Studies on Bronchodilator Activity of Salvia officinalis (Sage): Possible Involvement of K+ Channel Activation and Phosphodiesterase Inhibition

2015 ◽  
Vol 29 (9) ◽  
pp. 1323-1329 ◽  
Author(s):  
Anwarul-Hassan Gilani ◽  
Najeeb-ur Rehman ◽  
Aslam Khan ◽  
Khalid M. Alkharfy
Keyword(s):  
Salvia Officinalis ◽  
K Channel ◽  
Phosphodiesterase Inhibition ◽  
Channel Activation ◽  
Bronchodilator Activity

scholarly journals ATP-Dependent K+ Channel Activation in Isolated Normal and Hypertensive Newborn and Adult Porcine Pulmonary Vessels

1997 ◽  
Vol 42 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Piet J Boels ◽  
Beirong Gao ◽  
Joan Deutsch ◽  
Sheila G Haworth
Keyword(s):  
K Channel ◽  
Channel Activation ◽  
Pulmonary Vessels

scholarly journals Molecular Determinants of Humanether-à-go-go-Related Gene 1 (hERG1) K+Channel Activation by NS1643

2010 ◽  
Vol 79 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Morten Grunnet ◽  
Jennifer Abbruzzese ◽  
Frank B. Sachse ◽  
Michael C. Sanguinetti
Keyword(s):  
K Channel ◽  
Related Gene ◽  
Channel Activation ◽  
Molecular Determinants

K+ channel activation and low-threshold Ca2+ spike of rat cerebellar Purkinje cells in vitro

Neuroreport ◽  
2003 ◽  
Vol 14 (2) ◽  
pp. 167-171 ◽  
Author(s):  
Pauline Cavelier ◽  
Thomas Desplantez ◽  
Huguette Beekenkamp ◽  
Jean-Louis Bossu
Keyword(s):  
Purkinje Cells ◽  
K Channel ◽  
Channel Activation ◽  
Low Threshold ◽  
Cerebellar Purkinje Cells

scholarly journals Blockage of the HERG human cardiac K+ channel by the gastrointestinal prokinetic agent cisapride

1997 ◽  
Vol 273 (5) ◽  
pp. H2534-H2538 ◽  
Author(s):  
Saeed Mohammad ◽  
Zhengfeng Zhou ◽  
Qiuming Gong ◽  
Craig T. January
Keyword(s):  
Ventricular Arrhythmias ◽  
Current Amplitude ◽  
Hek293 Cells ◽  
K Channel ◽  
Delayed Rectifier ◽  
Patch Clamp Recording ◽  
Channel Activation ◽  
Prokinetic Agent ◽  
Tail Current ◽  
Herg Channels

Cisapride, a gastrointestinal prokinetic agent, is known to cause long Q-T syndrome and ventricular arrhythmias. The cellular mechanism is not known. The human ether-á-go-go-related gene ( HERG), which encodes the rapidly activating delayed rectifier K+current and is important in cardiac repolarization, may serve as a target for the action of cisapride. We tested the hypothesis that cisapride blocks HERG. The whole cell patch-clamp recording technique was used to study HERG channels stably expressed heterologously in HEK293 cells. Under voltage-clamp conditions, cisapride block of HERG is dose dependent with a half-maximal inhibitory concentration of 6.5 nM at 22°C ( n = 25 cells). Currents rapidly recovered with drug washout. The onset of block by cisapride required channel activation indicative of open or inactivated state blockage. Block of HERG with cisapride after channel activation was voltage dependent. At −20 mV, 10 nM cisapride reduced HERG tail-current amplitude by 5%, whereas, at +20 mV, the tail-current amplitude was reduced by 45% ( n = 4 cells). At −20 and +20 mV, 100 nM cisapride reduced tail-current amplitude by 66 and 90%, respectively. We conclude that cisapride is a potent blocker of HERG channels expressed in HEK293 cells. This effect may account for the clinical occurrence of Q-T prolongation and ventricular arrhythmias observed with cisapride.

NO causes perinatal pulmonary vasodilation through K+-channel activation and intracellular Ca2+release

1999 ◽  
Vol 276 (6) ◽  
pp. L925-L932 ◽  
Author(s):  
Connie B. Saqueton ◽  
Robert B. Miller ◽  
Valerie A. Porter ◽  
Carlos E. Milla ◽  
David N. Cornfield
Keyword(s):  
Channel Blocker ◽  
Control Period ◽  
Left Pulmonary Artery ◽  
Competitive Inhibitor ◽  
Late Gestation ◽  
K Channel ◽  
Channel Activation ◽  
Pulmonary Vasodilation ◽  
Voltage Dependent ◽  
Intracellular Ca

Evidence suggests that nitric oxide (NO) causes perinatal pulmonary vasodilation through K+-channel activation. We hypothesized that this effect worked through cGMP-dependent kinase-mediated activation of Ca2+-activated K+ channel that requires release of intracellular Ca2+ from a ryanodine-sensitive store. We studied the effects of 1) K+-channel blockade with tetraethylammonium, 4-aminopyridine, a voltage-dependent K+-channel blocker, or glibenclamide, an ATP-sensitive K+-channel blocker; 2) cyclic nucleotide-sensitive kinase blockade with either KT-5823, a guanylate-sensitive kinase blocker, or H-89, an adenylate-sensitive kinase blocker; and 3) blockade of intracellular Ca2+ release with ryanodine on NO-induced pulmonary vasodilation in acutely prepared late-gestation fetal lambs. N-nitro-l-arginine, a competitive inhibitor of endothelium-derived NO synthase, was infused into the left pulmonary artery, and tracheotomy was placed. The animals were ventilated with 100% oxygen for 20 min, followed by ventilation with 100% oxygen and inhaled NO at 20 parts/million (ppm) for 20 min. This represents the control period. In separate protocols, the animals received an intrapulmonary infusion of the different blockers and were ventilated as above. Tetraethylammonium ( n = 6 animals) and KT-5823 ( n = 4 animals) attenuated the response, whereas ryanodine ( n = 5 animals) blocked NO-induced perinatal pulmonary vasodilation. 4-Aminopyridine ( n = 5 animals), glibenclamide ( n = 5 animals), and H-89 ( n = 4 animals) did not affect NO-induced pulmonary vasodilation. We conclude that NO causes perinatal pulmonary vasodilation through cGMP-dependent kinase-mediated activation of Ca2+-activated K+ channels and release of Ca2+ from ryanodine-sensitive stores.

Levcromakalim- and Isoprenaline-induced Relaxation of Human Isolated Airways—Role of the Epithelium and of K+ Channel Activation

1994 ◽  
Vol 7 (3) ◽  
pp. 195-203 ◽  
Author(s):  
J.L. Black ◽  
P.R.A. Johnson ◽  
K.O. McKay ◽  
D. Carey ◽  
C.L. Armour
Keyword(s):  
K Channel ◽  
Channel Activation
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