Role of Anions in Nitric Oxide-Induced Short-Circuit Current Increase in Isolated Porcine Ciliary Processes

2004 ◽  
Vol 45 (9) ◽  
pp. 3213 ◽  
Author(s):  
Renyi Wu ◽  
Ke Yao ◽  
Josef Flammer ◽  
Ivan O. Haefliger
Keyword(s):  
Nitric Oxide ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Current Increase ◽  
Ciliary Processes

Prostaglandin-induced recovery of barrier function in porcine ileum is triggered by chloride secretion

1999 ◽  
Vol 276 (1) ◽  
pp. G28-G36 ◽  
Author(s):  
Anthony T. Blikslager ◽  
Malcolm C. Roberts ◽  
Robert A. Argenzio
Keyword(s):  
Short Circuit ◽  
Second Messengers ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Ringer Solution ◽  
Signal Recovery ◽  
Osmotic Gradient ◽  
Current Increase ◽  
Ussing Chambers

We have previously shown that PGI2 and PGE2 have a synergistic role in restoring electrical transepithelial resistance ( R) in ischemia-injured porcine ileum via the second messengers Ca2+ and cAMP. Because Ca2+ and cAMP stimulate Cl− secretion, we assessed the role of PG-induced Cl−secretion in recovery of R. Mucosa from porcine ileum subjected to ischemia for 45 min was mounted in Ussing chambers and bathed in indomethacin and Ringer solution. Addition of PGs stimulated a twofold increase in R, which was preceded by elevations in short-circuit current (increase of 25 μA/cm2). The PG-induced effect on R was partially inhibited with bumetanide, an inhibitor of Cl− secretion. The remaining elevations in R were similar in magnitude to those induced in ischemic tissues by amiloride, an inhibitor of Na+ absorption. Treatment with 10−4 M 8-bromo-cGMP or 300 mosM mucosal urea resulted in elevations in R similar to those attained with PG treatment. PGs signal recovery of Rvia induction of Cl−secretion and inhibition of Na+absorption, possibly by establishing a transmucosal osmotic gradient.

scholarly journals Ultrathin Cu(In,Ga)Se2 Solar Cells with Ag/AlOx Passivating Back Reflector

Energies ◽  
2021 ◽  
Vol 14 (14) ◽  
pp. 4268
Author(s):  
Jessica de Wild ◽  
Gizem Birant ◽  
Guy Brammertz ◽  
Marc Meuris ◽  
Jef Poortmans ◽  
...  
Keyword(s):  
Surface Roughness ◽  
Solar Cells ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Short Circuit Current Density ◽  
Open Circuit ◽  
Electron Microscopic ◽  
Current Increase ◽  
Time Resolved ◽  
Cigs Solar Cells

Ultrathin Cu(In,Ga)Se2 (CIGS) absorber layers of 550 nm were grown on Ag/AlOx stacks. The addition of the stack resulted in solar cells with improved fill factor, open circuit voltage and short circuit current density. The efficiency was increased from 7% to almost 12%. Photoluminescence (PL) and time resolved PL were improved, which was attributed to the passivating properties of AlOx. A current increase of almost 2 mA/cm2 was measured, due to increased light scattering and surface roughness. With time of flight—secondary ion mass spectroscopy, the elemental profiles were measured. It was found that the Ag is incorporated through the whole CIGS layer. Secondary electron microscopic images of the Mo back revealed residuals of the Ag/AlOx stack, which was confirmed by energy dispersive X-ray spectroscopy measurements. It is assumed to induce the increased surface roughness and scattering properties. At the front, large stains are visible for the cells with the Ag/AlOx back contact. An ammonia sulfide etching step was therefore applied on the bare absorber improving the efficiency further to 11.7%. It shows the potential of utilizing an Ag/AlOx stack at the back to improve both electrical and optical properties of ultrathin CIGS solar cells.

Enhancement of the performance of CdS/CdTe heterojunction solar cell using TiO2/ZnO bi-layer ARC and V2O5 BSF layers: A simulation approach

2020 ◽  
Vol 92 (2) ◽  
pp. 20901
Author(s):  
Abdul Kuddus ◽  
Md. Ferdous Rahman ◽  
Jaker Hossain ◽  
Abu Bakar Md. Ismail
Keyword(s):  
Solar Cell ◽  
Short Circuit ◽  
Photovoltaic Performance ◽  
Short Circuit Current ◽  
Short Circuit Current Density ◽  
Open Circuit ◽  
Heterojunction Solar Cell ◽  
Back Surface ◽  
Heterojunction Solar Cells

This article presents the role of Bi-layer anti-reflection coating (ARC) of TiO2/ZnO and back surface field (BSF) of V2O5 for improving the photovoltaic performance of Cadmium Sulfide (CdS) and Cadmium Telluride (CdTe) based heterojunction solar cells (HJSCs). The simulation was performed at different concentrations, thickness, defect densities of each active materials and working temperatures to optimize the most excellent structure and working conditions for achieving the highest cell performance using obtained optical and electrical parameters value from the experimental investigation on spin-coated CdS, CdTe, ZnO, TiO2 and V2O5 thin films deposited on the glass substrate. The simulation results reveal that the designed CdS/CdTe based heterojunction cell offers the highest efficiency, η of ∼25% with an enhanced open-circuit voltage, Voc of 0.811 V, short circuit current density, Jsc of 38.51 mA cm−2, fill factor, FF of 80% with bi-layer ARC and BSF. Moreover, it appears that the TiO2/ZnO bi-layer ARC, as well as ETL and V2O5 as BSF, could be highly promising materials of choice for CdS/CdTe based heterojunction solar cell.

Protein kinase C potentiates cAMP-stimulated mouse duodenal mucosal bicarbonate secretion in vitro

2004 ◽  
Vol 286 (5) ◽  
pp. G814-G821 ◽  
Author(s):  
Bi-Guang Tuo ◽  
Jimmy Y. C. Chow ◽  
Kim E. Barrett ◽  
Jon I. Isenberg
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Duodenal Mucosa ◽  
Bicarbonate Secretion ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Ussing Chambers ◽  
Duodenal Bicarbonate Secretion

PKC has been shown to regulate epithelial Cl- secretion in a variety of models. However, the role of PKC in duodenal mucosal bicarbonate secretion is less clear. We aimed to investigate the role of PKC in regulation of duodenal mucosal bicarbonate secretion. Bicarbonate secretion by murine duodenal mucosa was examined in vitro in Ussing chambers using a pH-stat technique. PKC isoform expression and activity were assessed by Western blotting and in vitro kinase assays, respectively. PMA (an activator of PKC) alone had no effect on duodenal bicarbonate secretion or short-circuit current ( Isc). When PMA and dibutyryl-cAMP (db-cAMP) were added simultaneously, PMA failed to alter db-cAMP-stimulated duodenal bicarbonate secretion or Isc ( P > 0.05). However, a 1-h preincubation with PMA potentiated db-cAMP-stimulated duodenal bicarbonate secretion and Isc in a concentration-dependent manner (from 10-8 to 10-5M) ( P < 0.05). PMA preincubation had no effects on carbachol- or heat-stable toxin-stimulated bicarbonate secretion. Western blot analysis revealed that PKCα, -γ, -ϵ, -θ, -μ, and -ι/λ were expressed in murine duodenal mucosa. Ro 31–8220 (an inhibitor active against PKCϵ, -α, -β, and -γ), but not Gö 6983 (an inhibitor active against PKCα, -γ, -β, and -δ), reversed the potentiating effect of PMA on db-cAMP-stimulated bicarbonate secretion. PMA also time- and concentration-dependently increased the activity of PKCϵ, an effect that was prevented by Ro 31–8220 but not Gö 6983. These results demonstrate that activation of PKC potentiates cAMP-stimulated duodenal bicarbonate secretion, whereas it does not modify basal secretion. The effect of PKC on cAMP-stimulated bicarbonate secretion is mediated by the PKCϵ isoform.

scholarly journals Coupling of epithelial Na+ and Cl− channels by direct and indirect activation by serine proteases

2012 ◽  
Vol 303 (9) ◽  
pp. C936-C946 ◽  
Author(s):  
Veronika Gondzik ◽  
Wolf Michael Weber ◽  
Mouhamed S. Awayda
Keyword(s):  
Serine Proteases ◽  
Collecting Duct ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Epithelial Cell Line ◽  
Extracellular Proteases ◽  
Direct Role ◽  
Renal Epithelial Cell ◽  
Transport Pathways

The mammalian collecting duct (CD) is continuously exposed to urinary proteases. The CD expresses an epithelial Na+ channel (ENaC) that is activated after cleavage by serine proteases. ENaC also exists at the plasma membrane in the uncleaved form, rendering activation by extracellular proteases an important mechanism for regulating Na+ transport. Many exogenous and a small number of endogenous extracellular serine proteases have been shown to activate the channel. Recently, kallikrein 1 (KLK1) was shown to increase γENaC cleavage in the native CD indicating a possible direct role of this endogenous protease in Na+ homeostasis. To explore this process, we examined the coordinated effect of this protease on Na+ and Cl− transport in a polarized renal epithelial cell line (Madin-Darby canine kidney). We also examined the role of native urinary proteases in this process. Short-circuit current ( Isc) was used to measure transport of these ions. The Isc exhibited an ENaC-dependent Na+ component that was amiloride blockable and a cystic fibrosis transmembrane conductance regulator (CFTR)-dependent Cl− component that was blocked by inhibitor 172. Apical application of trypsin, an exogenous S1 serine protease, activated IENaC but was without effects on ICFTR. Subtilisin an exogenous S8 protease that mimics endogenous furin-type proteases activated both currents. A similar activation was also observed with KLK1 and native rat urinary proteases. Activation with urinary proteases occurred within minutes and at protease concentrations similar to those in the CD indicating physiological significance of this process. ENaC activation was irreversible and mediated by enhanced cleavage of γENaC. The activation of CFTR was indirect and likely dependent on activation of an endogenous apical membrane protease receptor. Collectively, these data demonstrate coordinated stimulation of separate Na+ and Cl− transport pathways in renal epithelia by extracellular luminal proteases. They also indicate that baseline urinary proteolytic activity is sufficient to modify Na+ and Cl− transport in these epithelia.

An electrogenic amino acid transporter in the apical membrane of cultured human bronchial epithelial cells

1998 ◽  
Vol 275 (5) ◽  
pp. L917-L923 ◽  
Author(s):  
Luis J. V. Galietta ◽  
Luciana Musante ◽  
Leila Romio ◽  
Ubaldo Caruso ◽  
Annarita Fantasia ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Amino Acid ◽  
Epithelial Cells ◽  
Apical Membrane ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Bronchial Epithelial Cells ◽  
Maximal Effect ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

We performed Ussing chamber experiments on cultured human bronchial epithelial cells to look for the presence of electrogenic dibasic amino acid transport. Apical but not basolaterall-arginine (10–1,000 μM) increased the short-circuit current. Maximal effect and EC50were ∼3.5 μA/cm2and 80 μM, respectively, in cells from normal subjects and cystic fibrosis patients. The involvement of nitric oxide was ruled out because a nitric oxide synthase inhibitor ( NG-nitro-l-arginine methyl ester) did not decrease the arginine-dependent current. Apicall-lysine,l-alanine, andl-proline, but not aspartic acid, were also effective in increasing the short-circuit current, with EC50values ranging from 26 to 971 μM. Experiments performed with radiolabeled arginine demonstrated the presence of an Na+-dependent concentrative transporter on the apical membrane of bronchial cells. This transporter could be important in vivo to maintain a low amino acid concentration in the fluid covering the airway surface.

Histamine augments colonic secretion in guinea pig distal colon

1990 ◽  
Vol 258 (3) ◽  
pp. G432-G439 ◽  
Author(s):  
Y. Z. Wang ◽  
H. J. Cooke ◽  
H. C. Su ◽  
R. Fertel
Keyword(s):  
Short Circuit ◽  
Nordihydroguaiaretic Acid ◽  
Short Circuit Current ◽  
Intestinal Secretion ◽  
Distal Colon ◽  
H2 Antagonist ◽  
Colonic Secretion ◽  
Set Up ◽  
Colonic Transport

We tested the hypothesis that the role of histamine in the control of intestinal secretion is mediated by prostaglandins (PGs). The effects of histamine on ion transport were examined in muscle-stripped sheets of mucosa/submucosa set up in flux chambers. Histamine evoked a transient concentration-dependent increase in short-circuit current (Isc) that was reduced by the Cl- transport inhibitor bumetanide. Histamine also caused the release of PGE2. The Isc response to histamine was reduced by indomethacin and piroxicam, which block PG formation, but not by nordihydroguaiaretic acid, which prevents production of lipoxygenase products. 2-Methylhistamine, but not dimaprit, evoked a concentration-dependent increase in Isc. The Isc response to histamine was reduced by the H1-blocker pyrilamine, but not by the H2-antagonist cimetidine. In addition to its direct effect, histamine augmented the responses of endogenously released neurotransmitters with and without indomethacin and hexamethonium. Tetrodotoxin (TTX) reduced the Isc response to 10(-3) M histamine. In the presence of TTX, exogenous histamine amplified the responses to PGs, vasoactive intestinal polypeptide, 2-chloroadenosine, bethanechol, and carbachol. These results suggest that histamine acts at H1-receptors on cells within the gut to mediate intestinal Cl- secretion in part by releasing PGs and by augmenting the actions of endogenously released neurotransmitters. Our results indicate that histamine has a role in the regulation of colonic transport function.

Activation of KCNQ (KV7) K+ channels in enteric neurons inhibits epithelial Cl- secretion in mouse distal colon

2021 ◽  
Author(s):  
Andrew J. Nickerson ◽  
Trey S. Rottgen ◽  
Vazhaikkurichi M. Rajendran
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Therapeutic Benefit ◽  
Enteric Neurons ◽  
Intestinal Epithelial ◽  
Cell Monolayers ◽  
Neuronal Populations ◽  
Irritable Bowel

KV7 (KCNQ) K+ channels are expressed in many neuronal populations, and play an important role in regulating membrane potential by generating a hyper-polarizing K+ current and decreasing cell excitability. However, the role of KV7 channels in the neural regulation of intestinal epithelial Cl- secretion is not known. Cl- secretion in mouse distal colon was measured as a function of short circuit current (ISC), while pharmacological approaches were used to test the hypothesis that activation of KV7 channels in enteric neurons would inhibit epithelial Cl- secretion. Flupirtine, a non-selective KV7 activator, inhibited basal Cl- secretion in mouse distal colon and abolished or attenuated the effects of drugs that target various components of enteric neurotransmission, including tetrodotoxin (NaV channel blocker), Veratridine (NaV channel activator), Nicotine (nicotinic acetylcholine receptor agonist) and Hexamethonium (nicotinic antagonist). In contrast, flupritine did not block the response to epithelium-targeted agents VIP (endogenous VPAC receptor ligand) or carbachol (non-selective cholinergic agonist). Flupirtine inhibited Cl- secretion in both full-thickness and seromuscular-stripped distal colon (containing the submucosal, but not myenteric plexus), but generated no response in epithelial T84 cell monolayers. KV7.2 and KV7.3 channel proteins were detected by immunofluorescence in whole-mount preparations of the submucosa from mouse distal colon. ICA 110381 (KV7.2/7.3 specific activator) inhibited Cl- secretion comparably to flupirtine. We conclude that KV7 channel activators inhibit neurally-driven Cl- secretion in the colonic epithelium, and may therefore have therapeutic benefit in treating pathologies associated with hyper-excitable enteric nervous system, such as irritable bowel syndrome with diarrhea (IBS-D).

Inhibition of amiloride-sensitive sodium-channel activity in distal lung epithelial cells by nitric oxide

1998 ◽  
Vol 274 (3) ◽  
pp. L378-L387 ◽  
Author(s):  
Jin Wen Ding ◽  
John Dickie ◽  
Hugh O’Brodovich ◽  
Yutaka Shintani ◽  
Bijan Rafii ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Cell Function ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Lung Epithelial Cells ◽  
Flufenamic Acid ◽  
Activated Macrophages ◽  
Lung Epithelial ◽  
Distal Lung

Distal lung epithelial cells (DLECs) play an active role in fluid clearance from the alveolus by virtue of their ability to actively transport Na+ from the alveolus to the interstitial space. The present study evaluated the ability of activated macrophages to modulate the bioelectric properties of DLECs. Low numbers of lipopolysaccharide (LPS)-treated macrophages were able to significantly reduce amiloride-sensitive short-circuit current ( I sc) without affecting total I sc or monolayer resistance. This was associated with a rise in the flufenamic acid-sensitive component of the I sc. The effect was reversed by the addition of N-monomethyl-l-arginine to the medium, implying a role for nitric oxide. We hypothesized that macrophages exerted their effect by expressing inducible nitric oxide synthase (iNOS) in DLECs. The products of LPS-treated macrophages increased the levels of iNOS protein and mRNA transcripts in DLECs as well as causing a rise in iNOS activity. Immunofluorescence microscopy of LPS-stimulated macrophage-DLEC cocultures with anti-nitrotyrosine antibodies provided evidence for the generation of peroxynitrite in macrophages but not in DLECs. These data indicate that activated macrophages in the lung may contribute to impaired resolution of acute respiratory distress syndrome and suggest a novel mechanism whereby nitric oxide might alter cell function by altering its ion-transporting phenotype.

Role of nutrient HCO3(-) in protection of amphibian gastric mucosa

1980 ◽  
Vol 239 (6) ◽  
pp. G536-G542
Author(s):  
R. Schiessel ◽  
A. Merhav ◽  
J. B. Matthews ◽  
L. A. Fleischer ◽  
A. Barzilai ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Experimental Conditions ◽  
Slow Decline ◽  
Alkaline Tide ◽  
Artificial Gastric Juice ◽  
Rapid Drop

In in vitro bullfrog fundic mucosa inhibited with 10(-3) M metiamide and exposed to a luminal pH of 2 a progressive slow decline in potential difference (PD) and short-circuit current (Isc) and a rise in resistance (R) were observed when the nutrient solution (N) contained 18 mM HCO3(-), but these changes were restored by an N containing 50 mM HCO3(-). Substitution of PO4(3-) or N-tris(hydroxymethyl)-methyl-2-aminoethanesulfonic acid for NHO3(-) in N caused a rapid drop in PD and Isc in inhibited tissues, changes that could be prevented by 10(-4) M histamine. Ulceration occurred more frequently in metiamide-inhibited gastric sacs exposed to artificial gastric juice with an N of 18 mMHCO3(-) than with 50 mM HCO3(-), but histamine prevented ulceration in the 18 mM HCO3(-) solution. JnetCl approximated Isc under most experimental conditions in inhibited mucosa and was reduced dramatically as were both Jn leads to sCl and Js leads to nCl when HCO3(-) was removed from N. In histamine-stimulated tissues, removal of nutrient HCO3(-) did not influence Cl- transport. Our results are consistent with the proposal that HCO3(-) in N supports normal Cl- flux and that the alkaline tide of actively secreting oxyntic cells can do the same in the absence of ambient HCO3(-).

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