Gamma radiation affects active electrolyte transport by rabbit ileum: basal Na and Cl transport

1986 ◽  
Vol 250 (4) ◽  
pp. G540-G545 ◽  
Author(s):  
P. J. Gunter-Smith

The effect of whole-body gamma radiation (5-12 Gy) on electrolyte transport by rabbit ileum in vitro was assessed for 1-96 h postirradiation using the short-circuit technique and radioisotopic fluxes. Although there was no effect of radiation on short-circuit current (Isc), transepithelial potential, or resistance 1 h after exposure, by 24 h the basal parameters of ileal segments isolated from irradiated animals were significantly greater than those of sham-irradiated controls. The Isc increased in a dose-dependent fashion and was greatest 24 h postexposure. Isotope flux experiments revealed that the increased Isc following irradiation resulted in part from a stimulation of active serosal-to-mucosal net Cl flux. There was no observable change in net Na transport. The results demonstrate that radiation exposure alters cellular transport processes, which may contribute to the fluid and electrolyte imbalance observed following radiation exposure.

1980 ◽  
Vol 239 (6) ◽  
pp. G463-G472 ◽  
Author(s):  
M. Donowitz ◽  
Y. H. Tai ◽  
N. Asarkof

The effect of serotonin on active electrolyte transport was evaluated in vitro in epithelial sheets of rabbit ileum, gallbladder, and colon under short-circuited conditions. Serotonin added to the serosal surface of rabbit ileum caused a dose-dependent short-lived increase in short-circuit current and a more prolonged equal effect on net Na and Cl fluxes. The latter consisted primarily of inhibition of mucosal-to-serosal fluxes of both Na and Cl. In addition serosal serotonin decreased ileal Na influx from the mucosal solution into the epithelium, suggesting an effect on Na absorption. Serotonin did not alter all aspects of ileal absorptive function and did not affect glucose-dependent Na absorption. Consistent with serotonin acting by inhibiting NaCl absorption in the ileum, serotonin induced equal inhibition of net Na and Cl absorption in rabbit gallbladder (which has a linked Na and Cl absorptive process) but had no effect on rabbit colon (which lacks a linked Na and Cl absorptive process). In addition, adenosine 3',5'-cyclic monophosphate and serotonin both appeared to alter the same ileal NaCl absorptive process, since following stimulation of ileal secretion with the maximum concentration of theophylline, addition of serotonin did not cause any further effects.


Peptides ◽  
1994 ◽  
Vol 15 (8) ◽  
pp. 1431-1436 ◽  
Author(s):  
Fadia R. Homaidan ◽  
Shao Hua Tang ◽  
Mark Donowitz ◽  
Geoffrey W.G. Sharp

1983 ◽  
Vol 245 (5) ◽  
pp. G668-G675 ◽  
Author(s):  
E. S. Foster ◽  
T. W. Zimmerman ◽  
J. P. Hayslett ◽  
H. J. Binder

To determine the effect of corticosteroids on active transport processes, unidirectional fluxes of 22Na, 36Cl, and 42K were measured under short-circuit conditions across isolated stripped distal colonic mucosa of the rat in control, secondary hyperaldosterone, and dexamethasone-treated animals. In controls net sodium and chloride fluxes (JNanet and JClnet) and short-circuit current (Isc) were 6.6 +/- 2.2, 7.6 +/- 1.6, and 1.3 +/- 0.2 mu eq X h-1 X cm-2, respectively. Although aldosterone increased Isc to 7.3 +/- 0.5 mu eq X h-1 X cm-2, JNanet (6.9 +/- 0.7 mu eq X h-1 X cm-2) was not altered and JClnet was reduced to 0 compared with controls. Dexamethasone also stimulated Isc but did not inhibit JClnet. In Cl-free Ringer both aldosterone and dexamethasone produced significant and equal increases in JNanet and Isc. Theophylline abolished JNanet in control animals but not in the aldosterone group. Aldosterone reversed net potassium absorption (0.58 +/- 0.11 mu eq X h-1 X cm-2) to net potassium secretion (-0.94 +/- 0.08 mu eq X h-1 X cm-2). Dexamethasone reduced net potassium movement to 0 (-0.04 +/- 0.12 mu eq X h-1 X cm-2). These studies demonstrate that 1) corticosteroids stimulate electrogenic sodium absorption and 2) aldosterone, but not dexamethasone, inhibits neutral NaCl absorption and stimulates active potassium secretion. The effects of mineralocorticoids and glucocorticoids on electrolyte transport are not identical and may be mediated by separate and distinct mechanisms.


1975 ◽  
Vol 228 (6) ◽  
pp. 1808-1814 ◽  
Author(s):  
HN Nellans ◽  
RA Frizzell ◽  
SG Schultz

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.


1975 ◽  
Vol 229 (2) ◽  
pp. 438-443 ◽  
Author(s):  
DW Powell ◽  
SM Morris ◽  
DD Boyd

The nature of the transmural electrical potential difference and the characteristics of water and electrolyte transport by rabbit esophagus were determined with in vivo and in vitro studies. The potential difference of the perfused esophagus in vivo was -28 +/- 3 mV (lumen negative). In vitro the potential difference was -17.9 +/- 0.6 mV, the short-circuit current 12.9 +/- 0.6 muA/cm2, and the resistance 1,466 +/- 43 ohm-cm2. Net mucosal-to-serosal sodium transport from Ringer solution in the short-circuited esophagus in vitro accounted for 77% of the simultaneously measured short-circuit current and net serosal-to-mucosal chloride transport for 14%. Studies with bicarbonate-free, chloride-free, and bicarbonate-chloride-free solutions suggested that the net serosal-to mucosal transport of these two anions accounts for the short-circuit current not due to sodium absorption. The potential difference and short-circuit current were saturating functions of bathing solution sodium concentration and were inhibited by serosal ouabain and by amiloride. Thus active mucosal-to-serosal sodium transport is the major determinant of the potential difference and short-circuit current in this epithelium.


Gut ◽  
1998 ◽  
Vol 42 (2) ◽  
pp. 200-207 ◽  
Author(s):  
G K Collington ◽  
I W Booth ◽  
S Knutton

Background and aims—The pathophysiology of enteropathogenic Escherichia coli (EPEC) diarrhoea remains uncertain. EPEC adhere to enterocytes and transduce signals which produce a characteristic “attaching and effacing” (A/E) lesion in the brush border membrane. The present in vitro study was designed to determine whether signal transduction by EPEC also influences electrolyte transport.Methods—Caco-2 cell monolayers were rapidly infected with wild type EPEC strain E2348/69, or the signal transduction-defective mutant 14.2.1(1), and mounted in Ussing chambers.Results—Strain E2348/69 stimulated a rapid but transient increase in short circuit current (Isc) which coincided with A/E lesion formation; this Isc response was absent on infection with strain 14.2.1(1). While the initial rise inIsc induced by E2348/69 was partially (∼35%) dependent on chloride, the remainder possibly represents an influx of sodium and amino acid(s) across the apical membrane.Conclusions—The study directly shows that, after initial adhesion, EPEC induce major alterations in host cell electrolyte transport. The observed Isc responses indicate a rapid modulation of electrolyte transport in Caco-2 cells by EPEC, including stimulation of chloride secretion, for which signal transduction to host cells is a prerequisite.


1989 ◽  
Vol 77 (2) ◽  
pp. 161-166 ◽  
Author(s):  
K. J. Moriarty ◽  
N. B. Higgs ◽  
M. Woodford ◽  
L. A. Turnberg

1. Cholera toxin stimulates intestinal secretion in vitro by activation of mucosal adenylate cyclase. However, it has been proposed that cholera toxin promotes secretion in vivo mainly through an indirect mechanism involving enteric neural reflexes. 2. We examined this hypothesis further by studying the influence of neuronal blockade on cholera toxin-induced changes in fluid transport across rabbit ileum in vitro. Mucosa, stripped of muscle layers, was mounted in flux chambers and luminal application of crude cholera toxin (2 μg/ml) caused a delayed but sustained rise in the short-circuit current, electrical potential difference and Cl− secretion. Pretreatment with the nerve-blocking drug, tetrodotoxin (5 × 10−6 mol/l serosal side), failed to influence the secretory response to cholera toxin, and addition of tetrodotoxin at the peak response to cholera toxin also had no effect. 3. That tetrodotoxin could block neurally mediated secretagogues was confirmed by the demonstration that the electrical responses to neurotensin (10−7 mol/l and 10−8 mol/l) were blocked by tetrodotoxin (5 × 10−6 mol/l). Furthermore, the response to cholera toxin of segments of ileum, which included the myenteric, submucosal and mucosal nerve plexuses, was not inhibited by tetrodotoxin. 4. We conclude that cholera toxin-induced secretion in rabbit ileum in vitro is not mediated via a neurological mechanism.


1983 ◽  
Vol 245 (4) ◽  
pp. G562-G567 ◽  
Author(s):  
J. H. Sellin ◽  
R. C. DeSoignie

The effect of glucocorticoids on intestinal ion transport was studied in ileum in vitro from control and methylprednisolone (MP)-treated (40 mg im for 2 days) rabbits under the following conditions: a) basal rates of Na and Cl transport, b) the response to an individual absorptive stimulus (alanine, glucose, or epinephrine), and c) the response to a combination of the three absorptive stimuli. The results indicate that MP 1) increases basal absorption of Na and Cl and secretion of bicarbonate (as measured by residual ion flux), 2) does not alter the specific transport pathways stimulated by maximal doses of alanine, glucose, or epinephrine, but 3) significantly increases the absorptive capacity of ileum. After addition of combined alanine, glucose, and epinephrine, MP-treated ileum absorbed 15.8 mueq X cm-2 X h-1 Na (vs. 6.6 in controls, P less than 0.001) and 9.5 mueq X cm-2 X h-1 Cl (vs. 4.1 in controls, P less than 0.005). Additionally MP did not alter the Na dependence of either the short-circuit current or Cl absorption found in controls, although there appears to be a portion of residual ion flux insensitive to epinephrine inhibition. These data suggest that the MP-induced increase in absorptive capacity is due to an increase in a postapical transport step, most probably the Na pump.


2019 ◽  
Vol 76 (Suppl 1) ◽  
pp. A53.3-A54
Author(s):  
Minh Do ◽  
Avinash Ramkissoon ◽  
Colin Berriault ◽  
Paul Villeneuve ◽  
Paul Demers

Background and objectivesIncreases in leukemia risk after exposure to gamma radiation have been well-demonstrated among nuclear energy workers and atomic bomb survivors. Although uranium miners are also exposed to gamma radiation, its health effects are not well characterized, and assumed to be insignificant relative to the effects of radon decay products. The objective of this study is to quantify the effects of whole-body gamma radiation exposure on the incident risk of leukemia among Ontario Uranium Miners.MethodsBased on a retrospective cohort of 28 546 uranium miners, leukemia cases were identified through record linkages with the Canadian Cancer Registry and Canadian Mortality Database. Gamma doses were estimated through dose prediction models and badge dosimeter readings collated by the National Dose Registry, blinded from case status. Person-years at risk of leukemia were stratified by exposure category, calendar period of employment, and attained age at risk. Poisson regression was used to model the risk (RR) of incident leukemia at increasing levels of cumulative gamma radiation exposure, adjusting for calendar period and attained age.ResultsBetween 1969 and 2005, 116 incident cases of leukemia were identified. On average, these miners were employed for 4.4 years with a mean cumulative dose of 5.25 millisieverts (mSv). With exposure lagged by 2 years, preliminary analyses showed that when compared to the referent group (0 mSv), those with >30 mSv of cumulative gamma dose had a non-statistically significant increase in the risk of leukemia diagnosis (RR=2.04, 95% CI: 0.93, 4.51) with increasing, linear trend (p=0.08).ConclusionsAlthough our results did not show a statistically significant relationship between gamma radiation and leukemia incidence, it is likely due to low statistically power. Future work may include pooling the Ontario Uranium Miners cohort with other similar cohorts to better quantify the potential associated risks.


1982 ◽  
Vol 243 (1) ◽  
pp. G36-G41 ◽  
Author(s):  
S. Guandalini ◽  
M. C. Rao ◽  
P. L. Smith ◽  
M. Field

Diarrheagenic strains of Escherichia coli have been shown to produce a heat-stable enterotoxin (ST) that simulates guanylate cyclase, increases short-circuit current (Isc), and inhibits active Cl absorption in the intestine. In rabbit ileum, the ion transport effects are smaller than those produced by cAMP-related agonists. Because ST may be a selective cGMP agonist, we further explored its mode of action in rabbit ileum. ST inhibits net Na and net Cl absorption. ST also inhibits the same fraction of Cl influx across the brush border that theophylline inhibits. At maximal doses, ST and 8-bromo-cGMP (8-Br-cGMP) had nearly equal, nonadditive effects of Isc that were about 66% of that produced by 8-Br-cAMP. ST increased mucosal cGMP concentration 16-fold, whereas epinephrine, an inhibitor of secretion, increased cGMP concentration by only 30%. This is insufficient to alter ion transport because doses of ST that increased cGMP concentration by 100% failed to alter Cl fluxes. Furthermore, epinephrine did not increase cGMP concentration in isolated enterocytes. We conclude that 1) cGMP mediates ST effects on ion transport, and 2) although ST and cAMP-related agonists have the same antiabsorptive effects, ST is less effective in stimulating electrogenic Cl secretion.


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