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PubMed1988

Influence of prostaglandins on unidirectional zinc fluxes across the small intestine of the rat.

1. The regulatory role of prostaglandins (PGs) E2 and F2 alpha on the zinc transport rate across the jejunal segments of rats was examined by employing the Ussing chamber technique. The Zn flux rate from mucosa to serosa across jejunal segments (Jms) was 5.24 (SE 1.54) nmol/h per cm2 (n 48) and that from serosa to mucosa (Jsm) was 15.16 (SE 2.38) nmol/h per cm2 (n 48) when both sides of the segment were bathed with Ringer's bicarbonate solution containing 0.5 mM-zinc chloride and 3 mM-L-histidine. 2. When 5.0 or 50 microM of either PGE2 or PGF2 alpha were added to the serosal side of the tissue, Jsm generally decreased and Jms generally increased, compared with controls. On the other hand, when PGE2 or PGF2 alpha was added to the mucosal side of the tissue, Jms either did not change or increased while Jsm had a tendency to decrease. 3. The Zn uptake capacity of tissue increased significantly when PG was added to the serosal side of the tissue-bathing medium, but not when PG was added to the mucosal side. The uptake capacity of mucosal Zn by jejunal segments was approximately twice that of serosal Zn. 4. When PG was included in the tissue-bathing medium, the short-circuit current, potential difference and conductance between the mucosa- and serosa-bathing media generally decreased. 5. These results suggest that (a) PGs influence Zn flux rate not by chelating Zn and carrying it across the mucosal cell membrane but by interacting with the cytosolic components, (b) it is the serosal PGs which control the Zn flux rate and (c) PGs play a part in triggering a transduction mechanism in the intestinal Zn transport process.

Animals↗
PubMed2004

Apical sodium-glucose co-transport can be regulated by blood-borne glucose in the ruminal epithelium of sheep (Ovis aries, Merino breed).

The intestinal Na-dependent D-glucose co-transporter (SGLT)-1 in sheep is under dietary regulation by luminal substrates. The aim of the present study was to find out whether the SGLT-1 in the forestomach of sheep is also regulated by sugars. Furthermore, the location of a possible glucosensor (luminal v. intracellular v. basolateral) was to be elucidated. Ruminal epithelia of sheep (Ovis aries, Merino breed) were pre-incubated in Ussing chambers with various substrates on the mucosal (i.e. luminal) or serosal (i.e. blood) side. This pre-incubation period was followed by a second pre-incubation period without the tested substrates (washout period). Thereafter, apical D-glucose uptake by ruminal epithelial cells was determined with 200 mumol D-[(14)C]glucose/l in the absence or co-presence of the SGLT-1 inhibitor, phlorizin. Pre-incubation with D-glucose on the mucosal side had no significant effect on apical D-glucose uptake (P>0.05). In contrast, pre-incubation with D-glucose, D-mannose, 3-O-methyl-d-glucose or sucrose on the serosal side significantly increased D-glucose uptake compared with mannitol-treated controls (P<0.05). Serosal pre-incubation with cellobiose or D-xylose had no effect. The stimulation of d-glucose uptake by serosal D-glucose pre-incubation was concentration dependent, with maximal stimulation at about 10 mmol/l. We conclude that the ruminal SGLT-1 can be up-regulated in a concentration-dependent manner by blood-borne D-glucose via an extracellular sugar-sensing mechanism.

Animals↗
PubMed1975

Quantitation of conductance pathways in antral gastric mucosa.

The magnitude of cellular and shunt conductance of Necturus gastric antral mucosa was studied by (a) comparing the cellular PD response to transepithelial PD response during changes of ionic activity in the serosal bathing solution and (b) by measurement of current spread within the epithelial sheet. Using constant product KCl changes cellular resistance was 6,788 omegacm2 and shunt resistance was 1,803 omegacm2. Deletion of HCO3- from the serosal solution produced similar but quantitatively smaller changes in PD. Using HCO3- deletion cellular resistance was 7,338 omegacm2 and shunt resistance was 1,973 omegacm2. Measurement of current spead within the mucosa avoids changing ionic gradients yet gave very similar results; cellular resistance was 8,967 omegacm2 and shunt resistance was 2,947 omegacm2. The shunt contribution to transepithelial conductance ranged from 75.2 to 79.0%. Shunt selectivity was assessed using KCl dilution potentials, where mucosal dilution gave a small change in tissue PD compatible with an anion/cation selectivity ratio of 1.16 across the shunt, whereas serosal dilution effect was dominated by a PD change across the serosal membrane of the cell.

Animals↗
PubMed1980

Control of active proton transport in turtle urinary bladder by cell pH.

The rate of active H+ secretion (JH) across the luminal cell membrane of the turtle bladder decreases linearly with the chemical (delta pH) or electrical potential gradient (delta psi) against which secretion occurs. To examine the control of JH from the cell side of the pump, acid-base changes were imposed on the cellular compartment by increasing serosal[HCO3-] at constant PCO2 or by varying PCO2 at constant [HCO3-]. When serosal [HCO3-] was increased from 0 to 60 mM, cell [H+] decreased, as estimated by the 5,5-dimethyloxazoladine-2,4-dione method. JH was a saturable function of cell [H+], with an apparent Km of 25 nM. When PCO2 was varied between 1 and 20% at various serosal Km of 25 nM. When PCO2 was varied between 1 and 20% at various serosal [HCO3-], the PCO2 required to reach a maximal JH increased with [HCO3-] so that JH was a function of cell [H+] rather than of cell [HCO3-] or CO2. The proton pump was controlled asymmetrically with respect to the pH component of the electrochemical potential for protons, microH. On the cell side of the pump, a delta pH of < 1 U was required to vary JH between maximal and zero values, whereas on the luminal side a delta pH of 3 U was required. Cell [H+] regulates JH by determining the availability of H+ to the pump in a relationship resembling Michaelis-Menten kinetics. Increasing luminal [H+] generates an energy barrier at a luminal pH near 4.4 that equals the free energy (per H+ translocated) of the metabolic driving reaction.

Acid-Base Equilibrium↗
PubMed1981

Regulation of the sodium permeability of the luminal border of toad bladder by intracellular sodium and calcium: role of sodium-calcium exchange in the basolateral membrane.

Sodium movement across the luminal membrane of the toad bladder is the rate-limiting step for active transepithelial transport. Recent studies suggest that changes in intracellular sodium regulate the Na permeability of the luminal border, either directly or indirectly via increases in cell calcium induced by the high intracellular sodium. To test these proposals, we measured Na movement across the luminal membrane (th Na influx) and found that it is reduced when intracellular Na is increased by ouabain or by removal of external potassium. Removal of serosal sodium also reduced the influx, suggesting that the Na gradient across the serosal border rather than the cell Na concentration is the critical factor. Because in tissues such as muscle and nerve a steep transmembrane sodium gradient is necessary to maintain low cytosolic calcium, it is possible that a reduction in the sodium gradient in the toad bladder reduces luminal permeability by increasing the cell calcium activity. We found that the inhibition of the influx by ouabain or low serosal Na was prevented, in part, by removal of serosal calcium. To test for the existence of a sodium-calcium exchanger, we studied calcium transport in isolated basolateral membrane vesicles and found that calcium uptake was proportional to the outward directed sodium gradient. Uptake was not the result of a sodium diffusion potential. Calcium efflux from preloaded vesicles was accelerated by an inward directed sodium gradient. Preliminary kinetic analysis showed that the sodium gradient changes the Vmax but not the Km of calcium transport. These results suggest that the effect of intracellular sodium on the luminal sodium permeability is due to changes in intracellular calcium.

Animals↗
PubMed1987

Interactions of sodium transport, cell volume, and calcium in frog urinary bladder.

The volume of individual cells in intact frog urinary bladders was determined by quantitative microscopy and changes in volume were used to monitor the movement of solute across the basolateral membrane. When exposed to a serosal hyposmotic solution, the cells swell as expected for an osmometer, but then regulate their volume back to near control in a process that involves the loss of KCl. We show here that volume regulation is abolished by Ba++, which suggests that KCl movements are mediated by conductive channels for both ions. Volume regulation is also inhibited by removing Ca++ from the serosal perfusate, which suggests that the channels are activated by this cation. Previously, amiloride was observed to inhibit volume regulation: in this study, amiloride-inhibited, hyposmotically swollen cells lost volume when the Ca++ ionophore A23187 was added to Ca++-replete media. We attempted to effect volume changes under isosmotic conditions by suddenly inhibiting Na+ entry across the apical membrane with amiloride, or Na+ exit across the basolateral membrane with ouabain. Neither of these Na+ transport inhibitors produced the expected results. Amiloride, instead of causing a decrease in cell volume, had no effect, and ouabain, instead of causing cell swelling, caused cell shrinkage. However, increasing cell Ca++ with A23187, in both the absence and presence of amiloride, caused cells to lose volume, and Ca++-free Ringer's solution (serosal perfusate only) caused ouabain-blocked cells to swell. Finally, again under isosmotic conditions, removal of Na+ from the serosal perfusate caused a loss of volume from cells exposed to amiloride. These results strongly suggest that intracellular Ca++ mediates cell volume regulation by exerting a negative control on apical membrane Na+ permeability and a positive control on basolateral membrane K+ permeability. They also are compatible with the existence of a basolateral Na+/Ca++ exchanger.

Animals↗
PubMed1992

Electrophysiological effects of basolateral [Na+] in Necturus gallbladder epithelium.

In Necturus gallbladder epithelium, lowering serosal [Na+] ([Na+]s) reversibly hyperpolarized the basolateral cell membrane voltage (Vcs) and reduced the fractional resistance of the apical membrane (fRa). Previous results have suggested that there is no sizable basolateral Na+ conductance and that there are apical Ca(2+)-activated K+ channels. Here, we studied the mechanisms of the electrophysiological effects of lowering [Na+]s, in particular the possibility that an elevation in intracellular free [Ca2+] hyperpolarizes Vcs by increasing gK+. When [Na+]s was reduced from 100.5 to 10.5 mM (tetramethylammonium substitution), Vcs hyperpolarized from -68 +/- 2 to a peak value of -82 +/- 2 mV (P less than 0.001), and fRa decreased from 0.84 +/- 0.02 to 0.62 +/- 0.02 (P less than 0.001). Addition of 5 mM tetraethylammonium (TEA+) to the mucosal solution reduced both the hyperpolarization of Vcs and the change in fRa, whereas serosal addition of TEA+ had no effect. Ouabain (10(-4) M, serosal side) produced a small depolarization of Vcs and reduced the hyperpolarization upon lowering [Na+]s, without affecting the decrease in fRa. The effects of mucosal TEA+ and serosal ouabain were additive. Neither amiloride (10(-5) or 10(-3) M) nor tetrodotoxin (10(-6) M) had any effects on Vcs or fRa or on their responses to lowering [Na+]s, suggesting that basolateral Na+ channels do not contribute to the control membrane voltage or to the hyperpolarization upon lowering [Na+]s. The basolateral membrane depolarization upon elevating [K+]s was increased transiently during the hyperpolarization of Vcs upon lowering [Na+]s. Since cable analysis experiments show that basolateral membrane resistance increased, a decrease in basolateral Cl- conductance (gCl-) is the main cause of the increased K+ selectivity. Lowering [Na+]s increases intracellular free [Ca2+], which may be responsible for the increase in the apical membrane TEA(+)-sensitive gK+. We conclude that the decrease in fRa by lowering [Na+]s is mainly caused by an increase in intracellular free [Ca2+], which activates TEA(+)-sensitive maxi K+ channels at the apical membrane and decreases apical membrane resistance. The hyperpolarization of Vcs is due to increase in: (a) apical membrane gK+, (b) the contribution of the Na+ pump to Vcs, (c) basolateral membrane K+ selectivity (decreased gCl-), and (d) intraepithelial current flow brought about by a paracellular diffusion potential.

Amiloride↗
PubMed2002

Initial uptake and absorption of nonheme iron and absorption of heme iron in humans are unaffected by the addition of calcium as cheese to a meal with high iron bioavailability.

BACKGROUND: Quantitative data on the mucosal uptake and serosal transfer of nonheme-iron absorption in humans and the effects of calcium on these components are limited. OBJECTIVE: Our objective was to measure the initial mucosal uptake and the subsequent serosal transfer of nonheme iron and to determine the effects of adding calcium to a meal on both heme- and nonheme-iron retention. DESIGN: Whole-gut lavage and whole-body scintillation counting methods were applied to determine the 8-h uptake of nonheme iron and the 2-wk retention (absorption) of heme and nonheme iron in healthy adults (n = 17) after the consumption of meals of radiolabeled food. RESULTS: The initial uptake and absorption of nonheme iron were 11% and 7%, respectively, and the absorption of heme iron was 15%. Two-thirds of the nonheme iron taken up by the mucosa within 8 h was retained by the body after 2 wk (serosal transfer index: 0.63). Serum ferritin correlated inversely with the initial uptake and absorption of nonheme iron, but not with the nonheme serosal transfer index or the absorption of heme iron. Adding calcium (127 mg in cheese) to the meal did not affect absorption. CONCLUSIONS: On the basis of its association with serum ferritin, the initial mucosal uptake was the primary control point for nonheme-iron absorption. An apparent reduction in heme-iron absorption associated with the lavage procedure suggested that uptake of heme iron may take longer and proceed further through the intestine than that of nonheme iron. The absorption of both forms of iron was unaffected by the addition of cheese to this meal with high iron bioavailability.

Administration, Oral↗
PubMed2003

In-vitro and in-vivo histochemical and thermal studies using a thermal balloon endometrial ablation system for varying treatment times.

BACKGROUND: To assess the immediate zone of thermal necrosis (ZTN) using an enzyme histochemical staining technique and serosal temperatures for the Cavaterm endometrial balloon ablation system for different treatment times. METHODS: A thermal balloon ablation was performed initially post- (n = 6) and subsequently pre-hysterectomy (n = 15). Eight to 12 tissue blocks from each uterus were sectioned and stained using diaphorase respiratory enzyme techniques. Patients in the in-vivo group had temperature measurements taken from four serosal points, a myometrial gradient profile, the balloon surface and the endocervical canal. RESULTS: The serosal temperature sensors did not demonstrate any rise in temperature above 44.1 degrees C. The mean temperature at the anterior wall, posterior wall, fundus and cornual areas was 37.1 (SD 1.3), 36.8 (SD 1.0), 37.4 (SD 1.8) and 36.7 degrees C (SD 1.0), respectively. The immediate mean maximum ZTN was greatest for the 15-min treatment time (3.1 mm, SD 1.5) compared to the 10- and 7-min treatment times (3.0 mm, SD 1.4 and 2.2 mm, SD 0.7, respectively). The maximum ZTN recorded was 5.6 mm. No full thickness injuries were demonstrated either histochemically or suggested by the temperature studies. CONCLUSIONS: This study confirms that Cavaterm thermal balloon ablation produces a reproducible thermal injury without evidence of serosal heating. Results suggest that the treatment time could be reduced to 10-min with no detrimental effect on the clinical outcomes. This hypothesis is currently being evaluated by clinical trials.

Female↗
PubMed1981

Effect of carbenoxolone on alkaline secretion by isolated amphibian gastric and duodenal mucosa.

The influence of carbenoxolone sodium on HCO-3 transport has been examined in spontaneously alkalinizing amphibian antral (Necturus and Rana catesbeiana) and proximal duodenal (Rana catesbeiana) mucosa and in cimetidine-treated fundic mucosa (Rana temporaria) in vivo. Low concentrations of carbenoxolone (10(-6)-10(-4) mol/l, serosal side and 10(-5) mol/l, luminal side) did not affect the secretory rate or electrical properties of these tissues. In the stomach a higher concentration of carbenoxolone (10(-3) mol/l, serosal side) caused an immediate fall in transmucosal potential difference (PD) and electrical resistance. There was an initial decrease in the rate of HCO-3 transport followed by an increase in titratable alkalinization due to passive permeation of base from the serosal bathing solution. The non-steroidal anti-inflammatory agent ibuprofen (3 x 10(-3) mol/l, serosal side) inhibited alkaline secretion while the bile salt sodium taurocholate (10(-4) mol/l, luminal side) converted net alkaline secretion to a titratable acidity in cimetidine-treated fundus. Pretreatment of the mucosa with carbenoxolone (10(-4) mol/l) did not influence the response to taurocholate but when added with ibuprofen it potentiated the inhibitory effect of this drug on fundic alkaline secretion. In contrast, prostaglandin E2 (10(-6) mol/l) markedly reduced the inhibition of fundic alkaline secretion caused by ibuprofen. The anti-ulcer properties of carbenoxolone do not appear to be related to effects on gastroduodenal HCO-3 transport.

Animals↗
PubMed1990

Comparison of the basolateral K+ conductance of the epithelial cells in frog gastric fundus mucosa.

Frog stomach transepithelial potential difference (Vt) and resistance (Rt) as well as the voltage divider ratio (VDR) and serosal membrane potential (VS) of surface epithelial (SEC) and oxyntic (OC) cells were recorded at rest and during stimulation with histamine. Serosal membrane K+ permeability was tested by sudden elevation of serosal K+ concentration from 4 to 13 mmol l-1. Stimulation decreased both Vt and Rt and increased VDR of the OC (from 9.4 +/- SD 3.0 to 14.4 +/- 4.1, n = 10, P less than 0.001), while VS remained virtually unchanged (-66.3 +/- 4.5 mV, n = 10); in SEC, however, VDR as well as VS increased, the latter from -67.3 +/- 5.9 to -75.7 +/- 7.3 mV, n = 9, P less than 0.001. Elevation of serosal K+ reversibly diminished Vt and Vs in both cell types. The transepithelial response to K+ increased after stimulation. However, the cell potential response delta Vs,K increased only in the SEC (from +16.0 +/- 2.9 to +18.5 +/- 2.6 mV, n = 9, P less than 0.001) but not significantly in the OC. We conclude that in frog stomach both OC and SEC are stimulated by histamine: the SEC respond with a hyperpolarization, which reflects an increase in their basolateral K+ conductance; the OC do not respond with a hyperpolarization, possibly because histamine increases the basolateral membrane K+ conductance as well as other ion conductances which have not yet been identified.

Animals↗
PubMed1982

Kinins stimulate net chloride secretion by the rat colon.

1 Short circuit current (SCC), transepithelial conductance and ion fluxes were measured across the isolated descending colon of the rat in response to bradykinin or kallidin. 2 Kinins added to the serosal bath caused immediate increases in SCC but were ineffective when added to the mucosal bath. Increases in SCC were accompanied by significant increases in transepithelial conductance. Threshold kinin concentration was 0.5nM and maximal increases were seen at 50-100 nM. 3 A rat glandular kallikrein (7nM) or mellitin (2 microM) also increased SCC if added to the serosal bath. 4 Responses to kinins were unaffected by mucosal amiloride (100 micron) but attenuated or blocked by serosal frusemide (100 microM), indomethacin (1 microM) or mepacrine (50 microM). 5 Replacement of chloride ion in the serosal bath by gluconate and sulphate ions abolished responses to kinins which reappeared after chloride re-addition. 6 Measurement of 36Cl, 22Na and 86Rb fluxes across the tissue showed that the kinin-induced increase in SCC resulted principally from increased net chloride secretion. Effects upon 22Na or 86Rb flux were minimal and made no contribution to the current responses observed in this tissue. 7 The results prove that kinins stimulate net chloride secretion in the rat colon, most probably via a prostaglandin-dependent pathway.

Animals↗
PubMed1986

Neuropeptide Y: a powerful modulator of epithelial ion transport.

Neuropeptide Y (NPY) is a major gut peptide localized in the intestinal mucosa of several mammalian species. Ileal mucosa from rabbit and guinea-pig was mounted in Ussing chambers in order to study the effect of NPY on short circuit current. Neuropeptide Y inhibited the short circuit current when applied to the serosal side of the tissue. The maximum change in short circuit current was -50 +/- 6 microA cm-2 in the rabbit ileum and -49 +/- 14 microA cm-2 in the guinea-pig ileum. The EC50 was 3 X 10(-8) M in both species. Pretreatment of rabbit ileum with the alpha 2-adrenoceptor antagonist, yohimbine (1 X 10(-6) M) for 10 min did not reduce the response of the tissue to neuropeptide Y (1 X 10(-7) M). When applied serosally to rabbit ileal mucosa, the related peptide YY caused a maximum change in short circuit current of -60 +/- 13 microA cm-2; the EC50 was 2 X 10(-9) M. Isotopic flux studies in rabbit ileum showed that 1 X 10(-7) M neuropeptide Y enhanced mucosal-to-serosal Na+ and Cl- fluxes and reduced serosal-to-mucosal Cl- flux. Replacement of chloride with gluconate on both sides of the tissue significantly reduced the change in short circuit current produced by neuropeptide Y (1 X 10(-7) M), as did a similar replacement of bicarbonate. It is concluded that neuropeptide Y and peptide YY are the most potent neurotransmitters or hormones so far described in their ability to attenuate electrogenic transport in the small intestine.

Animals↗
PubMed1993

Absorption of insulin in the peritoneal cavity in a diabetic animal model.

This study was conducted to determine if different anatomical sites within the peritoneal cavity have different capacities for portal insulin absorption. Diabetic male Sprague-Dawley rats were studied. They were anesthetized and injected with streptozotocin. Blood glucose was measured before and after insulin (1 U/kg) was applied directly to the omentum, serosal surface of cecum, or parietal peritoneum or injected subcutaneously. In a control group, blood glucose was measured at intervals without administering insulin. In addition, insulin labeled with radioactive iodine (125I) was applied to the same three locations in the peritoneal cavity or injected intravenously. Animals were sacrificed at 1, 5, 15, or 30 mins, and radioactivity was measured in excised livers and in blood samples. Blood glucose in the omental group responded to insulin with a greater hypoglycemic effect than in the peritoneal and control groups. The percentage of radioactivity recovered in liver was significantly higher in the omental than in the serosal and peritoneal groups at 1 and 5 mins. The ratio of liver-to-blood radioactivity was also significantly higher in omental than in serosal and peritoneal groups and higher in the serosal than in the peritoneal group at 5 mins. The data suggest that, in this model, the omentum is a better site for insulin absorption than serosa or parietal peritoneum and that significant portal venous absorption of insulin occurs.

Animals↗
PubMed1982

Intestinal handling of bisacodyl and picosulphate by everted sacs of the rat jejunum and stripped colon.

Bisacodyl (BIS) is the acetic acid di-ester of the laxative diphenol 2-(4,4'-dihydroxydiphenyl)methyl-pyridine. A HPLC-method which permits the simultaneous determination of BIS and its monodesacetylated (MONO) as well as totally desacetylated (DES) form, has been used to study the intestinal handling of BIS (20 nmol/ml), when the compound was incubated for 60 min. at the mucosal side of the preparations specified. In the jejunal mucosal fluid, BIS disappeared completely in short time, and there was a nearly equivalent rise in DES. MONO was transitory present. Hydrolysis was also rapid in mucosal fluid which had been in contact with jejunal sacs for 30 sec., but BIS was stable in blank incubations. Hydrolysis of BIS was slower by colonic than by jejunal sacs, and all three molecular forms were present during incubation. It seemed still slower in mucosal fluid which had been in contact with colonic sacs for 5 min. BIS just as DES accumulated in the jejunal and colonic serosal fluid mainly as conjugates (greater than 95%), and DES was in all cases the only unconjugated metabolite present. Drug accumulation in jejunal serosal fluid was the same whether BIS or DES was added. However, more drug seemed to accumulate on the serosal side of colonic sacs when incubated with BIS instead of DES. In similar experiments with picosulphate, which is the sulphuric acid di-ester analogue of BIS, free DES was not detected in the mucosal fluid during incubation. The amounts of laxative accumulating in the serosal fluid were less than 1/10 of those observed with BIS.

Animals↗
PubMed1984

Effects of standard diuretics and ortho-vanadate on sodium transport across isolated frog skin.

Frog (Rana temporaria) skins were studied in an Ussing type lucite chamber adapted to diminish tissue edge damage. The transepithelial electrical potential difference, short circuit current and direct current (DC) resistance of skins mounted in this chamber were 56, 20 and 24% higher, respectively, than those of skins mounted in a conventional chamber. Amiloride, triamterene, ouabain and ortho-vanadate inhibited short circuit current and net mucosal to serosal flux of 22Na. Amiloride and triamterene had rapid onsets of action and were effective only when administered to the mucosal (pond) side of the skin. Ouabain and ortho-vanadate had slower onsets of action and were effective only when administered to the serosal side of the skin. Steady state of effects of these drugs was not reached within the three-hour period of the experiments. The inhibitory effect of ortho-vanadate was blocked by adding a disulfonic stilbene derivative (DIDS) to the serosal side of the skin. Serosal prostaglandin E2 stimulated the short-circuit current and decreased the DC resistance. Thiazides, acetazolamide and loop diuretics had no effects on Na+ transport by frog skin. Thus, frog skin seems to be a useful model only in studies of the mode of action and the structure-activity relationship of diuretic which act by inhibiting sodium entry or Na+-K+-ATPase activity.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1980

The role of bicarbonate ions and of adenosine 3',5'-monophosphate (cAMP) in chloride transport by epithelial cells of bullfrog small intestine.

In an HCO3-free medium, isolated segments of bullfrog small intestine, stripped of their external muscle layers, displayed a small, serosal positive PD that did not, on the average, differ significantly from zero. Similarly, in this medium, the mean values of Isc and of net Na+ and Cl- absorption under short-circuit conditions did not differ significantly from zero. External HCO3- (25 mM) induced a highly significant serosal negative PD and Isc and a large net absorption of Cl-. Net Cl- absorption exceeded Isc, i.e., there was a significant net flux, JR, which was consistent with a net secretion of HCO3-. The ratio of the internal Cl-activity of the absorptive cells (alpha Cli) to its equilibrium value was larger in the presence than in the absence of HCO3-. In the presence of HCO3-, cAMP, added to the serosal medium, reversed the serosal negative PD and Isc, and inhibited, though it did not completely abolish, net Cl- absorption. JR was unchanged; tissue Cl- and alpha Cli were reduced, and tissue Na+ decreased and tissue K+ increased. When HCO3- and Cl- were removed from the bathing medium, the electrical response of the tissue to cAMP, though greatly attenuated, was not completely abolished. Under these conditions, cAMP induced a significant net Na+ absorption. A model for ion transport in the absorptive cells of the small intestine is proposed that is consistent with these findings.

Animals↗
PubMed1988

Flux of calcium across the sheep rumen wall in vivo and in vitro.

Experiments were carried out in vivo and in vitro to study the flux of Ca2+ across the sheep rumen wall. Buffer solutions with five different Ca2+ concentrations in the range 0.2-3.6 mmol l-1 were introduced into the isolated, emptied and washed reticulo-rumen for 1 h to determine Ca2+ net flux. Phosphate concentrations were either kept constant at 8 mmol l-1, or varied so as to maintain a constant phosphate/Ca2+ ratio of 2:1. Under both conditions there was a Ca2+ net secretion into the rumen at Ca2+ concentrations below approximately 1 mmol l-1 whereas Ca2+ net absorption occurred at higher Ca2+ concentrations and linearly increased with increasing Ca2+ concentrations. When phosphate concentrations were reduced to 4.3 and 0.6 mmol l-1 (Ca2+, 3 mmol l-1) Ca2+ net absorption was reduced by about 50% and completely abolished, respectively. The unidirectional (mucosal-to-serosal or serosal-to-mucosal) Ca fluxes in vitro, JCams and JCasm, were measured in Ussing chambers with computer-controlled voltage clamp. Under short-circuit current conditions (Ca2+ and phosphate, 2 mmol l-1) there was a significant net flux of Ca2+ from the mucosal to the serosal side. This net flux of Ca2+ was abolished when ouabain was added to the serosal solution, indicating that the unidirectional Ca2+ flux JCams and, hence, the net flux of Ca2+ was dependent upon active Na+ transport accomplished by the Na, K-ATPase system. Under voltage clamp conditions, the net flux of Ca2+ was greatly increased at a potential difference PD = -25 mV (serosa negative) but disappeared at PD = +25 mV (serosa positive). Analysis of the unidirectional Ca2+ fluxes JCams and JCasm under varying potential differences indicated that both Ca2+ fluxes consisted of a PD-dependent and a PD-independent component. The results show that the reticulo-rumen participates in Ca2+ absorption in sheep.

Animals↗