Potassium-induced contraction in smooth muscle.

Karaki, Hideaki; Urakawa, Norimoto; P, Kutsky

doi:10.1540/jsmr1965.20.427

Cited by 47 publications

(30 citation statements)

References 103 publications

(114 reference statements)

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“…To test the ability of (-)-epicatechin to inhibit the influx of extracellular Ca 2 þ , we used high K þ solution to induce contraction of HIMA. High K þ depolarizes the smooth muscle cell membrane and opens voltage-gated Ca 2 þ channels, resulting in an influx of extracellular Ca 2 þ and an activation of contractile machinery (Karaki et al, 1984). We found that, under these conditions, (-)-epicatechin was able to relax HIMA rings significantly.…”

Section: Discussionmentioning

confidence: 72%

Mechanisms underlying the vasorelaxation of human internal mammary artery induced by (-)-epicatechin

Novakovic

Marinko

Vranic

et al. 2015

European Journal of Pharmacology

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Section: Discussionmentioning

confidence: 72%

Mechanisms underlying the vasorelaxation of human internal mammary artery induced by (-)-epicatechin

Novakovic

Marinko

Vranic

et al. 2015

European Journal of Pharmacology

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“…A high K + concentration induces smooth muscle contraction through the membrane depolarization-VDCC opening-calcium influx pathway [42, 43]. For this reason, the relaxant characteristic of TSU-68 was tested under conditions of high K + .…”

Section: Resultsmentioning

confidence: 99%

Relaxing Effect of TSU-68, an Antiangiogenic Agent, on Mouse Airway Smooth Muscle

Tan

Lei

Lü

et al. 2017

Cell Physiol Biochem

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Background/Aims: Recently, some small-molecule compounds that were designed for cancer therapy have acquired new roles in the treatment of pulmonary diseases. However, drug screening aimed at abnormal muscle contraction is still limited. TSU-68 is a potent, orally administered, small-molecule agent that can reduce the vascular endothelial growth factor (VEGF)-induced Ca²⁺ increase in endothelial cells. We questioned whether TSU-68 could also affect calcium influx and relax airway smooth muscle (ASM) cells. The current study aimed to investigate these effects and to explore the underlying mechanisms. Methods: The effects of TSU-68 on ASM cells were studied in mice using a series of biophysiological techniques, including force measurement and patch-clamp experiments. Results: TSU-68 inhibited high K⁺ or acetylcholine chloride (ACh)-induced pre-contracted mouse tracheal rings in a concentration-dependent manner. Further research demonstrated that the TSU-68-induced ASM relaxation was mediated by calcium, which was decreased by blocking voltage-dependent Ca²⁺ channels (VDCCs) and non-selective cation channels (NSCCs). Conclusion: Our data indicated that TSU-68 relaxes tense ASM by reducing the intracellular Ca²⁺ concentration through blocking VDCCs and NSCCs, which suggested that this small molecule might be useful in the treatment of abnormal smooth muscle.

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“…A high K + concentration causes the contraction of smooth muscle through the membrane depolarization-VDCC open-calcium influx pathway [35, 36]. The high K + (80 mM)-induced contraction was blocked by AELL in a dose-dependent manner (Fig.…”

Section: Resultsmentioning

confidence: 99%

Nelumbo nucifera leaves extracts inhibit mouse airway smooth muscle contraction

Yang¹,

Lü²,

Zhao

et al. 2017

BMC Complement Altern Med

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BackgroundAlkaloids extracted from lotus leaves (AELL) can relax vascular smooth muscle. However, whether AELL has a similar relaxant role on airway smooth muscle (ASM) remains unknown. This study aimed to explore the relaxant property of AELL on ASM and the underlying mechanism.MethodsAlkaloids were extracted from dried lotus leaves using the high temperature rotary evaporation extraction method. The effects of AELL on mouse ASM tension were studied using force measuring and patch-clamp techniques.ResultsIt was found that AELL inhibited the high K+ or acetylcholine chloride (ACh)-induced precontraction of mouse tracheal rings by 64.8 ± 2.9%, or 48.8 ± 4.7%, respectively. The inhibition was statistically significant and performed in a dose-dependent manner. Furthermore, AELL-induced smooth muscle relaxation was partially mediated by blocking voltage-dependent Ca2+ channels (VDCC) and non-selective cation channels (NSCC).ConclusionAELL, which plays a relaxant role in ASM, might be a new complementary treatment to treat abnormal contractions of the trachea and asthma.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-017-1674-7) contains supplementary material, which is available to authorized users.

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Potassium-induced contraction in smooth muscle.

Cited by 47 publications

References 103 publications

Mechanisms underlying the vasorelaxation of human internal mammary artery induced by (-)-epicatechin

Mechanisms underlying the vasorelaxation of human internal mammary artery induced by (-)-epicatechin

Relaxing Effect of TSU-68, an Antiangiogenic Agent, on Mouse Airway Smooth Muscle

Nelumbo nucifera leaves extracts inhibit mouse airway smooth muscle contraction

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