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

scholarly journals H 2 O 2 -Induced Dilation in Human Coronary Arterioles: Role of Protein Kinase G Dimerization and Large-Conductance Ca 2+ -Activated K + Channel Activation

2012 ◽  
Vol 110 (3) ◽  
pp. 471-480 ◽  
Author(s):  
David X. Zhang ◽  
Lena Borbouse ◽  
Debebe Gebremedhin ◽  
Suelhem A. Mendoza ◽  
Natalya S. Zinkevich ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase G ◽  
K Channel ◽  
Channel Activation ◽  
Coronary Arterioles

ATP-dependent K+ channel activation reduces loss of opioid dilation after brain injury

1998 ◽  
Vol 274 (5) ◽  
pp. H1674-H1683 ◽  
Author(s):  
William M. Armstead
Keyword(s):  
Brain Injury ◽  
K Channel ◽  
Channel Activation ◽  
Calcium Dependent ◽  
Cranial Window ◽  
Pial Artery ◽  
Cgmp Analog ◽  
Newborn Pigs ◽  
The Brain

ATP-dependent K+(KATP) channel function is impaired after fluid percussion brain injury (FPI). Additionally, the nitric oxide (NO) releaser sodium nitroprusside and a cGMP analog elicit pial dilation via KATP channel activation, whereas opioids such as methionine enkephalin (Met) elicit pial dilation via NO and KATP channel activation. Decremented Met dilation contributes to reductions in pial artery diameter and altered cerebral hemodynamics after FPI. This study was designed to investigate the role of KATP channel activation before FPI in the loss of opioid dilation subsequent to FPI in newborn pigs equipped with a closed cranial window. FPI was produced by allowing a pendulum to strike a piston on a saline-filled cylinder that was fluid coupled to the brain via a hollow screw in the cranium. FPI blunted dilation to Met (7 ± 1, 11 ± 1, and 17 ± 1% before FPI vs. 1 ± 1, 4 ± 1, and 6 ± 1% after FPI for 10−10, 10−8, and 10−6 M Met, respectively). Met-associated elevation in cerebrospinal fluid (CSF) cGMP was similarly blunted (350 ± 12 and 636 ± 12 fmol/ml before FPI vs. 265 ± 5 and 312 ± 17 fmol/ml after FPI for control and 10−6 M Met, respectively). In piglets pretreated with cromakalim (10−10 M) 20 min before FPI, Met dilation was partially restored (7 ± 1, 10 ± 1, and 15 ± 1% before FPI vs. 4 ± 1, 7 ± 1, and 11 ± 1% after FPI for 10−10, 10−8, and 10−6 M Met, respectively). Met cGMP release was similarly partially restored (400 ± 9 and 665 ± 25 fmol/ml before FPI vs. 327 ± 11 and 564 ± 23 fmol/ml after FPI for control and 10−6 Met, respectively). Cromakalim (10−10 M) had no effect on pial diameter itself but prevented pial artery constriction by FPI (148 ± 5 to 124 ± 5 μm vs. 139 ± 4 to 141 ± 4 μm in the absence vs. presence of cromakalim pretreatment, respectively). In contrast, pretreatment with a subthreshold concentration of NS-1619, a calcium-dependent K+ channel agonist, did not restore vascular and biochemical parameters after FPI. These data indicate that prior KATP channel activation reduces the loss of opioid dilation after FPI.

Flow-mediated NO release from endothelial cells is independent of K+ channel activation or intracellular Ca2+

1995 ◽  
Vol 269 (4) ◽  
pp. C863-C869 ◽  
Author(s):  
W. C. O'Neill
Keyword(s):  
Endothelial Cells ◽  
K Channel ◽  
No Production ◽  
Channel Activation ◽  
Aortic Endothelial Cells ◽  
K Channels ◽  
Microcarrier Beads ◽  
Nitrite Production ◽  
No Release

The role of K+ channels and intracellular [Ca2+] in flow-induced nitric oxide (NO) production was investigated in bovine aortic endothelial cells in culture. NO release (measured as nitrite production) and K+ channel activity (measured as 86Rb+ efflux) were measured in cells grown on collagen-coated microcarrier beads and perfused in a column. An eightfold increase in flow produced a rapid (within 1 min), sustained, and reversible sixfold increase in NO release. Efflux of 86Rb+ also increased but rapidly returned to baseline and then transiently decreased when flow was decreased. This was probably due to boundary layer washout rather than to K+ channel activation, because an identical pattern was seen for release of [3H]ouabain. Neither tetraethylammonium nor increasing medium [K+] to block K+ currents prevented flow-induced NO release. Removal of medium Ca2+ or chelation of intracellular Ca2+ also did not block flow-mediated NO release. The results demonstrate that flow rapidly increases NO release from endothelial cells but that this increase in NO release is not dependent on activation of K+ channels or changes in intracellular [Ca2+].

scholarly journals Cyclic AMP-mediated inhibition of gallbladder contractility: role of K+ channel activation and Ca2+ signaling

2004 ◽  
Vol 143 (8) ◽  
pp. 994-1005 ◽  
Author(s):  
Sara Morales ◽  
Pedro J Camello ◽  
Gary M Mawe ◽  
María J Pozo
Keyword(s):  
Cyclic Amp ◽  
K Channel ◽  
Channel Activation ◽  
Gallbladder Contractility

scholarly journals Adrenomedullin Reduces Gender-Dependent Loss of Hypotensive Cerebrovasodilation after Newborn Brain Injury through Activation of ATP-Dependent K Channels

2007 ◽  
Vol 27 (10) ◽  
pp. 1702-1709 ◽  
Author(s):  
William M Armstead ◽  
Monica S Vavilala
Keyword(s):  
Brain Injury ◽  
Clinical Intervention ◽  
K Channel ◽  
Dependent Manner ◽  
Channel Activation ◽  
Cranial Window ◽  
Pial Artery ◽  
Newborn Brain ◽  
Newborn Pigs

Cerebrovascular dysregulation during hypotension occurs after fluid percussion brain injury (FPI) in the newborn pig owing to impaired K channel function. This study was designed to (1) determine the role of gender and K channel activation in adrenomedullin (ADM) cerebrovasodilation, (2) characterize the role of gender in the loss of hypotensive cerebrovasodilation after FPI, and (3) determine the role of gender in the ability of exogenous ADM to modulate hypotensive dysregulation after FPI. Lateral FPI (2 atm) was induced in newborn male and female newborn pigs (1 to 5 days old) equipped with a closed cranial window, n = 6 for each protocol. Adrenomedullin-induced pial artery dilation was significantly greater in female than male piglets and blocked by the KATP channel antagonist glibenclamide, but not by the Kca channel antagonist iberiotoxin. Cerebrospinal fluid ADM was increased from 3.8 ± 0.7 to 14.6 ± 3.0 fmol/mL after FPI in female but was unchanged in male piglets. Hypotensive pial artery dilation was blunted to a significantly greater degree in male versus female piglets after FPI. Topical pretreatment with a subthreshold vascular concentration of ADM (10−10 mol/L) before FPI reduced the loss of hypotensive pial artery dilation in both genders, but protection was significantly greater in male versus female piglets. These data show that hypotensive pial artery dilation is impaired after FPI in a gender-dependent manner. By unmasking a gender-dependent endogenous protectant, these data suggest novel gender-dependent approaches for clinical intervention in the treatment of perinatal traumatic brain injury.

Enhanced role of K+ channels in relaxations of hypercholesterolemic rabbit carotid artery to NO

1995 ◽  
Vol 269 (3) ◽  
pp. H805-H811 ◽  
Author(s):  
S. Najibi ◽  
R. A. Cohen
Keyword(s):  
Carotid Artery ◽  
Sodium Nitroprusside ◽  
Channel Blocker ◽  
Isometric Tension ◽  
K Channel ◽  
K Channels ◽  
Rabbit Carotid Artery ◽  
Cyclic Monophosphate ◽  
Endothelium Dependent Relaxation

Endothelium-dependent relaxations to acetylcholine remain normal in the carotid artery of hypercholesterolemic rabbits, but unlike endothelium-dependent relaxations of normal rabbits, they are inhibited by charybdotoxin, a specific blocker of Ca(2+)-dependent K+ channels. Because nitric oxide (NO) is the mediator of endothelium-dependent relaxation and can activate Ca(2+)-dependent K+ channels directly or via guanosine 3',5'-cyclic monophosphate, the present study investigated the role of Ca(2+)-dependent K+ channels in relaxations caused by NO, sodium nitroprusside, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-Brc-GMP) in hypercholesterolemic rabbit carotid artery. Isometric tension was measured in rabbit carotid artery denuded of endothelium from normal and hypercholesterolemic rabbits which were fed 0.5% cholesterol for 12 wk. Under control conditions, relaxations to all agents were similar in normal and hypercholesterolemic rabbit arteries. Charybdotoxin had no significant effect on relaxations of normal arteries to NO, sodium nitroprusside, or 8-BrcGMP, but the Ca(2+)-dependent K+ channel blocker significantly inhibited the relaxations caused by each of these agents in the arteries from hypercholesterolemic rabbits. By contrast, relaxations to the calcium channel blocker nifedipine were potentiated to a similar extent by charybdotoxin in both groups. In addition, arteries from hypercholesterolemic rabbits relaxed less than normal to sodium nitroprusside when contracted with depolarizing potassium solution. These results indicate that although nitrovasodilator relaxations are normal in the hypercholesterolemic rabbit carotid artery, they are mediated differently, and to a greater extent, by Ca(2+)-dependent K+ channels. These data also suggest that K+ channel-independent mechanism(s) are impaired in hypercholesterolemia.

scholarly journals Calnexin revealed as an ether-a-go-go chaperone by getting mutant worms up and going

2018 ◽  
Vol 150 (8) ◽  
pp. 1059-1061
Author(s):  
Jonathan T. Pierce
Keyword(s):  
Ion Channels ◽  
Dynamic Control ◽  
Cell Types ◽  
K Channel ◽  
Membrane Domains ◽  
Excitable Cells ◽  
Patch Clamp Recording ◽  
Cell Excitability ◽  
Distinct Membrane

The role of ion channels in cell excitability was first revealed in a series of voltage clamp experiments by Hodgkin and Huxley in the 1950s. However, it was not until the 1970s that patch-clamp recording ushered in a revolution that allowed physiologists to witness how ion channels flicker open and closed at angstrom scale and with microsecond resolution. The unexpectedly tight seal made by the patch pipette in the whole-cell configuration later allowed molecular biologists to suck up the insides of identified cells to unveil their unique molecular contents. By refining these techniques, researchers have scrutinized the surface and contents of excitable cells in detail over the past few decades. However, these powerful approaches do not discern which molecules are responsible for the dynamic control of the genesis, abundance, and subcellular localization of ion channels. In this dark territory, teams of unknown and poorly understood molecules guide specific ion channels through translation, folding, and modification, and then they shuttle them toward and away from distinct membrane domains via different subcellular routes. A central challenge in understanding these processes is the likelihood that these diverse regulatory molecules may be specific to ion channel subtypes, cell types, and circumstance. In work described in this issue, Bai et al. (2018. J. Gen. Physiol. https://doi.org/10.1085/jgp.201812025) begin to shed light on the biogenesis of UNC-103, a K+ channel found in Caenorhabditis elegans.

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