Species Differences in Inhibitory Effect of Li+ on High K+-lnduced Contraction in the Ileal Longitudinal Smooth Muscle

Hori, Masaru; Nakaya, Michiaki; Noda, Kazue; Shimizu, Kazumasa; Nakajyo, Shinjiro; Urakawa, Norimoto

doi:10.1254/jjp.48.113

Cited by 3 publications

(2 citation statements)

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“…Fifthly, in guinea pig taenia coli, Li substitution for external Na inhibited the contraction induced by 60 mM KC1 without change of the trans membrane potential [25]. Furthermore, 45Ca uptake [26] was also inhibited without effect on K-induced elevation of [Ca]i [27], These authors suggested that a change of cytosolic electrolytes (e.g., Li) plays a more dominant role than the entry of Ca in the development of K-induced contraction [28]. Finally, a small K-induced contraction in some muscles in Ca-free, Mg-free solutions has also been observed [29,30].…”

Section: Introductionmentioning

confidence: 99%

A Revisitation on the Mechanism of Action of KCI-lnduced Vascular Smooth Muscle Contraction: A Key Role of Cation Binding to the Plasma Membrane

Kravtsov¹,

Kwan²

1995

Neurosignals

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Aortic rings of Sprague-Dawley rats developed reproducible contractions in Ca-free, nominally Mg-free (2 µM), Na-free, K solution, but not in Ca-free, nominally Mg-free, K-free, Na solution. Further reduction of the residual Mg by 0.5 µM EDTA in the above solutions potentiated this K-induced contraction and allowed the development of a relatively small contraction in Na-rich medium, respectively. The amplitude of EDTA-enhanced, K-induced contraction was almost the same as the amplitude of contraction induced in K-rich ([K] = 142 mM), Ca-containing (2.5 mM) solution. Such K-induced contraction was completely inhibited by 38 mM Na and by 3 mM of Mg (and Ni or Cd). Nifedipine (1 µM) also inhibited aortic smooth muscle contraction produced in K-EDTA, Ca-free solution. Modulators of Ca in sarcoplasmic reticulum (ryanodine, caffeine and norephinephrine), Ca-ionophore (A-23187) and protein kinase C inhibitor (Calphostin C) had no effect on EDTA-enhanced, K-induced contraction. It was suggested that K-induced contraction in rat aorta is not dependent on the increase in cytosolic Ca following membrane depolarization, is not a result of the release of Ca from intracellular stores, and is not due to change of Ca sensitivity upon the activation of protein kinase C. We propose that the competition of K for Mg and Na at external binding sites on the plasma membranes of the smooth muscle cells is primarily responsible for the development of vascular contraction.

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Section: Introductionmentioning

confidence: 99%

A Revisitation on the Mechanism of Action of KCI-lnduced Vascular Smooth Muscle Contraction: A Key Role of Cation Binding to the Plasma Membrane

Kravtsov¹,

Kwan²

1995

Neurosignals

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“…Treatment of guinea pig ileal muscle with 68.4 mM Li+ solution increased the cellular Li+ content to 10-20 mmol/kg wet wt. in 30-60 min (8) and the inhibitory effect increased with the accumulation of Li+ in the cell (9)(10)(11). Recently, we have reported that Li+-induced relaxation is not due to a decrease in cytosolic Ca 2+ level ([Ca2+];) and that Li+ relaxes Ca 2+-induced contraction in permeabilized tissue (11).…”

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confidence: 98%

The Inhibitory Effect of Li+ on Contractile Elements of Intestinal Smooth Muscle

Hori

Shimizu

Nakajyo

et al. 1995

Japanese Journal of Pharmacology

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ABSTRACT-The mechanism of the inhibitory effect of Li+ on contraction was examined in guinea pig ileal longitudinal smooth muscle. Li+-substitution (68.4 mM) reversed contractions induced by high K+ (45.4 mM), carbachol (1 teM) and histamine (1 tM) without changing the cytosolic Ca" level. Li+ also had no effect on the increase in 45Ca2+ uptake stimulated by high K+. High K+ transiently increased myosin light chain (MLC) phosphorylation, reaching a peak at 6-9 sec. Li+-substitution inhibited the high K+-induced MLC phosphorylation. In permeabilized ileal strips, contraction induced by 1 1iM Ca 2+ was inhibited by 10 mM Lit The inhibitory effect was antagonized by increasing the concentration of Ca 2+ or calmodulin. In the permeabilized muscle in which MLC was previously thiophosphorylated with 1 mM ATPIS and 3 PM Ca2+, ATP induced contraction in Ca 21 free buffer. Li+ added during this contraction did not show an inhibitory effect. In contrast, when 30 mM Li+ was added during the thiophosphorylation, the contraction induced by the subsequent addition of ATP was inhibited. Li+ (30 mM) changed neither the rate of relaxation induced by removing external Ca 21 in permeabilized muscle nor the rate of dephosphorylation of MLC induced by crude phosphatase extracted from the ileum. Li+ (15 mM), on the other hand, inhibited the rate of phosphorylation of MLC caused by crude MLC kinase extracted from the ileum. Li+ did not inhibit the calmodulin activity as measured with the (Ca 2+ + Mg2+)-ATPase activity of the erythrocyte membrane. These results suggest that the inhibitory effect of Li+ on contractions is attributable to the inhibition of MLC kinase in guinea pig ileum. Keywords: Li+ (lithium ion), Smooth muscle (intestine), Contractile element, Myosin light chain kinase, Cytosolic Ca 2+ levelLi+ has been shown to have various biological actions such as inhibition of phosphatidylinositol turnover (1, 2) and adenylate cyclase (3, 4). In intestinal smooth muscle, Li+ relaxes contractions induced by high concentrations of KCl and receptor agonists (5 -7). Treatment of guinea pig ileal muscle with 68.4 mM Li+ solution increased the cellular Li+ content to 10-20 mmol/kg wet wt. in 30-60 min (8) and the inhibitory effect increased with the accumulation of Li+ in the cell (9-11). Recently, we have reported that Li+-induced relaxation is not due to a decrease in cytosolic Ca 2+ level ([Ca2+];) and that Li+ relaxes Ca 2+-induced contraction in permeabilized tissue (11). The purpose of the present experiments is to further clarify the mechanism for the inhibitory effect of Li+ in guinea pig ileal smooth muscle. Preparations and solutionsIleum was isolated from male guinea pigs (300 -400 g) after stunning by a sharp blow on the neck and exsanguination. Longitudinal smooth muscle strips, approximately 5-mm-wide and 10-mm-long, were prepared. Normal physiological salt solution (PSS) contained: 136.9 mM NaCl, 5.4 mM KCI, 1.5 mM CaC12, 1.0 MM MgC12, 23.8 mM NaHCO3 and 5.5 mM glucose. High K+ solutions were made by hyperosmotically add...

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Inhibitory effect of lithium on muscle contractions caused by various stimulants in guinea-pig ileum

Hori

Shimizu

Nakajyo

et al. 1989

European Journal of Pharmacology

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Species Differences in Inhibitory Effect of Li+ on High K+-lnduced Contraction in the Ileal Longitudinal Smooth Muscle

Cited by 3 publications

References 17 publications

A Revisitation on the Mechanism of Action of KCI-lnduced Vascular Smooth Muscle Contraction: A Key Role of Cation Binding to the Plasma Membrane

A Revisitation on the Mechanism of Action of KCI-lnduced Vascular Smooth Muscle Contraction: A Key Role of Cation Binding to the Plasma Membrane

The Inhibitory Effect of Li+ on Contractile Elements of Intestinal Smooth Muscle

Inhibitory effect of lithium on muscle contractions caused by various stimulants in guinea-pig ileum

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