Inhibitory effects of large Ca2+-activated K+-channel blockers on β-adrenergic- and NO-donor-mediated relaxations of human and guinea-pig airway smooth muscles

1997 ◽  
Vol 357 (1) ◽  
pp. 77-86 ◽  
Author(s):  
E. Corompt ◽  
G. Bessard ◽  
S. Lantuejoul ◽  
E. Naline ◽  
C. Advenier ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Smooth Muscles ◽  
K Channel ◽  
Channel Blockers ◽  
Inhibitory Effects ◽  
No Donor

Effects of K+-channel blockers on cochlear potentials in the guinea pig

1993 ◽  
Vol 68 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Wang Jian ◽  
Li Qian-hong ◽  
Dong Wei-jia ◽  
Chen Ji-sheng
Keyword(s):  
Guinea Pig ◽  
K Channel ◽  
Channel Blockers ◽  
Cochlear Potentials

Inhibitory effects of class I and IV antiarrhythmic drugs on the Na+-activated K+ channel current in guinea pig ventricular cells

1998 ◽  
Vol 358 (6) ◽  
pp. 641-648 ◽  
Author(s):  
Katsumi Mori ◽  
Satoru Kobayashi ◽  
Toshihiro Saito ◽  
Yoshiaki Masuda ◽  
H. Nakaya
Keyword(s):  
Guinea Pig ◽  
Antiarrhythmic Drugs ◽  
Class I ◽  
K Channel ◽  
Inhibitory Effects ◽  
Channel Current ◽  
Ventricular Cells

Effects of Y-26763, A Novel K-Channel Opener, on Electrical Responses of Smooth Muscles in the Guinea Pig Bladder

1996 ◽  
Vol 155 (4) ◽  
pp. 1454-1458 ◽  
Author(s):  
Hikaru Hashitani ◽  
Hikaru Suzuki ◽  
Joichi Kumazawa
Keyword(s):  
Guinea Pig ◽  
Smooth Muscles ◽  
K Channel ◽  
Channel Opener ◽  
K Channel Opener ◽  
Electrical Responses

Effect of K(+)-channel blockers on ACh-induced hyperpolarization and relaxation in mesenteric arteries

1997 ◽  
Vol 272 (5) ◽  
pp. H2306-H2312 ◽  
Author(s):  
G. Chen ◽  
D. W. Cheung
Keyword(s):  
Significant Inhibition ◽  
Mesenteric Arteries ◽  
K Channel ◽  
Channel Blockers ◽  
Inhibitory Effects ◽  
Similar Extent ◽  
Nitric Oxide Synthase Inhibitor ◽  
Rat Mesenteric Artery ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Acetylcholine (ACh) induces endothelium-dependent hyperpolarization in the rat mesenteric artery in the presence of the nitric oxide synthase inhibitor N omega-nitro-L-arginine. We have now studied the effects of K(+)-channel blockers on the hyperpolarization responses to ACh in resting and norepinephrine-contracted rat mesenteric arteries. We also measured tension simultaneously to determine whether the inhibitory effects of these agents on relaxation could be correlated to their effects on hyperpolarization. Glibenclamide had no significant effect on the hyperpolarization or relaxation. Tetraethylammonium (TEA, 5 mM) inhibited the hyperpolarization to ACh significantly to a similar extent in both the resting and norepinephrine-stimulated arteries. Charybdotoxin (100–150 nM) caused only a small but significant inhibition. Apamin (0.3 microM) was the most effective in inhibiting the hyperpolarization in resting arteries. It was less effective in the norepinephrine-contracted arteries. A combination of apamin and charybdotoxin completely abolished the hyperpolarization responses in both conditions. The relaxation to ACh was correlated to hyperpolarization. In all cases, the inhibition of the relaxation by the K(+)-channel blockers could be accounted for by their effects on the hyperpolarization. These results indicate that Ca(2+)-activated K(+)-channels, especially those sensitive to apamin, may be the major ion channels mediating endothelium-dependent hyperpolarization to ACh.

K+ channel opening mediates hyperpolarizations by nitric oxide donors and IJPs in opossum esophagus

1995 ◽  
Vol 268 (5) ◽  
pp. G831-G842 ◽  
Author(s):  
F. S. Cayabyab ◽  
E. E. Daniel
Keyword(s):  
Nitric Oxide ◽  
Soluble Guanylate Cyclase ◽  
Equilibrium Potential ◽  
K Channel ◽  
Resting Membrane Potential ◽  
Channel Blockers ◽  
No Donor ◽  
No Donors ◽  
Circular Smooth Muscle ◽  
Ionic Mechanisms

The ionic mechanisms by which nitric oxide (NO) or a related compound mediates the inhibitory junction potentials (IJPs) of the opossum esophageal circular smooth muscle were studied using microelectrodes and double sucrose gap. The NO donors, 3-morpholino-sydnonimine hydrochloride and sodium nitroprusside, induced 15- to 20-mV hyperpolarizations that reversed near the potassium equilibrium potential as did the IJPs. They inhibited the IJPs and decreased electrotonic potentials (increased conductance) even during restoration of the resting membrane potential by application of depolarizing current. Quinine was more efficacious than apamin in inhibiting the IJPs or NO donor hyperpolarizations, whereas the other K+ channel blockers tested (tetraethylammonium, charybdotoxin, 4-aminopyridine, Cs+, and glibenclamide) were without effect. Glibenclamide abolished the hyperpolarizing effects of the K+ channel opener BRL-34915. Low Cl- Krebs (isethionate substitutions) caused hyperpolarizations, increased electrotonic potentials, and reduced IJPs. The neural blockers, tetrodotoxin, omega-conotoxin GVIA, and N omega-nitro-L-arginine methyl ester, inhibited IJPs but not the responses to NO donors, indicating a postjunctional effect. Methylene blue and cystamine, soluble guanylate cyclase inhibitors, suppressed IJPs and responses to NO donors. We conclude that NO mediates esophageal IJPs, which depend on guanosine 3',5'-cyclic monophosphate elevation and activation of quinine- and apamin-sensitive K+ channels.

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