenaline is known to enter smooth muscle cells of cat arteries (Avakian & Gillespie, 1968) and so probably has an opportunity to act directly on any cell component.…”

Section: Discussionmentioning

confidence: 99%

Mechanical response with reversed electrical response to noradrenaline by Ca‐deprived arterial smooth muscle

Keatinge¹

1972

The Journal of Physiology

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SUMMARY1. When sheep carotid arteries had become electrically active after 30 min in Ca-free saline, noradrenaline 0 1 mm caused almost as much contraction as it did with Ca 1P25 mm present; it also caused slight electrical depolarization, usually with increased spike frequency, followed by electrical quiescence.2. In Ca-free saline with EDTA the arteries became profoundly depolarized, and their mechanical responses greatly reduced, within a few minutes. The mechanical responses to noradrenaline that remained were accompanied by electrical repolarization or, after longer periods in EDTA, by no electrical change.3. This residual mechanical responsiveness to noradrenaline, always tested at 360 C, declined on average 26 times as rapidly during exposure to EDTA at 360 C as at 5°C and was not reduced by increasing the concentration of EDTA from 1P25 to 12-5 mm. This temperature-sensitivity was significantly too high to be explained by a diffusion-limited process 4. The results suggest that most of the tissue Ca responsible for contractility in simple Ca-free saline was either free in the extracellular space or in cellular stores that were discharged within a few minutes when free extracellular Ca was removed. They also indicate a small resistant Ca store which did not communicate with the exterior by diffusion, and part of which noradrenaline could utilize for contraction by means not dependent on depolarization conducted from the cell membrane.

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Section: Discussionmentioning

confidence: 99%

Mechanical response with reversed electrical response to noradrenaline by Ca‐deprived arterial smooth muscle

Keatinge¹

1972

The Journal of Physiology

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“…The action of excitatory neurotransmitters on most smooth muscle tissues is accompanied by an increase of the K+ efflux (Durbin & Jenkinson, 1961;Briggs & Melvin, 1961;Jenkinson & Morton, 1967;Burgen & Spero, 1968;Droogmans, Raeymaekers & Casteels, 1977;Casteels, Kitamura, Kuriyama & Suzuki, 1977; Bolton & Clark, i981; Bolton & Clapp, 1984). For some tissues this effect has been partly explained by the concomitant change of resting potential (Bolton, Clark, Kitamura & Lang, 1981).…”

Section: Introductionmentioning

confidence: 99%

Dependence on calcium of potassium‐ and agonist‐induced changes in potassium permeability of rabbit ear artery.

Casteels¹,

Droogmans²

1985

The Journal of Physiology

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solutions, whereas the maintained component is largely independent of [Ca2+]0. 4. Stimulation with noradrenaline during depolarization of the tissues with K+ induces, after a transient increase of the efflux rate, an inhibition of the K+-induced increase of the efflux rate. Both phases of the noradrenaline action are due to activation of a-adrenoreceptors.5. Exposure to Ca2+-free medium induces a progressive increase of the 86Rb+ efflux rate, which reaches a new steady-state value after about 60 min. Stimulation with noradrenaline after this 60 min exposure to Ca2+-free solution no longer induces a significant effect. Stimulation with noradrenaline after shorter exposures to Ca2+-free solution immediately increases the 86Rb+ efflux to a value close to the steady-state value obtained after prolonged exposure to Ca2+-free medium. Washing out the agonist has no effect on the rate constant. It will only return to its control value after exposure to solutions containing Ca2+.6. This recovery of the rate constant by external Ca2+ also occurs in the presence of 1 mM-Mn2+ in the perfusion fluid. On re-exposure of the tissues in the presence of 1 mM-Mn2+ to Ca2+-free solution the rate constant of the 86 Rb+ efflux increases at once to the steady-state value observed in Ca2+-free solution. This increase proceeds gradually if the tissues have been re-exposed in the absence of Mn2+.7. It is concluded that K+ permeability might be regulated by [Ca2+]

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“…The consequent block of the spike generation then results in the relaxation of the muscle, in the manner proposed by JENKINSON and MORTON (1967a). On the other hand, acetylcholine might increase Na-, K-and Ca-permeabilities of the depolarized membrane (EVANS, SCHILD and THESLEFF, 1958;DURBIN and JENKINSON, 1961;SCHILD, 1964;JENKIN-SON and MORTON, 1967b).…”

Section: Resultsmentioning

confidence: 99%

Effects of Noradrenaline and Isoprenaline on the Electrical and Mechanical Activities of Guinea Pig Depolarized Taenia Coli

Magaribuchi

Kuriyama²

1972

Jpn.J.Physiol

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Summary The effects of noradrenaline and isoprenaline on the electrical and mechanical properties of depolarized smooth muscle of the guinea pig taenia coli were investigated by the double sucrose gap method. 1. Noradrenaline (10-7-10-5 g/ml) decreased the membrane resistance at any given concentration of excess K ion. When increased K ion concentration accelerated the spike discharges, noradrenaline blocked the spike generation as a result of the consequent reduction in membrane resistance, thus causing relaxation. When the excess K ion depolarized the muscle and no spike generation was observed due to depolarization block, noradrenaline no longer caused relaxation of the tissue. Phentolamine (10-5 g/ml) completely blocked the effect of noradrenaline. 2. Acetylcholine (10-5 g/ml) and noradrenaline (10-5 g/ml) reduced the membrane resistance and blocked the spike generation to the same extent in 59 mm K-Krebs solution. However, acetylcholine enhanced and noradrenaline reduced the contraction. 3. Isoprenaline (10-7-10-5 g/ml) reduced the tonic response of the contraction without any marked changes in the membrane resistance, membrane potential and membrane activity, at any given concentration of excess K ion. 4. Isoprenaline (10-7-10-5 g/ml) did not reduce the tonic response evoked by excess K ion in Na-free solution. It is suggested that external Na ion might be important for the reduction of the internal free Ca ion concentration. In the Cl-deficient (C6H5S0O3), excess K+ condition, isoprenaline again had no effect on the depolarized muscle. 5. When Ca ion in the excess K-Krebs solution was replaced by Sr and Ba ions, the effect of isoprenaline on the tonic response was markedly suppressed. 6. Ouabain (10-5-10-4 g/ml) reduced the membrane resistance and the tonic response evoked by excess K+ (below 59 mm) solution. In

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The effect of noradrenaline on the permeability of depolarized intestinal smooth muscle to inorganic ions

Cited by 56 publications

References 36 publications

Mechanical response with reversed electrical response to noradrenaline by Ca‐deprived arterial smooth muscle

Mechanical response with reversed electrical response to noradrenaline by Ca‐deprived arterial smooth muscle

Dependence on calcium of potassium‐ and agonist‐induced changes in potassium permeability of rabbit ear artery.

Effects of Noradrenaline and Isoprenaline on the Electrical and Mechanical Activities of Guinea Pig Depolarized Taenia Coli

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