Mechanisms and properties of sodium transport in locust rectum

1987 ◽  
Vol 65 (12) ◽  
pp. 3084-3092 ◽  
Author(s):  
K. Black ◽  
J. Meredith ◽  
B. Thomson ◽  
J. Phillips ◽  
T. Dietz
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Water Soluble ◽  
Neurosecretory System ◽  
Apical Plasma Membrane ◽  
Organic Substrates ◽  
Active Process ◽  
Soluble Factors ◽  
Flux Formula ◽  
Net Flux

Steady-state fluxes of 22Na+ were measured as a function of external Na+ concentration across locust recta mounted as flat sheets under short-circuit conditions. A net flux [Formula: see text] at all concentrations confirmed that absorption was an active process obeying Michaelis–Menten kinetics with Kt of 17 mM and Vmax of 1.5 to 2.5 μequiv. cm−2 h−1. [Formula: see text] was not affected by cAMP, was independent of external Cl− levels and stimulated short-circuit current (i.e., Cl− transport), and was partially inhibited by amiloride and ouabain but not by vanadate. Using intracellular electrodes, a small Na+ conductance that was not due to cotransport with organic substrates was identified in the apical plasma membrane. A semiquantitative model for Na+ absorption in this epithelium is proposed. We surveyed the locust neurosecretory system for water-soluble factors that might control rectal Na+ reabsorption.

Active transport of magnesium across the isolated midgut of Hyalophora cecropia

1975 ◽  
Vol 63 (2) ◽  
pp. 313-320
Author(s):  
J. L. Wood ◽  
A. M. Jungreis ◽  
W. R. Harvey
Keyword(s):  
Steady State ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Potassium Transport ◽  
Magnesium Concentration ◽  
Magnesium Transport ◽  
Wet Weight ◽  
Net Flux ◽  
Burk Plot

1. The 28Mg-measured net flux of magnesium from lumen-side to haemolymph-side of the isolated and short-circuited midgut was 1.97 +/− 0.28 mu-equiv cm(−2) /(−1) in 8 mM-Mg2+. 2. The magnesium-influx shows a delay before the tracer steady-state is attained, indicating the existence of a magnesium-transport pool equivalent to 6.7 mu-equiv/g wet weight of midgut tissue. 3. Magnesium depresses the short-circuit current produced the midgut but not the potassium transport, the depression being equal to the rate of magnesium transport. 4. Magnesium transport yields a linear Lineweaver-Burk plot with an apparent Km of 34 mM-Mg2+ and an apparent Vmax of 14.9 mu-equiv cm(−1) /(−1). 5. Magnesium is actively transported across the midgut and contributes to the regulation of the haemolymph magnesium concentration in vivo.

Suppression of gastric acid secretion by furosemide in isolated gastric mucosa of guinea pig

1980 ◽  
Vol 239 (6) ◽  
pp. G532-G535 ◽  
Author(s):  
A. Ayalon ◽  
A. Corcia ◽  
G. Klemperer ◽  
S. R. Caplan
Keyword(s):  
Guinea Pig ◽  
Acid Secretion ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Electrical Conductance ◽  
Short Circuit Current ◽  
Cl Transport ◽  
Consequent Reduction ◽  
Net Flux ◽  
Mucosal Side

The effect of furosemide on acid secretion and Cl- transport was studied in isolated fundic mucosa of the guinea pig. Furosemide (10(-3) M), applied to the serosal side produced an immediate effect on the short-circuit current (Isc), lowering it by 47 +/- 2%. Potential difference decreased by 29 +/- 3%, electrical conductance by 18 +/- 4%, acid secretion by 38 +/- 1%, and net flux of Cl- from serosal-to-mucosal side by 37%. Application of the drug to the mucosal side produced similar effects on acid secretion and on the electrical parameters. It is suggested that furosemide blocks the entrance of Cl-, by the Na+--Cl- cotransport mechanism, through the basolateral membrane of the secreting cell. The consequent reduction in electrogenic Cl- transport would cause Isc and acid secretion to decrease. A reduction of Cl- conductance of the apical membrane, upon mucosal application of the drug, would cause similar effects on acid secretion and Cl- transport.

Nucleotides regulate NaCl transport in mIMCD-K2 cells via P2X and P2Y purinergic receptors

1999 ◽  
Vol 277 (4) ◽  
pp. F552-F559 ◽  
Author(s):  
David E. McCoy ◽  
Amanda L. Taylor ◽  
Brian A. Kudlow ◽  
Katherine Karlson ◽  
Margaret J. Slattery ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Apical Membrane ◽  
Collecting Duct ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Extracellular Nucleotides ◽  
P2x Receptor ◽  
Apical Plasma Membrane ◽  
Receptor Subtypes ◽  
Nacl Transport

Extracellular nucleotides regulate NaCl transport in some epithelia. However, the effects of nucleotide agonists on NaCl transport in the renal inner medullary collecting duct (IMCD) are not known. The objective of this study was to determine whether ATP and related nucleotides regulate NaCl transport across mouse IMCD cell line (mIMCD-K2) epithelial monolayers and, if so, via what purinergic receptor subtypes. ATP and UTP inhibited Na+ absorption [measured via Na+ short-circuit current[Formula: see text])] and stimulated Cl− secretion [measured via Cl−short-circuit current ([Formula: see text])]. Using selective P2 agonists, we report that P2X and P2Y purinoceptors regulate [Formula: see text] and[Formula: see text]. By RT-PCR, two P2X receptor channels (P2X3, P2X4) and two P2Y G protein-coupled receptors (P2Y1, P2Y2) were identified. Functional localization of P2 purinoceptors suggest that [Formula: see text] is stimulated by apical membrane-resident P2Y purinoceptors and P2X receptor channels, whereas[Formula: see text] is inhibited by apical membrane-resident P2Y purinoceptors and P2X receptor channels. Together, we conclude that nucleotide agonists inhibit[Formula: see text] across mIMCD-K2 monolayers through interactions with P2X and P2Y purinoceptors expressed on the apical plasma membrane, whereas extracellular nucleotides stimulate [Formula: see text]through interactions with P2X and P2Y purinoceptors expressed on the apical plasma membrane.

Aspects of electrolyte transport across isolated dog retinal pigment epithelium

1986 ◽  
Vol 250 (5) ◽  
pp. F781-F784 ◽  
Author(s):  
S. Tsuboi ◽  
R. Manabe ◽  
S. Iizuka
Keyword(s):  
Retinal Pigment Epithelium ◽  
Apical Membrane ◽  
Short Circuit ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Short Circuit Current ◽  
Bathing Solution ◽  
Apical Side ◽  
Net Flux ◽  
Net Fluxes

Transport of Na and Cl across the isolated dog retinal pigment epithelium (RPE) choroid was investigated. Under the short-circuit condition, a net Na flux was observed from choroid to retina and a net Cl flux was determined in the opposite direction. The current created by the net flux of these two ions was larger than the short-circuit current (SCC). Addition of 10(-5) M ouabain to the apical side inhibited net fluxes of both Na and Cl, whereas it reduced the SCC 84%. Addition of 10(-4) M furosemide to the apical side inhibited net Cl flux but had no effect on the net Na transport. The 10(-4) M furosemide reduced the SCC 38%. These drugs had no effect when applied to the basal side. Thus the transport of both Na and Cl depends on the Na-K-ATPase in the apical membrane of the dog RPE. A furosemide-sensitive neutral carrier at the apical membrane is suggested for the transport of Cl. Replacement of HCO3 with SO4 in the bathing solution caused an increase in the SCC, indicating the choroid-to-retina movement of HCO3 across the short-circuited dog RPE choroid.

Action of adenosine on chloride active transport of isolated frog cornea

1979 ◽  
Vol 237 (2) ◽  
pp. F121-F127
Author(s):  
B. S. Spinowitz ◽  
J. A. Zadunaisky
Keyword(s):  
Rana Catesbeiana ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Adenyl Cyclase ◽  
Naturally Occurring ◽  
Chloride Pump ◽  
Net Flux ◽  
The One ◽  
Sustained Increase

Addition of adenosine (10–7 to 10–4 M) to the tear side of isolated corneas (Rana catesbeiana) produced a rapid, sustained increase in short-circuit current, potential difference, and radioisotopic chloride net flux. The increased net chloride flux accounted for the increased short-circuit current. Adenosine, a known activator of adenyl cyclase in other tissues, exerted its effects on chloride transport through a receptor different from the one described for epinephrine and prostaglandins in the corneal epithelium. Propranolol inhibited the epinephrine response but not the adenosine effect. Dipolyphloretin phosphate inhibited prostaglandin responses but did not affect the adenosine stimulation of chloride transport. Adenine and/or ribose, parts of the adenosine molecule, had no stimulatory effect, but 5'-AMP had a partial effect.The activation of the chloride pump with DBcAMP blocked the response to adenosine. Adenosine interacted with the effects of theophylline. Adenosine, a naturally occurring molecule, stimulated chloride transport by activation of adenyl cyclase through a separate membrane receptor in the corneal eqithelium.

Evidence that prostaglandin E2 stimulates chloride secretion in cultured A6 renal epithelial cells

1986 ◽  
Vol 250 (3) ◽  
pp. F511-F515 ◽  
Author(s):  
R. Keeler ◽  
N. L. Wong
Keyword(s):  
Epithelial Cells ◽  
Prostaglandin E2 ◽  
Short Circuit ◽  
Basal Medium ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Apical Surface ◽  
Renal Epithelial Cells ◽  
Apical Side ◽  
Net Flux

The effects of prostaglandin E2 (PGE2) on the transport of sodium and chloride were studied in cultured A6 renal epithelial cells. PGE2 on the basolateral but not the apical surface increased transmonolayer short-circuit current (Isc) and conductance. These changes could not be inhibited with amiloride or furosemide in the apical medium. Flux measurements showed that although Isc and net flux of sodium were equal in unstimulated cells, after addition of PGE2 the current increased with no corresponding changes in bidirectional or net flux of sodium. Immersing the cells in sodium-free or chloride-free media inhibited the effects of PGE2. Measurements of the simultaneous fluxes of sodium and chloride showed that after PGE2 was added there was a net flux of chloride from the basal to the apical side (secretion) that was equal to the change in Isc. The effects of PGE2 were inhibited by furosemide in the basal medium. We conclude that PGE2 stimulates a process of chloride secretion in A6 cells.

Purification and characteristics of the chloride transport stimulating factor from locust corpora cardiaca: a new peptide

1980 ◽  
Vol 58 (10) ◽  
pp. 1851-1860 ◽  
Author(s):  
J. E. Phillips ◽  
W. Mordue ◽  
J. Meredith ◽  
J. Spring
Keyword(s):  
Chloride Transport ◽  
Short Circuit ◽  
Gel Filtration ◽  
Short Circuit Current ◽  
Water Soluble ◽  
Cellulose Acetate Electrophoresis ◽  
Corpora Cardiaca ◽  
Ph Range ◽  
And Storage ◽  
Layer Chromatography

Corpora cardiaca (CC), cAMP, and hemolymph all increase short-circuit current (Isc) and electropotential difference (PD) across locust rectum by stimulating electrogenic transport of Cl− from the lumen. Using ΔIsc as a bioassay, we have purified the water-soluble stimulant (CTSH) from CC using gel filtration chromatography, DEAE-Sephadex anion exchange, cellulose acetate electrophoresis, and thin-layer chromatography. A single peak of CTSH activity was observed after all these procedures, although small amounts of CTSH activity occasionally remained in the high molecular weight (MW) protein precipitate. CTSH was purified more than 100-fold on Bio-Gel P-30 columns. It has a MW of 8 000 – 12 000, is destroyed by trypsin digestion, and has a net negative charge over the pH range (5–10) at which it is most stable. Various properties (i.e., stability at 20 °C, localization in CC, MW, Rf values) and reciprocal bioassay s indicate that CTSH is different from diuretic, antidiuretic, and adipokinetic hormones from locust CC. No difference in the properties of CTSH from glandular (GL) and storage lobes (SL) of CC were noted, although 80% of activity was in the SL. The concentration of purified CTSH required to cause maximal stimulation of rectal Isc is less than 7 nM.

Ion transport across rumen and omasum epithelium

1971 ◽  
Vol 262 (842) ◽  
pp. 301-305 ◽  
Keyword(s):  
Active Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Chloride Ions ◽  
Rumen Epithelium ◽  
Sodium Flux ◽  
Sodium System ◽  
Chloride Pump ◽  
Net Flux ◽  
Cattle And Sheep

The interior of the rumen in cattle and sheep is normally maintained at a potential of about — 40 mV relative to the blood. This potential depends primarily on the occurrence of an active transport of sodium from rumen to blood, since the potential, short-circuit current and the net sodium flux are simultaneously abolished by anoxia, ouabain and removal of sodium from the bathing solutions. There is an appreciable net flux of potassium from blood to rumen. There is also a substantial active transport of chloride in the same direction as sodium and it can be reduced by treatment with acetazolamide without affecting the potential or the sodium system. Nevertheless, sodium transport is reduced by the removal of chloride ions. Omasum epithelium is similar to rumen epithelium. However, the chloride pump appears to work in both directions in this tissue. Short-circuited omasum epithelium can also transport magnesium from omasum to blood.

Regulation of Na-Cl absorption in rabbit proximal colon in vitro

1987 ◽  
Vol 252 (1) ◽  
pp. G45-G51 ◽  
Author(s):  
J. H. Sellin ◽  
R. De Soignie
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Proximal Colon ◽  
Beta Agonist ◽  
Disulfonic Acid ◽  
Low Concentrations ◽  
Cotransport System ◽  
Net Flux

Ion transport in rabbit proximal colon (PC) in vitro is dominated by a Na-Cl cotransport system stimulated by epinephrine. To further characterize the regulation of Na-Cl transport, we tested the effects of specific adrenergic agonists on ion fluxes under short-circuit conditions. Additionally, we tested the effects of the transport inhibitors bumetanide, furosemide, and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS). Basal Na and Cl absorption were essentially nil [Na net flux (JNanet) = 0.3 +/- 0.4, and Cl net flux (JClnet) = -0.5 +/- 0.5 mu eq X cm-2 X h-1, means +/- SE]. The alpha 2-agonist clonidine significantly increased net Na and Cl absorption (delta JNanet = 3.0 +/- 0.6 mu eq X cm-2 X h-1, delta JClnet = 2.0 +/- 0.4 mu eq X cm-2 X h-1) with a minimal change in short-circuit current (delta Isc = 0.1 +/- 0.1 mu eq X cm-2 X h-1). The alpha 1-agonist phenylephrine and the beta-agonist isoproterenol did not alter ion transport. The alpha 2-blocker yohimbine (YOH) had a complex, concentration-dependent effect. At low concentrations (10(-6)-10(-8) M) YOH effectively inhibited epinephrine-stimulated cotransport. Compared with 10(-8)M YOH, 10(-6) YOH blocked 90% of the epinephrine-induced increases in Na and Cl absorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of carbenoxolone on glucocorticoid metabolism and Na transport in toad bladder

1989 ◽  
Vol 257 (4) ◽  
pp. F700-F704
Author(s):  
A. S. Brem ◽  
K. L. Matheson ◽  
T. Conca ◽  
D. J. Morris
Keyword(s):  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Water Soluble ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Base Line ◽  
Target Tissue ◽  
Glucocorticoid Metabolism ◽  
Transepithelial Sodium Transport

In humans, diminished 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) enzyme activity has been associated with sodium retention and hypertension. These studies show that the toad bladder, another target tissue epithelium displaying steroid-induced sodium transport, possesses the enzyme 11 beta-OHSD. The toad urinary bladder rapidly transformed corticosterone (3 x 10(-8) M) (50% by 10 min and 90% by 180 min) with 11-dehydrocorticosterone being the major metabolite. The 11-dehydrocorticosterone produced reached an apparent plateau when the tissue incubations were repeated with higher concentrations of corticosterone (10(-7) and 10(-6) M). Carbenoxolone sodium (2.5 x 10(-5) M), a water soluble derivative of glycyrrhetinic acid, markedly inhibited the metabolism of corticosterone (3 x 10(-8) M) to 11-dehydrocorticosterone similar to previous observations in the mammalian kidney. Carbenoxolone sodium (2.5 x 10(-5) M) did not significantly affect short-circuit current (SCC) in toad bladders when added to either the serosal or mucosal bath. However, when carbenoxolone sodium was added to the mucosal bath and 60 min later corticosterone 10(-6) M was placed in the serosal bath, bladders generated a SCC 2.07 +/- 0.17 (mean +/- SE) times above base line at 360 min compared with 1.48 +/- 0.11 in bladders exposed to corticosterone alone (P less than 0.02). In parallel experiments, carbenoxolone sodium in the mucosal bath enhanced the rise in SCC induced by cortisol 10(-6) M; 1.66 +/- 0.16 times above base line at 360 min compared with 1.07 +/- 0.14 with cortisol alone (P less than 0.02). We conclude that the toad bladder contains 11 beta-OHSD and inhibition of this enzyme with carbenoxolone sodium is associated with amplification of glucocorticoid-induced transepithelial sodium transport in this tissue. However, since the quantity of 11-dehydro-product produced appears to be limited, other factors in addition to inhibition of 11 beta-OHSD may play a role in this amplification of sodium transport.

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