scholarly journals The role of potassium channels and calcium in the relaxation mechanism of magnesium sulfate on the isolated rat uterus

2019 ◽  
Vol 71 (1) ◽  
pp. 5-11 ◽  
Author(s):  
Dragana Sokolovic ◽  
Dragana Drakul ◽  
Zorana Orescanin-Dusic ◽  
Nikola Tatalovic ◽  
Milica Pecelj ◽  
...  
Keyword(s):  
Potassium Channels ◽  
Potassium Channel ◽  
Contractile Activity ◽  
Specific Inhibitor ◽  
Relaxation Mechanism ◽  
Uterine Contractile ◽  
Dependent Inhibition ◽  
Calcium Activated Potassium Channels ◽  
Uterine Relaxation

MgSO4 is used as a tocolytic agent. It is considered to be a calcium channel antagonist, but a different mechanism of its action might be involved. The aim of this study was to examine the contribution of calcium concentrations and potassium channels in the mechanism of MgSO4-mediated uterine relaxation. Isolated uteri from female Wister rats were treated with increasing MgSO4 concentrations (0.1-30 mM). MgSO4 induced dose-dependent inhibition of spontaneous activity. Addition of Ca2+ (6 mM and 12 mM) stimulated uterine contractile activity and attenuated the inhibitory activity of MgSO4. In order to analyze the role of different subtypes of potassium channels, Ca2+-stimulated uteri were pretreated with glibenclamide (Glib), a selective ATP-sensitive potassium channel inhibitor (KATP), tetraethylammonium (TEA), a non-specific inhibitor of large conductance calcium-activated potassium channels (BKCa), and 4-aminopyridine (4-AP), a voltage-sensitive potassium channel inhibitor (Kv), at concentrations that had no effect per se. Pretreatment with 4-AP had no effect on MgSO4-mediated relaxation of Ca2+-stimulated uteri. The relaxing effect of MgSO4 was potentiated by pretreatment with glibenclamide. Pretreatment with TEA attenuated the MgSO4-mediated decrease in frequency. Our results suggest that MgSO4 acts as a general calcium antagonist that influences Ca2+-mediated potassium channels. Furthermore, it seems that MgSO4 uterine relaxation activity is partially mediated by selective ATP-sensitive potassium channels, suggesting an ATP-dependent role.

In vivo location and mechanism of EDHF-mediated vasodilation in canine coronary microcirculation

1999 ◽  
Vol 277 (3) ◽  
pp. H1252-H1259 ◽  
Author(s):  
Yasuhiro Nishikawa ◽  
David W. Stepp ◽  
William M. Chilian
Keyword(s):  
Nitric Oxide ◽  
Potassium Channels ◽  
Potassium Channel ◽  
Direct Evidence ◽  
Coronary Microcirculation ◽  
Combined Administration ◽  
Cytochrome P 450 ◽  
Coronary Arterioles

Responses of epicardial coronary arterioles to ACh were measured using stroboscopic fluorescence microangiography in dogs ( n = 38). ACh (0.1 and 0.5 μg ⋅ kg−1 ⋅ min−1ic) dilated small (<100 μm, 11 ± 2 and 19 ± 2%, respectively) and large (>100 μm, 6 ± 3 and 13 ± 3%, respectively) arterioles at baseline. Combined administration of N ω-monomethyl-l-arginine (l-NMMA; 1.0 μmol/min ic) and indomethacin (10 mg/kg iv) eliminated ACh-induced dilation in large coronary arterioles but only partially attenuated that in small arterioles. Suffusion of a buffer containing 60 mM KCl (high KCl) completely abolished cromakalim-induced dilation in arterioles and in combination with l-NMMA plus indomethacin completely blocked ACh-induced dilation in small arterioles. This indicated that the vasodilation to ACh that persists in small arterioles after administration of l-NMMA and indomethacin is mediated via a hyperpolarizing factor. The ACh-induced vasodilation remaining after l-NMMA and indomethacin was completely blocked by the large-conductance potassium-channel antagonist iberiotoxin or by epicardial suffusion of miconazole or metyrapone, inhibitors of cytochrome P-450 enzymes. These observations are consistent with the view that endothelium-derived hyperpolarizing factor (EDHF) is a product of cytochrome P-450 enzymes and produces vasodilation by the opening of large-conductance potassium channels. We conclude that ACh-induced dilation in large coronary arterioles is mediated mainly by nitric oxide (NO), whereas, in small arterioles both NO and EDHF mediate dilation to ACh. These data provide the first direct evidence for an in vivo role of EDHF in small coronary arterioles.

Role of ATP-sensitive potassium channels in the basilar artery

1993 ◽  
Vol 264 (1) ◽  
pp. H8-H13 ◽  
Author(s):  
F. M. Faraci ◽  
D. D. Heistad
Keyword(s):  
Potassium Channels ◽  
Basilar Artery ◽  
Cranial Window ◽  
Basal Tone ◽  
Dependent Inhibition ◽  
Baseline Diameter ◽  
Direct Activator ◽  
Sustained Increase

This study examined the hypothesis that activation of ATP-sensitive potassium channels produces vasodilation and contributes to dilator responses of the basilar artery to acetylcholine in vivo. Diameter of the basilar artery (baseline diam = 245 +/- 14 microns, means +/- SE) was measured through a cranial window in anesthetized rats. RP52891 (1 microM), a direct activator of ATP-sensitive potassium channels, increased the diameter of the basilar artery by 33 +/- 5%. Glibenclamide (1 microM), an inhibitor of ATP-sensitive potassium channels, did not alter baseline diameter but abolished responses of the basilar artery to RP52891. Topical application of acetylcholine (10 microM) for 3 min produced peak dilatation of 33 +/- 6% at 30 s and produced a sustained increase in diameter of 17 +/- 4%. Glibenclamide did not inhibit dilator responses of the basilar artery to acetylcholine. Nitro-L-arginine methyl ester (10 and 100 microM), which inhibits synthesis of endothelium-derived relaxing factor (EDRF), produced concentration-dependent inhibition of dilatation of the basilar artery in response to acetylcholine. Thus ATP-sensitive potassium channels are functional but do not appear to influence basal tone of the basilar artery. Dilator responses of the basilar artery to acetylcholine are dependent on formation of EDRF but not dependent on activity of glibenclamide-sensitive potassium channels.

126. Role of Calcium-Activated Potassium Channels in Myogenic Reactivity of Human Peripheral Microvasculature

2009 ◽  
Vol 151 (2) ◽  
pp. 232
Author(s):  
J. Feng ◽  
Y. Liu ◽  
K.R. Khabbaz ◽  
S.L. Alper ◽  
F.W. Sellke
Keyword(s):  
Potassium Channels ◽  
Calcium Activated Potassium Channels

scholarly journals The Unexpected Role of Calcium‐Activated Potassium Channels: Limitation of NO‐Induced Arterial Relaxation

2018 ◽  
Vol 7 (7) ◽  
Author(s):  
Johannes Schmid ◽  
Bettina Müller ◽  
David Heppeler ◽  
Dina Gaynullina ◽  
Mario Kassmann ◽  
...  
Keyword(s):  
Potassium Channels ◽  
Arterial Relaxation ◽  
Calcium Activated Potassium Channels

Exploring the Role of Calcium-Activated Potassium Channels in Alpha-Cell Function

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2172-P
Author(s):  
MATTHEW DICKERSON ◽  
MOLLY K. ALTMAN ◽  
PRASANNA DADI ◽  
NICHOLAS C. VIERRA ◽  
DAVID JACOBSON
Keyword(s):  
Potassium Channels ◽  
Cell Function ◽  
Alpha Cell ◽  
Calcium Activated Potassium Channels ◽  
Alpha Cell Function
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