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 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.

Changes in intracellular sodium with chloride secretion in dog tracheal epithelium

1986 ◽  
Vol 250 (4) ◽  
pp. C646-C650 ◽  
Author(s):  
S. R. Shorofsky ◽  
M. Field ◽  
H. A. Fozzard
Keyword(s):  
Steady State ◽  
Kinetic Models ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Tracheal Epithelium ◽  
Cl Secretion ◽  
Intracellular Na Activity ◽  
Sufficient Energy ◽  
Stimulation Of

Na-selective microelectrodes were employed to investigate the mechanism of Cl secretion by canine tracheal epithelium. In control tissues with a mean short-circuit current (Isc) of 30.1 microA/cm2, the intracellular Na activity (aiNa) was 10.7 mM. Following steady-state stimulation of Cl secretion with epinephrine (Isc = 126.4 microA/cm2), aiNa was 21.3 mM. These data indicate that there is sufficient energy in the Na gradient to drive Cl secretion by this tissue. When analyzed with simple kinetic models for the Na-K pump, they also suggest that the basolateral entry step involves the Na-K-2Cl cotransporter.

Network thermodynamic modeling of hormone regulation of active Na+ transport in cultured renal epithelium (A6)

1986 ◽  
Vol 250 (6) ◽  
pp. C978-C991 ◽  
Author(s):  
M. L. Fidelman ◽  
D. C. Mikulecky
Keyword(s):  
Steady State ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Hormone Regulation ◽  
Na Channels ◽  
Na Transport ◽  
Renal Epithelium ◽  
Ion Concentrations ◽  
Tight Junction Permeability

A network thermodynamic model was developed to describe steady-state ion flows (Na+,K+, and Cl-) and related electrical events in a cultured renal epithelium (A6) derived from toad kidney. Three hypotheses for explaining the steady-state increases in short-circuit current (SCC) produced by aldosterone and/or insulin were examined using the model. Changing only the number of basolateral Na+-K+ pumps produced virtually no change in SCC and was ruled out. Changing only the number of apical Na+ channels could produce sufficient increases in SCC but presented problems in the pattern of changes produced in cell ion concentrations and therefore appeared unlikely. Changing both apical and basolateral parameters in a balanced, coordinated manner produced the maximal changes in SCC with the minimal changes in cell ion concentrations and appeared to be the "best" hypothesis. In addition, it was found necessary for tight junction permeability to increase as active Na+ transport increased under open-circuit conditions. Simulations, using these results, compared favorably with experimental data on the stimulatory effects of aldosterone and insulin, both separately and together, on active Na+ transport.

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.

Studies on Locust Rectum: I. Stimulants of Electrogenic Ion Transport

1980 ◽  
Vol 86 (1) ◽  
pp. 211-223
Author(s):  
J. H. SPRING ◽  
J. E. PHILLIPS
Keyword(s):  
Steady State ◽  
Cyclic Amp ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Lag Time ◽  
Camp Concentration ◽  
Maximum Increase ◽  
Electrogenic Ion Transport ◽  
The Relationship ◽  
Stimulation Of

1. Homogenates of whole corpora cardiaca (CC) cause increases in the short-circuit current (Isc) and transepithelial electropotential difference (PD) across locust recta of 3-fold and 1.7-fold respectively, in comparison with the values for unstimulated steady-state recta. Maximum stimulation restores rectal ISC and PD to levels observed immediately after removing this organ from animals. 2. Cyclic-AMP causes a similar maximum increase in ISC and PD; however, the response exhibits a much shorter lag time and a faster rate of rise than is observed for stimulation with CC. 3. The addition of CC to the haemocoel side of everted rectal sacs caused whole tissue levels of cAMP in this organ to increase 3-fold. 4. The relationship between the logarithm of CC or cAMP concentration and the increase in ISC is linear, and the decline in ΔISC with time is also dosedependent. 5. Small maximum increases in ISC are caused by homogenates of ventral ganglia, whole brain and rectal tissue, but the concentration of the stimulatory activity in these locust tissues is clearly three orders of magnitude lower than in CC. 6. Inhibitors of HCO3—/H+ and Cl− transport in vertebrate systems, acetazolamide and thiocyanate, do not inhibit the stimulation of recta by CC or cAMP.

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.

Effects of biguanides on short-circuit current in frog skin

1984 ◽  
Vol 247 (2) ◽  
pp. F277-F281
Author(s):  
T. Saito ◽  
S. Yoshida
Keyword(s):  
Sodium Transport ◽  
Frog Skin ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Apical Surface ◽  
Sodium Permeability ◽  
Total Conductance ◽  
Mucosal Side ◽  
Stimulation Of

The addition of phenformin to the solution bathing the mucosal side of frog skin resulted in a sustained stimulation of short-circuit current accompanied by an increase in open-circuit potential and total conductance of the membrane. The flux of 22Na from the mucosal to the serosal side of the skin was increased by phenformin, whereas no significant effect on the flux from the serosal to the mucosal side was observed. The increases in the short-circuit current and total conductance with phenformin were completely abolished by the addition of 5 X 10(-5) M amiloride, which blocks sodium permeability at the apical surface of the membrane. Thus, the stimulation of active sodium transport in frog skin by phenformin would be due to the increase in the amiloride-sensitive sodium permeability of the membrane. Phenformin may prove to be a useful tool for the study of sodium transport in amphibian epithelia.

Effect of vasoactive intestinal peptide on ion transport across dog tracheal epithelium

1983 ◽  
Vol 55 (6) ◽  
pp. 1844-1848 ◽  
Author(s):  
I. Nathanson ◽  
J. H. Widdicombe ◽  
P. J. Barnes
Keyword(s):  
Epithelial Cells ◽  
Vasoactive Intestinal Peptide ◽  
Short Circuit ◽  
Statistical Significance ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Tracheal Epithelium ◽  
Cl Secretion ◽  
High Affinity ◽  
Stimulation Of

Under short-circuit conditions, vasoactive intestinal peptide (VIP) did not alter net Na+ movement but selectively stimulated net Cl- secretion across dog tracheal epithelium with a high affinity (Km congruent to 10(-8) M). The increase in Cl- secretion was not different from the rise in short-circuit current (Isc). However, stimulation of Cl- secretion was not maximal, because the addition of isoproterenol (10(-6) M) to VIP-treated tissues further increased the Isc by 54%. The effect of exogenous VIP was not blocked by a combination of atropine, phentolamine, propranolol (10(-5) or 10(-6) M), or tetrodotoxin (10(-6) M). Under open-circuit conditions, VIP caused an increase in the net secretion of Cl- and Na+, but the changes did not reach statistical significance. We conclude that VIP acts directly on receptors on the surface of epithelial cells to stimulate active Cl- secretion. The abundance of VIP nerves in the submucosa suggests that VIP may be important in regulation of fluid movement across the epithelium.

Effects of amino acids on chloride transport in Aplysia intestine

1981 ◽  
Vol 240 (1) ◽  
pp. R61-R69 ◽  
Author(s):  
G. A. Gerencser
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Electrical Characteristics ◽  
Glucose Stimulation ◽  
Flux Measurements ◽  
Short Circuit Currents ◽  
Stimulation Of

This investigation was principally undertaken to examine the mechanism by which organic solutes (amino acids) stimulate chloride transport across the Aplysia californica intestine. Isolated intestine, mounted between identical oxygenated seawater solutions, maintained stable transmural potential differences (serosa negative) and short-circuit currents for several hours at 25 degrees C. The addition of glycine to the mucosal solution stimulated rapid sustained increases in these electrical characteristics. The change in short-circuit increased curvilinearly with increasing concentrations of mucosal glycine. Mucosal glycine stimulated transmural potential difference and short-circuit current after mucosal phlorizin had partially inhibited D-glucose stimulation of the electrical characteristics. Mucosal glycine enhanced the transmural electrical characteristics. Mucosal glycine enhanced the transmural electrical characteristics after serosal ouabain had abolished them. The major portion of the amino acid-induced short-circuit current was carried by a net, active, chloride transfer from mucosa to serosa as determined by flux measurements. These results suggest that the amino acid-induced effect on chloride transport is mediated by a common mucosal membrane carrier for both sodium and the amino acid.

Role of calcium in mediating action of carbachol in T84 cells

1989 ◽  
Vol 257 (5) ◽  
pp. C976-C985 ◽  
Author(s):  
S. M. Wong ◽  
R. P. Lindeman ◽  
S. Parangi ◽  
H. S. Chase
Keyword(s):  
Transport Process ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
T84 Cells ◽  
Calcium Buffer ◽  
Relative Value ◽  
Induced Changes ◽  
Stimulation Of

To examine the role of calcium in mediating carbachol's action in secretory epithelia, we simultaneously measured intracellular free [Ca] [( Ca]i) and transepithelial chloride transport in T84 cells grown on collagen-coated filters. [Ca]i was measured with fura-2 and fluorescence microscopy and expressed as a relative value [( Ca]'i) normalized to control. Chloride transport was measured as the short-circuit current (Isc) with a voltage clamp. Monolayers were pretreated with cyclic AMP to augment the response of Isc to carbachol, a procedure that did not qualitatively change the response of the monolayer to carbachol. The carbachol-induced changes in Isc appeared to be dependent on the increase in [Ca]i. First, carbachol caused both Isc and [Ca]'i to increase in parallel. Isc increased from 32 +/- 5 to 70 +/- 9 microA and then declined to 57 +/- 16 microA while [Ca]'i increased from 72 +/- 14 to 156 +/- 22 nM and then declined to 133 +/- 45 nM. Second, the carbachol-induced increases in Isc and [Ca]'i were correlated. The greater the hormone-stimulated rise in [Ca]'i, the higher the increase in Isc. Third, carbachol's stimulation of Isc was blunted by preventing the calcium spike with the cellular calcium buffer 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetic acid (BAPTA). Although the carbachol-induced increase in [Ca]'i appeared necessary for the increase in Isc, it was not clear if carbachol's action was solely the result of an increase in [Ca]'i. Increasing [Ca]'i with ionomycin, although causing Isc and [Ca]'i to increase in parallel, failed to increase Isc to the levels observed with carbachol. These experiments suggest that although the carbachol-induced increase in Isc is dependent on the increase in [Ca]i, the hormone may activate a second process that increases the sensitivity of the calcium-activated transport process to changes in [Ca]i.

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