Hormonal control of chloride transport across locust rectum

1978 ◽  
Vol 56 (8) ◽  
pp. 1879-1882 ◽  
Author(s):  
J. Spring ◽  
J. Hanrahan ◽  
J. Phillips
Keyword(s):  
Chloride Transport ◽  
Short Circuit ◽  
Fold Increase ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Hormonal Control ◽  
Net Flux ◽  
Hemolymph Volume ◽  
Camp Levels

Rates of ion transport across locust recta were monitored in vitro by following fluxes of 22Na+ and 36Cl−, short-circuit current (Isc), and open-circuit electropotential difference (PD) across this epithelium for several hours. Corpora cardiaca (CC) homogenates, cAMP, theophylline, and hemolymph of recently fed locusts all stimulate electrogenic transport of Cl− across locust rectum, as indicated by a two- to three-fold increase in 36Cl− net flux, Isc, and PD. Cyclic AMP caused a Cl-dependent increase in PD across the lumen-facing but not the hemocoel-facing plasma membrane of the epithelial cells. We propose that a blood-borne factor, possibly from the CC, causes an elevation in cAMP levels in rectal tissue and that this second messenger acts by increasing Cl− entry into the cell from the rectal lumen. Additional fluid absorption accompanies the resulting increase in transport of NaCl, leading to an increase in the hemolymph volume of previously dehydrated locusts.

scholarly journals Further Observations on the Regulation of KCl ABSORPTION ACROSS LOCUST RECTUM

1985 ◽  
Vol 116 (1) ◽  
pp. 153-167
Author(s):  
J. W. HANRAHAN ◽  
J. E. PHILLIPS
Keyword(s):  
Chloride Transport ◽  
Short Circuit ◽  
Membrane Conductance ◽  
Short Circuit Current ◽  
Membrane Resistance ◽  
Open Circuit ◽  
High K ◽  
K Concentration ◽  
K Permeability

1. Electrophysiological and tracer flux techniques were used to studyregulation of KC1 reabsorption across locust recta. Physiologically high K+levels (100 mmolI−1) on the lumen side stimulated net 36Cl flux and reduced the theoretical energy cost of anion transport under open-circuit conductions. 2. The stimulation of short-circuit current (Ibc i.e. active C− absorption) by crude corpora cardiaca extracts (CC) was not dependent on exogenous Ca2+. Stimulations of Ibc were greatly enhanced in the presence of theophylline, indicating that the rate of synthesis of cAMP is increased by CC extracts. High CC levels lowered transepithelial resistance (Rt), suggesting that chloride transport stimulating hormone (CTSH) regulates both active Cl− absorption and counter-ion (K+) permeability. 3. High mucosal osmolarity or K+ concentration decreased Ibc and caused a disproportionately large increase in Rt, consistent with a decrease in theshunt (K+) conductance. Measurements of relative mucosal-to-serosal membrane resistance confirmed that high mucosal K+ levels reduced apical membrane conductance. Lowering mucosal pH to values observed in vivo atthe end of resorptive cycles also inhibited Ibc, apparently without affecting K+ permeability.

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.

Regulation of ion transport in porcine gallbladder: effects of VIP and norepinephrine

1989 ◽  
Vol 257 (1) ◽  
pp. C52-C57 ◽  
Author(s):  
S. M. O'Grady ◽  
P. J. Wolters ◽  
K. Hildebrand ◽  
D. R. Brown
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptor ◽  
Sulfonic Acid ◽  
Short Circuit ◽  
Fold Increase ◽  
Short Circuit Current ◽  
Maximal Effect ◽  
Camp Content ◽  
Flux Measurements

The objective of this study was to investigate the effects of vasoactive intestinal peptide (VIP) and norepinephrine (NE) on Na and Cl transport across the isolated porcine gallbladder. Serosal addition of either VIP or secretin increased the short-circuit current (Isc). The half-maximal effect for VIP was 84.3 nM. The effect of VIP was mimicked by 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP). Replacement of Cl with gluconate nearly abolished the effect of 8-BrcAMP on Isc, whereas HCO3 replacement with N-2-hydroxyethylpiperazine-N'-2-ethane-sulfonic acid buffer had no effect. Transepithelial flux measurements indicated that 8-BrcAMP stimulates net Cl secretion and inhibits Na absorption. Norepinephrine inhibits VIP-stimulated changes in Isc as well as the basal Isc. NE does not, however, reverse the effects of 8-BrcAMP on Isc. The effects of NE are antagonized by yohimbine (alpha 2-adrenergic receptor antagonist) but not prazosin (an alpha 1-adrenergic receptor antagonist). VIP causes a 2.5-fold increase in cAMP content in the gallbladder epithelium. This increase is blocked by NE. Serosal tetrodotoxin did not inhibit the peptide effects, indicating that VIP receptors are localized on the epithelium. Depolarization of submucosal nerves with veratrine inhibited the basal Isc and was reversible with yohimbine. This result indicated that sympathetic nerve pathways regulate Na and Cl absorption in vitro.

Effect of acetazolamide on sodium and chloride transport by in vitro rabbit ileum

1975 ◽  
Vol 228 (6) ◽  
pp. 1808-1814 ◽  
Author(s):  
HN Nellans ◽  
RA Frizzell ◽  
SG Schultz
Keyword(s):  
Cyclic Amp ◽  
Chloride Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Direct Interaction ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Membrane Component ◽  
Rabbit Ileum

Acetazolamide (8 mM) aboishes active Cl absorption and inhibits but does not abolish active Na absorption by stripped, short-circuited rabbit ileum. These effects are not accompanied by significant changes in the transmural electrical potential difference or short-circuit current. Studies of the undirectional influxes of Na andCl indicate that acetazolamide inhibits the neutral, coupled NaCl influx process at the mucosal membranes. This action appears to explain the observed effect of acetazolamide on active, transepithelial Na and Cl transport. Acetazolamide did not significantly inhibit either spontaneous or theophylline-induced Cl secretion by this preparation, suggesting that the theophylline-induced secretion may not simply be due tothe unmasking of a preexisting efflux process when the neutral influx mechanism is inhibited by theophylline. Finally, inhibition of the neutral NaCl influx process by acetazolamide does not appear to be attributable to an inhibition of endogenous HCO3production or an elevation in intracellular cyclic-AMP levels. Instead, it appearstheat the effect of acetazolamide is due to a direct interaction with a membrane component involved in the coupled influx process.

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)

Effects of lactose on calcium absorption and secretion by rat ileum

1984 ◽  
Vol 246 (3) ◽  
pp. G281-G285 ◽  
Author(s):  
M. J. Favus ◽  
E. Angeid-Backman
Keyword(s):  
Calcium Absorption ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Direct Effects ◽  
Dihydroxyvitamin D3 ◽  
Rat Ileum ◽  
Tissue Polarity ◽  
Net Flux ◽  
Absorptive Flux

The direct effects of lactose on net intestinal calcium absorption were determined by measuring unidirectional steady-state calcium fluxes in vitro under short-circuited conditions in segments of rat ileum. The isosmotic mucosal additions in segments of rat ileum. The isosmotic mucosal addition of lactose (160 mM) increased net calcium absorption (J net) by increasing the absorptive flux from mucosa to serosa (Jm----s) and reducing the secretory flux from serosa to mucosa (Js----m). Lactose also reduced tissue conductance and short-circuit current and reversed tissue polarity. 1,25-Dihydroxyvitamin D3 administration (50 ng/day for 4 days) increased J net from secretion to no net flux (Jm----s = Js----m), and lactose increased J net further to net absorption. Removal of sodium from the medium, like lactose addition, increased J net by increasing Jm----s and reducing Js----m. The replacement of medium sodium with choline abolished a further increase of J net by lactose. These results show that lactose increases net calcium absorption in the absence of transepithelial electrochemical or osmotic gradients. Transcellular calcium transport may be stimulated by lactose by hyperpolarization of the brush border as a result of reduced mucosal sodium.

Active hydrogen excretion and sodium absorption through isolated frog skin

1977 ◽  
Vol 233 (1) ◽  
pp. F46-F54 ◽  
Author(s):  
J. Ehrenfeld ◽  
F. Garcia-Romeu
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Sodium Concentration ◽  
Rana Esculenta ◽  
Open Circuit ◽  
Sodium Absorption ◽  
Ionic Balance ◽  
Proton Excretion ◽  
External Face

The in vitro skin of Rana esculenta was studied in open-circuit conditions. It was shown that when the external face is bathed in a 2-meq solution of NaCl, sodium is absorbed at a significantly higher rate than chloride. The ionic balance is maintained by excretion of hydrogen. With a mucosal solution of 2 meq Na2SO4 the equation relating sodium absorption to proton excretion is JnH+ = (-25 +/- 7) - (0.73 +/- 0.04) JnNa+. The correlation between the two variables is highly significant. Hydrogen excretion obeys saturation kinetics in relation to the sodium concentration of the mucosal solution. Maximum excretion occurs at a sodium concentration of 4 meq. When the mucosal solution is a 115-meq solution of Na2SO4 the net flux of sodium is 2.3 times higher than that of hydrogen. The balance is maintained by absorption of SO42-. The effects of various substances on the Na+ext/H+int exchange were studied. With a mucosal solution of 2 meq Na2SO4 and short-circuit conditions it was shown that the hydrogen excretion is active and nearly the same as in open circuit, the short-circuit current is equal (to within 8%) to the sum of the sodium and hydrogen net fluxes, and the correlation between the movements of the two ions is low. A model relating the active proton excretion with the sodium transport mechanism is proposed.

Studies on locust rectum. III. Stimulation of electrogenic chloride transport by hemolymph

1980 ◽  
Vol 58 (10) ◽  
pp. 1933-1939 ◽  
Author(s):  
J. H. Spring ◽  
J. E. Phillips
Keyword(s):  
Steady State ◽  
Filter Paper ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Simultaneous Measurements ◽  
Parallel Increase ◽  
Neuroendocrine Organ ◽  
Stimulation Of

Hemolymph was collected from recently fed desert locusts either by adsorption onto filter paper, or by centrifugation and methanol extraction. Whole hemolymph caused both the short-circuit current (Isc) and open-circuit transepithelial electropotential difference (PD) across locust recta mounted in Ussing-type chambers to double during the steady-state period. Methanol extracts of hemolymph caused similar but smaller increases in Isc. The transepithelial resistance (R) did not change. Simultaneous measurements of 36Cl− fluxes indicated that all of the increase in Isc following stimulation could be accounted for by a parallel increase in net Cl− absorption from the lumen side. With the exception of an initial small biphasic fluctuation in Isc, stimulation by hemolymph exhibited identical characteristics to those produced by submaximal dosages of corpora cardiaca (CC). Cardiatectomy drastically reduced the stimulatory activity of hemolymph, suggesting that this neuroendocrine organ is the source of the active factor (chloride transport stimulating hormone (CTSH)) in hemolymph.

scholarly journals Transport Properties of Locust Ileum in vitro: Effects of Cyclic Amp

1988 ◽  
Vol 137 (1) ◽  
pp. 361-385 ◽  
Author(s):  
B. Irvine ◽  
N. Audsley ◽  
R. Lechleitner ◽  
J. Meredith ◽  
B. Thomson ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Active Absorption ◽  
Rate Of Absorption ◽  
The Difference ◽  
In Vitro Effects ◽  
Resistance Decrease

1. Short-circuited locust ilea exhibited electrical properties remarkably similar to those of recta. The large short-circuit current (Isc) and transepithelial potential, both indicating net active absorption of anions, initially began to decline to zero but could be fully restored by adding cyclic AMP or extracts of corpus cardiacum and ventral abdominal ganglia to the haemocoel side. 2. Ion substitutions and radiotracer flux studies indicated that cyclic AMP-induced ΔIsc was due to electrogenic Cl− transport with kinetics identical to those of the rectum. Concurrent decreases in transileal resistance were due to increases in both Cl− and K+ (PK) permeabilities, most evident as a resistance decrease at the apical membrane. The ΔPK was blocked by basolateral addition of Ba2+, as observed for recta. 3. Everted ileal sacs under open-circuit conditions absorbed a slightly hyperosmotic NaCl-rich fluid and the rate of absorption was increased more than twofold by cyclic AMP. This contrasts with stimulated recta which absorb primarily KCl and a hyposmotic absorbate. Flux studies with short-circuited ilea demonstrated active absorption of Na+ (JnetNa), which was stimulated twofold by cyclic AMP. Removal of external Na+ had little effect on Isc, suggesting that JnetNa involves exchange for another cation, e.g. NH4+. 4. Ilea actively secreted acid at lower rates than do recta under open-circuit conditions. Under short-circuit conditions, cyclic AMP addition led to active alkalinization of the ileal lumen at high rates, and the large Isc represented the difference between active secretion of base equivalents and net absorption of Cl−. 5. The transport capacities of locust ilea and recta are compared in relation to their ultrastructure.

scholarly journals Cellular mechanisms and control of KCl absorption in insect hindgut

1983 ◽  
Vol 106 (1) ◽  
pp. 71-89 ◽  
Author(s):  
J. W. Hanrahan ◽  
J. E. Phillips
Keyword(s):  
Cyclic Amp ◽  
Apical Membrane ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Basal Membrane ◽  
Peptide Hormone ◽  
Open Circuit ◽  
Electrochemical Gradient ◽  
Cellular Mechanisms

The hindgut of the desert locust possesses an unusual chloride transport system. The isolated locust rectum absorbs chloride from the mucosal (lumen) to the serosal (haemolymph) side at a rate which is equal to the short-circuit current (Isc). Net chloride transport (JClnet) persists in nominally Na-free or HCO3(CO2)-free saline, is insensitive to normal inhibitors of NaCl co-transport and anion exchange, and is independent of the net electrochemical gradient for sodium across the apical membrane. However, active chloride transport is strongly dependent on mucosal potassium (Ka = 5.3 mM-K). Chloride entry across the apical membrane is active, whereas the net electrochemical gradient across the apical membrane is active, whereas the net electrochemical gradient across the basal membrane favours passive Cl exit from the cell. Although mucosal potassium directly stimulates ‘uphill’ chloride entry, there is no evidence for coupled KCl co-transport, nor would co-entry with potassium be advantageous energetically. Net chloride absorption and Isc are stimulated by a peptide hormone from the central nervous system which acts via cyclic-AMP. Cyclic-AMP increases Isc and JClnet approximately 1000% and transepithelial conductance (Gt) approximately 100%. Approximately half of the delta Gt during stimulation results from increased Cl conductance at the basal cell border. This increase is also reflected in a shift of the basal membrane e.m.f. towards the Nernst potential for chloride. The remainder of the cAMP-induced delta Gt is due to an elevation of apical membrane K conductance, which causes a 400% increase in transepithelial potassium permeability as estimated by radiotracer diffusion. Because of this stimulation of K conductance, potassium serves as the principal counterion for active chloride transport under open-circuit conditions. Very high luminal levels of K oppose the stimulatory actions of cAMP on active Cl transport and K conductance. These and other results have been incorporated into a cellular model for KCl absorption across this insect epithelium.

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