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Melatonin stimulates outward currents. (A) time course of the outward current at a test potential of +70 mV during the addition of 10 −5 mol l −1 melatonin (Mel), of bath solution (time control) and of 10 −5 mol l −1 melatonin in the presence of 3*10 −7 mol l −1 <t>iberiotoxin,</t> a specific BK channel inhibitor (Mel + IBTX). The application period of melatonin and of the bath solution, respectively, is indicated by the gray area; s—start of application, e—end of application; data points are the mean current during the last 200 ms of the voltage step. (B) Example traces of the outward current at the start (s) and the end (e) of melatonin application evoked by a voltage step from a holding potential of −40 mV to a test potential of +70 mV with duration 500 ms (left panel) and a voltage ramp from −70 mV to +100 mV providing the I‐V relationship (right panel), respectively. (C) Summarized data of the effect of melatonin (Mel) on the outward current, data are expressed as the ratio of the current at the end of the application period (I K (e)) to the initial current immediately at the start of the application period (I K (s)); test potential +70 mV; number of cells investigated appears on bar; * ‐ p < 0.05.
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Alomone Labs ibtx
Involvement of potassium channels in tectorigenin-induced vasorelaxation in porcine coronary arteries. ( A ) Effects of various potassium channel blockers on vasorelaxation induced by 30 µM tectorigenin. Pretreatment with glibenclamide (10 µM), iberiotoxin <t>(IbTX,</t> 200 nM), <t>tetraethylammonium</t> <t>(TEA,</t> 1 mM), apamin (100 nM), or charybdotoxin (1 µM) did not significantly affect the relaxant response ( p > 0.05), whereas 4-aminopyridine (4-AP, 1 mM) significantly attenuated tectorigenin-induced relaxation ( p < 0.05). ( B ) Concentration-dependent inhibitory effect of 4-AP (1 mM) on tectorigenin-induced relaxation. Significant inhibition was observed at 10 and 30 µM († p < 0.05 vs. corresponding tectorigenin alone), but not at 100 µM. ( C ) Comparison of the relaxant effects of 30 µM tectorigenin in porcine coronary arteries pre-contracted with either 100 nM U46619 or 80 mM KCl. Tectorigenin elicited significant vasorelaxation in U46619-pre-contracted rings but had negligible effect in KCl-contracted rings. Data are expressed as mean ± standard error of the mean (SEM) from four independent hearts. U46619 plateau (normalised to 60 mM KCl) was similar across groups ( p > 0.05; Supplementary Table 2).
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Alomone Labs bk channel currents
Involvement of potassium channels in tectorigenin-induced vasorelaxation in porcine coronary arteries. ( A ) Effects of various potassium channel blockers on vasorelaxation induced by 30 µM tectorigenin. Pretreatment with glibenclamide (10 µM), iberiotoxin <t>(IbTX,</t> 200 nM), <t>tetraethylammonium</t> <t>(TEA,</t> 1 mM), apamin (100 nM), or charybdotoxin (1 µM) did not significantly affect the relaxant response ( p > 0.05), whereas 4-aminopyridine (4-AP, 1 mM) significantly attenuated tectorigenin-induced relaxation ( p < 0.05). ( B ) Concentration-dependent inhibitory effect of 4-AP (1 mM) on tectorigenin-induced relaxation. Significant inhibition was observed at 10 and 30 µM († p < 0.05 vs. corresponding tectorigenin alone), but not at 100 µM. ( C ) Comparison of the relaxant effects of 30 µM tectorigenin in porcine coronary arteries pre-contracted with either 100 nM U46619 or 80 mM KCl. Tectorigenin elicited significant vasorelaxation in U46619-pre-contracted rings but had negligible effect in KCl-contracted rings. Data are expressed as mean ± standard error of the mean (SEM) from four independent hearts. U46619 plateau (normalised to 60 mM KCl) was similar across groups ( p > 0.05; Supplementary Table 2).
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Melatonin stimulates outward currents. (A) time course of the outward current at a test potential of +70 mV during the addition of 10 −5 mol l −1 melatonin (Mel), of bath solution (time control) and of 10 −5 mol l −1 melatonin in the presence of 3*10 −7 mol l −1 iberiotoxin, a specific BK channel inhibitor (Mel + IBTX). The application period of melatonin and of the bath solution, respectively, is indicated by the gray area; s—start of application, e—end of application; data points are the mean current during the last 200 ms of the voltage step. (B) Example traces of the outward current at the start (s) and the end (e) of melatonin application evoked by a voltage step from a holding potential of −40 mV to a test potential of +70 mV with duration 500 ms (left panel) and a voltage ramp from −70 mV to +100 mV providing the I‐V relationship (right panel), respectively. (C) Summarized data of the effect of melatonin (Mel) on the outward current, data are expressed as the ratio of the current at the end of the application period (I K (e)) to the initial current immediately at the start of the application period (I K (s)); test potential +70 mV; number of cells investigated appears on bar; * ‐ p < 0.05.

Journal: The FASEB Journal

Article Title: Orchestration of PKC ‐Mediated Inhibition and Calcium Release‐Mediated Activation of BK Currents in Rat Vascular Smooth Muscle Cells by Melatonin Confers a BK ‐Channel‐Dependent Restraint on Melatonin‐Induced Vasocontraction

doi: 10.1096/fj.202601214R

Figure Lengend Snippet: Melatonin stimulates outward currents. (A) time course of the outward current at a test potential of +70 mV during the addition of 10 −5 mol l −1 melatonin (Mel), of bath solution (time control) and of 10 −5 mol l −1 melatonin in the presence of 3*10 −7 mol l −1 iberiotoxin, a specific BK channel inhibitor (Mel + IBTX). The application period of melatonin and of the bath solution, respectively, is indicated by the gray area; s—start of application, e—end of application; data points are the mean current during the last 200 ms of the voltage step. (B) Example traces of the outward current at the start (s) and the end (e) of melatonin application evoked by a voltage step from a holding potential of −40 mV to a test potential of +70 mV with duration 500 ms (left panel) and a voltage ramp from −70 mV to +100 mV providing the I‐V relationship (right panel), respectively. (C) Summarized data of the effect of melatonin (Mel) on the outward current, data are expressed as the ratio of the current at the end of the application period (I K (e)) to the initial current immediately at the start of the application period (I K (s)); test potential +70 mV; number of cells investigated appears on bar; * ‐ p < 0.05.

Article Snippet: Iberiotoxin was obtained from Alomone.

Techniques: Control

Involvement of potassium channels in tectorigenin-induced vasorelaxation in porcine coronary arteries. ( A ) Effects of various potassium channel blockers on vasorelaxation induced by 30 µM tectorigenin. Pretreatment with glibenclamide (10 µM), iberiotoxin (IbTX, 200 nM), tetraethylammonium (TEA, 1 mM), apamin (100 nM), or charybdotoxin (1 µM) did not significantly affect the relaxant response ( p > 0.05), whereas 4-aminopyridine (4-AP, 1 mM) significantly attenuated tectorigenin-induced relaxation ( p < 0.05). ( B ) Concentration-dependent inhibitory effect of 4-AP (1 mM) on tectorigenin-induced relaxation. Significant inhibition was observed at 10 and 30 µM († p < 0.05 vs. corresponding tectorigenin alone), but not at 100 µM. ( C ) Comparison of the relaxant effects of 30 µM tectorigenin in porcine coronary arteries pre-contracted with either 100 nM U46619 or 80 mM KCl. Tectorigenin elicited significant vasorelaxation in U46619-pre-contracted rings but had negligible effect in KCl-contracted rings. Data are expressed as mean ± standard error of the mean (SEM) from four independent hearts. U46619 plateau (normalised to 60 mM KCl) was similar across groups ( p > 0.05; Supplementary Table 2).

Journal: Scientific Reports

Article Title: Tectorigenin induces vasorelaxation in porcine coronary arteries through activation of Kv channels and oestrogen receptor modulation

doi: 10.1038/s41598-025-20988-6

Figure Lengend Snippet: Involvement of potassium channels in tectorigenin-induced vasorelaxation in porcine coronary arteries. ( A ) Effects of various potassium channel blockers on vasorelaxation induced by 30 µM tectorigenin. Pretreatment with glibenclamide (10 µM), iberiotoxin (IbTX, 200 nM), tetraethylammonium (TEA, 1 mM), apamin (100 nM), or charybdotoxin (1 µM) did not significantly affect the relaxant response ( p > 0.05), whereas 4-aminopyridine (4-AP, 1 mM) significantly attenuated tectorigenin-induced relaxation ( p < 0.05). ( B ) Concentration-dependent inhibitory effect of 4-AP (1 mM) on tectorigenin-induced relaxation. Significant inhibition was observed at 10 and 30 µM († p < 0.05 vs. corresponding tectorigenin alone), but not at 100 µM. ( C ) Comparison of the relaxant effects of 30 µM tectorigenin in porcine coronary arteries pre-contracted with either 100 nM U46619 or 80 mM KCl. Tectorigenin elicited significant vasorelaxation in U46619-pre-contracted rings but had negligible effect in KCl-contracted rings. Data are expressed as mean ± standard error of the mean (SEM) from four independent hearts. U46619 plateau (normalised to 60 mM KCl) was similar across groups ( p > 0.05; Supplementary Table 2).

Article Snippet: For experimental assays, a range of pharmacological agents was utilised, including U46619, apamin, KT5720, KT5823, and L-NNA (Sigma-Aldrich, MO, USA); rolipram, vardenafil, and TEA (Santa Cruz Biotechnology, CA, USA); IbTX (Alomone Labs, Jerusalem, Israel); glibenclamide (Research Biochemicals International, MA, USA); TTX and 4-AP (Tocris Bioscience, Bristol, UK); CTX (Bachem, Bubendorf, Switzerland); and charybdotoxin, methyl-piperidino-pyrazole (MPP), and PHTPP (Cayman Chemical, MI, USA).

Techniques: Concentration Assay, Inhibition, Comparison