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PubMed1966

The origin of the glucose dependent increase in the potential difference across the tortoise small intestine.

1. Experiments were carried out to investigate the origin of the glucose dependent increase in the potential difference (p.d.) across the isolated intestinal mucosa of the tortoise.2. In addition to glucose, galactose, alpha-methyl glucoside, 3-0-methyl glucopyranose and sucrose also increased the transepithelial potential difference. There was no increase with either fructose or mannose.3. The use of micro-electrodes demonstrated that the change in the p.d. due to the presence of glucose was wholly accounted for by the increase in the p.d. across the serosal face of the epithelial cells.4. Diffusion potentials were produced across the isolated mucosa by varying the ionic composition of either the mucosal or serosal fluids. However, there was no reduction of the glucose dependent increase in the p.d. when the ionic concentration gradients across the serosal face of the cell were reversed.5. These results suggest that the increase in the p.d. associated with the active transfer of sugars across the small intestine was due to the presence of an electrogenic ion pump at the serosal face of the epithelial cell.

Journal Article↗
PubMed1972

Permeability of urinary bladder of Rana cancrivora to urea in the presence of oxytocin.

1. When Rana cancrivora collected from fresh water had been exposed for 3 days to saline solutions having osmolalities from 280 to 690 m-osmole/kg, urea concentrations in plasma and urine appeared to come into equilibrium, and were from 70 to 200 m-mole/l.2. Plasma urea level of fresh water R. cancrivora (48 m-mole/l.) was doubled (82 m-mole/l.) after 8 hr of exposure to 270 m-osmolal saline. It continued the same after 24 hr of exposure.3. When isolated urinary bladders of R. cancrivora were exposed to Ringer on the serosal aspect and one-fifth Ringer on the mucosal aspect, then in response to this osmotic difference of 190 m-osmole/kg, the rate of fluid movement (mucosa to serosa), which was 10.3(+/-2) mul./cm(2).hr, was not significantly altered when up to 60% of the NaCl of the Ringer solution was substituted by urea.4. Under the same circumstances, when oxytocin (50 m-u./ml.) was present in the serosal solution, the rate of fluid movement (mucosa to serosa) was 133.2(+/-7.9) mul./cm(2).hr in the absence of urea; it was progressively decreased by the presence of urea until, when 80% of the NaCl had been substituted by urea, the rate of fluid movement was reduced to 14.5(+/-4.0) mul./cm(2).hr.5. The diminished rate of fluid movement under the above circumstances could not be correlated with serosal urea concentration, with serosal availability of Na(+), nor with Na(+) concentration difference across the bladder wall. It appeared to be directly related to the ;non-urea osmotic difference' across the bladder wall provided by solutes other than urea.6. When isolated bladders were exposed to an osmotic difference of 190 m-osmole/kg, but having 25 mM urea present in the mucosal solution, then fluid moved from mucosa to serosa at a rate of 10.4(+/-1.3) mul./cm(2).hr in the absence of oxytocin and 124(+/-9) mul./cm(2).hr when oxytocin (50 m-u./ml.) was present. In the former case no urea passed across the bladder wall, but in the latter case urea passed from mucosa to serosa at a rate of 3.16(+/-0.3) mumole/cm(2).hr. The fluid moving from mucosa to serosa thus contained urea 25.5 m-mole/l.7. Vasotocin (10(-9)M), which is equipotent with oxytocin (50 m-u./ml.) in affecting permeability of the isolated urinary bladder to water, was also equipotent in producing a reduced rate of water fluid movement in the presence of 40% urea (vasotocin, 63 mul./cm(2).hr; oxytocin, 59 mul./cm(2).hr).8. When groups of frogs were cystectomized, and other groups of frogs were sham-operated, then after 48 hr of exposure to fresh water or to 300 m-osmolal saline the sham-operated frogs had plasma urea level raised from 20 m-mole/l. (fresh water) to 42 m-mole/l. (saline), while the cystectomized frogs had 20 m-mole/l. (fresh water) and 26 m-mole/l. (saline).9. The hypothesis is presented that hormone-induced permeability of the urinary bladder to urea contributes to the immediate adjustment of plasma urea level by which R. cancrivora survives when exposed to high environmental salinity.

Animals↗
PubMed1974

Active transport of iodide and other anions across the choroid plexus.

1. An in vitro preparation of the frog choroid plexus was used to study mechanisms of anion transport.2. It was observed that, in the absence of electrochemical potential gradients, there were net fluxes of I(-), SCN(-), TcO(4) (-), and Br(-) across the plexus, from the ventricular to the serosal surface. The net flux of I(-) reached a maximum at a concentration of 250 muM.3. On the basis of competition effects it was concluded that the affinity of the transport process for anions was: ClO(4) > ReO(4) approximately BF(4) > SCN approximately SeCN > I > NO(3) > Br > Cl.4. Ouabain, oligomycin, phloretin and 2,4-DNP inhibited the net transport of anions, but phlorrhizin, furosemide, 2,4,6-trinitro-m-cresolate, reducing agents, and antithyroid agents did not. Ouabain and phloretin were only effective on the ventricular side of the preparation.5. Anion transport required the presence of both Na and K. The requirement for Na was specific, but Rb, and to a lesser extent Cs, could substitute for K. Na in either the ventricular or the serosal fluids could partially stimulate anion transport, but K was only effective in the ventricular solution.6. TcO(4) (-), SCN(-) and I(-) were accumulated within the choroidal epithelium from the ventricular fluid, but not from the serosal fluid. Accumulation was inhibited by ouabain and ClO(4) (-).7. The unidirectional influx of I(-) across the apical cell membrane was about an order of magnitude greater than the flux across the epithelium. This flux was inhibited by ClO(4) (-), ouabain, and Na-free solutions.8. These experiments suggest the following mechanism for anion transport across the plexus: anions are actively transported into the epithelium, by a ouabain sensitive, Na/K dependent pump located in the brush border membrane. The anions are accumulated within the epithelium, and, finally, they pass into the serosal fluid down their electrochemical potential gradient. Relations between anion transport, Na/K transport, and Na/K ATPases are discussed.

Adenosine Triphosphatases↗
PubMed1977

Sucrose absorption by the rat small intestine in vivo and in vitro.

1. The absorption of glucose and fructose derived from sucrose has been studied using in vitro and in vivo loops of the rat jejunum.2. At low sucrose concentrations (1 and 10 mM) glucose appeared in the serosal compartment of the in vitro preparation at a faster rate than fructose, but at high sucrose concentrations (50 and 100 mM) the rates of serosal transfer of the two sugars were similar. Glucose and fructose appeared in the mucosal compartment, with the rate of fructose appearance exceeding that of glucose, at all the sucrose concentrations studied.3. Phlorizin (5 x 10(-5)M) added to the mucosal medium of the in vitro preparation abolished the serosal transfer of glucose derived from 50 mM sucrose, and reduced that of fructose by 75%.4. In the absence of sodium ions, the in vitro preparation failed to transfer glucose and fructose derived from 50 mM sucrose, into the serosal compartment.5. Glucose was actively accumulated in the whole gut wall of the in vivo preparation to concentrations higher than those in the plasma at 50 and 100 mM, but not at 10 mM sucrose concentrations. Fructose was also actively accumulated to about half the extent of glucose, but reached tissue concentrations greater than those in the plasma, at each sucrose concentration.6. The whole wall concentrations of glucose and fructose derived from sucrose added to the lumen continued to rise when the blood supply to the in vivo preparation was terminated.7. No increase in the in vivo whole wall concentrations of glucose and fructose were detected when sucrose was added to the lumen together with concentrations of glucose sufficient to saturate the monosaccharide transport systems.8. The results favour the view that disaccharide hydrolysis and resulting hexose transfer are sequential, separate events.

Animals↗
PubMed1978

Functional distinction between two transport mechanisms in rabbit gall-bladder epithelium by use of ouabain, ethacrynic acid and metabolic inhibitors.

1. Net fluid transport rate, transepithelial p.d. and resistance, and unidirectional Na+-fluxes were measured in rabbit gall-bladder preparations exposed on both sides to bicarbonate-Ringer solution in vitro. 2. Both ouabain and ethacrynic acid (ETCA) caused dose-dependent decreases of net fluid transport rate; ouabain inhibited fluid transport predominantly from the serosal side, whereas the inhibitory effect of ETCA was elicited mainly from the mucosal (luminal) side. Applied bilaterally, the ID50 for ouabain was 2.5 X 10(-6) M, and for ETCA 2.3 X 10(-4) M. After maximal inhibition at each concentration level of the two inhibitors fluid transport could not be reversed. 3. 2,4-Dinitrophenol (2,4-DNP) (2 X 10(-4) M) or substitution of O2 by N2 caused an 80% reversible decrease of net fluid transport. 4. The spontaneous p.d. across the rabbit gall-bladder was about 2.7 mV, mucosal side positive. 2,4-DNP, N2 and serosal application of ouabain depressed the p.d. after an initial hyperpolarization. This decrease was reversible during recovery from 2,4-DNP and N2, but irreversible after removal of ouabain at concentrations greater than or equal to 10(-4) M. Mucosal application of ETCA (10(-3) M) caused no decrease in p.d., which actually increased slightly. 5. Calculated passive serosal-to-mucosal Na+-fluxes changed in the same direction as did changes in conductance. 6. It is concluded that ETCA does not interfere primarily with the Na-K-ATPase or cellular oxidative metabolism. The data support the proposal that the pump responsible for isosmotic transepithelial fluid transfer is located in the luminal end of the cells. This pump is ETCA-sensitive. The ATPase-dependent Na-K pump, which can be inhibited by ouabain, is localized in the serosa-facing cell membrane. The data suggest that the inhibition of net fluid transport by ouabain is indirect and mediated by changes in intracellular ion concentrations. 7. The results support the concept that the transepithelial fluid transport mechanism is electroneutral, and suggest that the mucosa positive transepithelial p.d. is due to differences in electromotive forces arising from ion (mainly K+) diffusion across the mucosal and serosal cell membranes.

Animals↗
PubMed1979

Fluid movements across rabbit ileum coupled to passive paracellular ion movements.

1. Theophylline (10 mM) and choleragen (1 x 10(-6) g ml.-1) abolish net fluid absorption by everted sacs of rabbit ileum. Triaminopyrimidine (20 mM) and ethacrynate (0.1 mM) prevent this inhibition of net fluid movement. Replacing Ringer Cl- with isethionate prevents the theophylline-dependent decrease in fluid absorption also. 2. Ouabain (0.1 mM) abolishes net fluid movements in both control and theophylline-treated tissue. 3. With ouabain present, hypertonic NaCl (200 mM) in the mucosal solution causes net fluid secretion (serosal-mucosal flux). With theophylline added to both the mucosal and serosal solution, net fluid absorption (mucosal-serosal flux) is observed (P less than 0.001). Triaminopyrimidine (20 mM), or ethacrynate (0.1 mM), or replacement of Ringer Na+ with choline, or Ringer Cl- with isethionate all prevent the theophylline-induced reversal of osmotic flow. 4. Theophylline increases passive net flux of Na+ and Cl- from mucosal solution containing hypertonic (200 mM) NaCl+ ouabain (0.1 mM) across sheets of ileum into serosal solution containing mannitol Ringer + ouabain. The increased passive Na+ flux is blocked by triaminopyrimidine and the increased Na+ and Cl- fluxes are blocked by ethacrynate (0.1 mM). 5. The suggested route of increased NaCl leakage is via the paracellular pathway as it is inhibited by triaminopyrimidine. The increase, itself, is a consequence of the increased passive permeability of the mucosal border to Cl-, induced by theophylline or choleragen. Water is apparently electro-osmotically coupled to the paracellular Na+ leakage (100 mole water mole-1 Na+), hence increased passive leakage reverses osmotic flow. In active tissue the lateral intercellular space contains hypertonic NaCl, and hence increased leakage of NaCl across the tight-junction in theophylline or choleragen-treated tissue gives rise to net fluid secretion.

Animals↗
PubMed1980

Delayed development of amiloride-sensitive sodium transport in lamb distal colon.

1. Na transport has been measured in vitro across distal colons taken from fetal and early post-natal lambs. 2. The mucosal to serosal Na flux fell by half during the first three weeks of post-natal life. Similar falls were recorded for measured short-circuit current and open-circuit voltage. The net transport of Na, measured isotopically at all stages of development, corresponded approximately to that calculated from measurements of short-circuit current. 3. The serosal to mucosal flux of Na was approximately half the mucosal to serosal flux at all stages in development. 4. Amiloride affected neither the short-circuit current nor the mucosal to serosal flux of Na measured during the first five days of post-natal life. The short-circuit current of an increasing proportion of distal colons (30-70%) began to show some sensitivity to amiloride during the second to third week of post-natal life. Sensitivity of the short-circuit to inhibition by amiloride appeared to be fully developed in the 8-week-old lamb colon. 5. The serum concentration of aldosterone was high at birth. It then fell rapidly to levels approaching those found in fetuses in the last week of pregnancy. The serum concentration of cortisol was two orders of magnitude higher than for aldosterone. Changes in cortisol concentration during development paralleled those for aldosterone. 6. There appears to be no aldosterone-induced change in Na transport across lamb distal colon during the first week of post-natal development. Comparisons are made between this situation and that found in the neonatal pig, where aldosterone acts to increase Na reabsorption immediately after birth. Possible reasons for this species difference are discussed.

Aldosterone↗
PubMed1983

Relationship between intestinal motility, tone, water absorption and lymph flow in the rat.

The relations between motility, tone, water absorption rate (Jv) and lymph flow (J1), were studied in an exteriorized upper jejunal preparation in vivo, with its serosal side bathed in Krebs-Ringer or other solutions. Neither Jv nor J1 was correlated with motility. When the luminal fluid consisted of an isotonic solution of MgSO4, glucose or LiCl, motility was greatly increased with no increase in J1. When the serosal fluid consisted of an isotonic solution of mannitol, glucose or MgSO4, motility was depressed with a large decrease in tone, and Jv was increased by 51-83% with a decrease in J1. When the serosal fluid consisted of an isotonic solution of NaCl, Na2SO4, LiCl or KCl, motility was decreased with either no change or an increase in tone, and both Jv and J1 were much decreased. When isotonic choline Cl solution was employed as the serosal fluid, motility increased with an increase in tone, Jv became negative (fluid secretion), and J1 decreased to 0. Acetylcholine depressed motility but increased tone with a decrease in Jv and J1. Eserine increased both tone and motility with a decrease in Jv and J1. Serotonin caused no change in motility but increased tone with a decrease in Jv and J1. Noradrenaline and adrenaline depressed motility and reduced tone with an increase in Jv and J1. Isoprenaline abolished motility and reduced tone with a large increase in Jv but no change in J1. Pentobarbitone depressed motility and reduced tone with an increase in Jv but a decrease in J1. It is concluded that the intestine responds to various stimuli with a change in motility, or tone, or both. Intestinal motility per se does not produce lymph. Since an increase or decrease in tone always results in a decrease or increase in Jv, respectively, regardless of the nature of the conditions, a relaxation of the intestinal musculature appears to be associated with an increase in water absorption.

Adrenergic beta-Agonists↗
PubMed1984

Stimulation of electrolyte secretion in rabbit colon by adenosine.

Serosal addition of adenosine after inhibition of adenosine deaminase with deoxycoformycin increases short-circuit current (Isc) and tissue conductance of isolated epithelia of rabbit descending colon. In the presence of Cl this increase in Isc results from a reversal of electrically neutral Cl absorption to rheogenic Cl secretion. When Cl is absent the stimulating effect of adenosine on Isc is reduced to one-third and appears to be brought about by HCO3 secretion. Under all conditions active Na transport remains unaltered. Adenosine-induced electrolyte secretion is markedly decreased by serosal addition of furosemide and depends on the presence of Na on the serosal side of the tissue. The stoichiometry of the interaction of Na and Cl with the basolateral Cl entry mechanism appears to be 1:1. Under Na-free conditions adenosine elicits a current transient which is carried by Cl ions and which is not inhibited by furosemide. Hence this current transient seems to be brought about by rheogenic apical Cl efflux. All these findings suggest that the conductive step in transepithelial Cl secretion resides in the apical membrane. Hyperpolarization of the Na-transporting cells by luminal addition of amiloride does not enhance electrolyte secretion. The site of action of adenosine is the extracellular surface of the basolateral membrane, because (a) luminal addition of adenosine is ineffective, (b) nitrobenzylmercaptopurineriboside, a blocker of cellular nucleoside uptake, augments the effect of serosal adenosine, and (c) the intracellular metabolites of adenosine do not mediate the effect. From the rank-order of potency of adenosine and its analogues 5'-N-ethylcarboxamide adenosine and N6-cyclohexyladenosine it is concluded that the adenosine receptors involved in electrolyte secretion are of the Ra subtype. Theophylline partially inhibits the secretory effect. The intracellular mediator of adenosine appears to be cyclic AMP and/or cyclic GMP, since the tissue levels of both compounds are rapidly elevated after addition of adenosine and both cyclic AMP and cyclic 8-bromo-GMP are able to mimic the adenosine action.

Adenosine↗
PubMed1986

Acid secretion through the Rana esculenta skin: involvement of an anion-exchange mechanism at the basolateral membrane.

Kinetic and electrophysiological studies were carried out to characterize the efflux of HCO3- (or OH-) across the basolateral membrane of the proton-secreting cells of the frog skin epithelium bathed with dilute saline mucosal solutions. In control conditions, the acidification of the mucosal solution (JnH+) was correlated directly with serosal alkalinization. Cl- substitution in the serosal Ringer (by gluconate or methylsulphate ions) induced an inhibition of proton excretion (70% inhibition). Measurements of the basolateral membrane potential with conventional micro-electrodes and of cell Cl- activity (aCli) and proton activity with double-barrelled ion-sensitive micro-electrodes recorded a basolateral membrane depolarization of 5.1 +/- 0.7 mV (n = 12), a decrease in aCli from 14.5 +/- 1.6 mequiv l-1 to 1.8 +/- 0.3 mequiv l-1 (n = 12), and a cell pH increase from 7.18 +/- 0.04 to 7.32 +/- 0.06 (n = 12) after serosal Cl- replacement. 4,4'-diisothiocyanostilbene-2-2'-disulphonic acid (DIDS) (10(-4) M) and meclofenamate (5 X 10(-5) M) inhibit JHn+ by 34% and 53% respectively whereas bumetanide did not block JHn+. Depolarization of the basolateral membrane (2 mM-Ba2+ addition to the serosal solution) did not block proton excretion. We show that cell Cl- activity is maintained at a higher level than that predicted by the equilibrium potential, by a mechanism located at the basolateral membrane of the epithelium since the apical solution was Cl(-)-free. This mechanism is not sensitive to potential changes at the basolateral membrane in the range tested. An electroneutral Cl(-)-HCO3- exchange mechanism is the simplest hypothesis which can account for our results.

Animals↗
PubMed1989

The specificity of pyrimidine nucleoside transport and metabolism by rat jejunum in vitro.

1. 5-Methyluridine perfused through the lumen of isolated loops of rat jejunum gave rise to serosal thymine as the major species transported across the epithelial layer; no serosal 5-methyluridine was detected. 2. At 0.1 mM-luminal 5-methyluridine there was enhanced transmural transport of thymine (P less than 0.001) when compared with either 0.1 mM-thymine or 0.1 mM-thymidine as the luminal substrate for thymine transport. 3. At low luminal concentrations (0.025 mM) thymine was a significantly better substrate (P less than 0.001) for the transport of the free pyrimidine than either of the two nucleosides (thymidine or 5-methyluridine). 4. Luminal deoxyuridine gave rise to uracil as the major species appearing in the serosal secretion. High luminal concentrations of deoxyuridine (0.5 and 1.0 mM) gave rise to low levels of the nucleoside in the serosal fluid. 5. As a consequence of the specificity of the mucosal phosphorolysis the ribonucleosides are favoured over the deoxyribonucleosides as substrates for transmural pyrimidine transport.

Animals↗
PubMed1994

Enterotoxin Escherichia coli STa activates a nitric oxide-dependent myenteric plexus secretory reflex in the rat ileum.

1. Mucosally added enterotoxin Escherichia coli STa increased the electrogenic Cl- secretion measured as the short-circuit current (Isc) across isolated muscle-stripped and muscle-unstripped rat mid-ilea incubated in vitro. 2. Pretreatment with serosal L-NAME (N omega-nitro-L-arginine methyl ester) or tetrodotoxin (TTX) significantly reduced the maximum Isc and the duration of action of STa in the unstripped but not stripped ilea. D-NAME (serosal), indomethacin or 5-hydroxy-tryptamine-desensitization was ineffective on STa-induced Isc in either stripped or unstripped ilea. 3. Serosal capsaicin reduced the maximum Isc of STa and its duration of action in unstripped ilea. 4. L-Arginine induced a significantly larger increase in the Isc across unstripped ilea than across stripped ilea; this could be significantly reduced by serosal L-NAME or TTX, although these were ineffective in stripped ilea. 5. Pretreatment of anaesthetized rats with I.P. L-NAME suppressed the fluid secretion induced by luminal STa in ilea in vivo but had no effect on that induced by luminal carbachol. 6. Mucosal STa increased electrogenic Cl- secretion across intact rat ileum in vitro by activating a capsaicin-sensitive, nitric oxide-dependent myenteric plexus-mediated secretory reflex. The suppression by L-NAME of STa induced ileal fluid secretion in vivo probably involves the inhibition of this reflex.

Animals↗
PubMed1987

Regulation of intracellular pH in the stomach.

The following picture emerges from the relatively small literature concerned with pHi regulation in the stomach. Oxyntic cells have a H,K-ATPase at the luminal membrane and both Na+-H+ and Cl(-)-HCO3 exchangers at the serosal membrane. The intrinsic buffer capacity is 40-50 mM/pH. In the resting state, when the H, K-ATPase is inactive, pHi is 7.1. The Na+-H+ exchanger prevents acidic shifts of pHi, and the Cl(-)-HCO3 exchanger prevents alkaline shifts. The combined operation of the two appears to contribute directly to the net Cl- secretion (and short-circuit current) generated by resting OC. In the stimulated state, H+ secretion into the gland lumen via the H,K-ATPase increases, and Cl- movement across the serosal membrane via exchange for HCO3 doubles or triples; however, pHi remains roughly constant (delta pHi less than or equal to 0.1 units). The large increase in Cl- and HCO3 movement across the serosal membrane requires one (or all) of the following events: The anion exchanger changes its characteristics (Km or Vmax); [Cl-]i decreases; or other membrane mechanisms must be activated. Chief cells also have a pHi of 7.1 and a Bi of 40-50 mM/pH. They exhibit Na+-dependent and Cl(-)-dependent changes of pHi that are consistent with the presence of both Na+-H+ and Cl(-)-HCO3 exchangers. The Na+-dependent changes of pHi are larger and the Cl(-)-dependent changes are smaller in CC than in OC. Surface cells exhibit changes of AO fluorescence that indicate that there is a Na+-H+ exchanger and a HCO3 conductance. The H+ permeability of the luminal membranes of all cells is very low, while that of the serosal membrane (via the cation and anion exchangers) is high.

Animals↗
PubMed2005

T staging of gastric cancer: role of multi-detector row CT.

PURPOSE: To evaluate retrospectively the accuracy of multi-detector row computed tomography (CT) in the assessment of serosal invasion in patients with gastric cancer. MATERIALS AND METHODS: The Ethics Committee does not require approval or informed consent for retrospective studies. Forty-one consecutive patients (24 men, 17 women; mean age, 68 years) with gastric cancer were included in this study. All patients were given 600 mL of tap water to drink and were positioned prone or supine on the scanning table. The detector row configuration included four detector rows, a section thickness of 1.25 mm, a pitch of 6, and a reconstruction interval of 0.63 mm. Transverse and multiplanar reconstruction images were simultaneously evaluated by two independent observers to assess the depth of tumor invasion in the gastric wall (ie, T stage). T staging at multi-detector row CT was compared with T staging at histologic evaluation (reference standard), which was performed by means of surgical or histologic examination of the resected specimen. We also calculated the sensitivity, specificity, and accuracy of multi-detector row CT for each observer in the assessment of serosal invasion. RESULTS: Analysis of interobserver agreement showed substantial or almost perfect agreement (nonweighted kappa value of 0.78 and weighted kappa value of 0.85). Correct assessment of gastric wall invasion was 80% and 85% for observers 1 and 2, respectively. The sensitivity, specificity, and accuracy of multi-detector row CT in the assessment of serosal invasion were 90%, 95%, and 93%, respectively, for observer 1 and 80%, 97%, and 93%, respectively, for observer 2. Overstaging occurred in six patients, and understaging occurred in five patients. All understaged tumors were scirrhous subtype gastric cancer. CONCLUSION: Multi-detector row CT scanning of patients with gastric cancer gave 93% accuracy in the assessment of serosal invasion in patients with gastric cancer.

Adult↗
PubMed1984

Chloride movement across basolateral membrane of Necturus gallbladder epithelium.

The relative Cl- and K+ sensitivity of the basolateral membrane potential of the in vitro Necturus gallbladder epithelium was determined. Tissues were punctured with two conventional glass microelectrodes to simultaneously measure the intracellular voltage (Vcs) and the voltage across the subepithelial connective tissue (Vse). Increasing the serosal K+ concentration from 2.5 to 25 mM caused a rapid monotonic depolarization of Vcs without changes of Vse. Reduction of serosal Cl- concentration (98 to 8 mM) caused a transient change of Vse. Thus the difference between Vcs and Vse more accurately reflected the basolateral membrane voltage (Vc) after Cl- concentration changes. The changes of Vc were small and biphasic in response to the decrease of serosal Cl- concentration. Perfusion of a low-ionic-strength solution in the mucosal chamber decreased the current that normally passes through the epithelium. Consistent with the notion that the basolateral voltage changes are attenuated by parallel pathways, the K+-induced depolarization increased by 80% under these conditions. The changes of Vc in response to Cl- substitutions were not different from those of tissue bathed in control solution. Thus the basolateral membrane voltage is relatively insensitive to changes of serosal Cl- concentration. I conclude that Cl- movement across the basolateral membrane is not attributable to simple electrodiffusion, and Cl- exit from these cells at this membrane must be electroneutral.

Animals↗
PubMed1985

Alpha 2-adrenergic receptor-mediated regulation of intestinal calcium transport.

The role of alpha 2-adrenergic receptors in the regulation of intestinal Ca2+ transport was studied in vitro in rabbit proximal colon and distal ileum. Unidirectional mucosal-to-serosal and serosal-to-mucosal fluxes (Jm----s and Js----m) of 45Ca2+ were measured across isolated mucosal sheets bathed on both sides with identical Ringer solutions (1.25 mM Ca2+) and short-circuited. In the proximal colon, mucosal-to-epithelial influx (Jm----e) of Ca2+ was also determined. Proximal colonic mucosa secreted Ca2+ (in nmol X h-1 X cm-2, Jm----s = 12.1 and Js----m = 42.2). Epinephrine (10 microM) abolished Ca2+ secretion (Jm----s = 24.1 and Js----m = 24.9) but did not affect Jm----e (21.4 in controls and 23.6 after epinephrine). These effects were mediated by alpha 2-adrenergic receptors: yohimbine abolished the effect of epinephrine, but prazosin and propranolol did not; furthermore, clonidine mimicked the effects of epinephrine, whereas methoxamine and isoproterenol had no effect. Ileal mucosa did not transport Ca2+ spontaneously; epinephrine (10 microM) increased Jm----s in the ileum without affecting Js----m, thereby stimulating net Ca2+ absorption. The mechanism for these alpha 2-receptor-mediated effects was examined in proximal colon. The effect of epinephrine on Jm----s was dependent on serosal Na+ but was unaffected by ouabain or the Na+-Ca2+ exchange inhibitor, benzamil. The effect of epinephrine on Js----m was dependent on serosal Na+ and was blocked by both ouabain and benzamil. In the absence of epinephrine benzamil did not alter Jm----s or Js----m.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1986

Active K transport across rabbit distal colon: relation to Na absorption and Cl secretion.

We measured isotopic unidirectional fluxes of K to elucidate the mechanisms of active K transport across the distal colon of the rabbit. Separate pathways for active K absorption and active K secretion were detected using various transport inhibitors and stimulators. The rate and direction of net K transport depend on the activities of these two pathways. K absorption was reduced by orthovanadate (both solutions) or serosal Ba, consistent with ATPase-dependent uptake of K across the apical membrane and exit via a Ba-sensitive basolateral K conductance. K secretion was inhibited by serosal ouabain or mucosal Ba, indicating that K secretion involves basolateral uptake via the Na-K pump and apical exit via a Ba-sensitive K conductance. Active K secretion appears to be electrogenic, since inhibition by ouabain produced equivalent changes in the net K flux and short-circuit current. Addition of bumetanide to the serosal solution or the removal of either Na or Cl from the serosal solution inhibited K secretion; mucosal solution amiloride was without effect. These results indicate that this K secretory process is independent of electrogenic Na absorption but is mechanistically similar to Cl secretory processes. Both epinephrine and prostaglandin E2 (PGE2) stimulate K secretion, but only PGE2 also stimulates Cl secretion. The response to these secretogogues suggests that the mechanisms underlying K and Cl secretion are closely linked but can be regulated independently.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1979

Drug uptake into everted intestinal sacs. II. Inhibition of secretion by hypertonicity.

Mucosal hypertonicity, metabolic inhibitors, or absence of glucose and oxygen enhance mucosal-to-serosal influx of the cationic drug, pralidoxime (PAM), into sacs of everted rat jejunum in vitro. Conversely, efflux of PAM, which is twice the influx rate, is inhibited by mucosal hypertonicity or cyanide and iodoacetate. When sacs containing PAM, 0.87 mM, and glucose, 10 mM, were placed in identical drug- and sugar-containing mediums, the inside (serosal) concentration of PAM fell by over half in 120 min, whereas that of glucose more than doubled. Mucosal hypertonicity depressed PAM efflux and glucose influx regardless of serosal osmolarity. Although azide and mucosal hypertonicity each depressed glucose uptake and oxygen consumption while accelerating net PAM influx, azide more effectively depressed glucose and oxygen uptake, whereas hypertonicity caused greater acceleration of PAM uptake. Hypertonicity did not affect PAM binding to intestinal tissue. Varying mucosal pH did not change PAM or glucose uptake. Thus, mucosal hypertonicity apparently enhances net mucosal-to-serosal transfer of PAM by blocking its active secretion from serosa to mucosa.

Animals↗