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PubMed1990

Calcium dependence of BAY K 8644 effects on the rabbit gall-bladder.

In the present study, we characterized the effects of the calcium (Ca2+) channel activator BAY K 8644 on sodium (Na+) absorption and transepithelial potential difference (Pd) in the rabbit gall-bladder. In gall-bladders mounted in an Ussing chamber it was observed that serosal BAY K 8644 (10(-5) M) inhibited Na+ absorption in the presence, but not in the absence of serosal Ca2+. Serosal nifedipine (a Ca2+ channel antagonist) at 10(-5) M did not reverse the Na+ transport inhibition caused by BAY K 8644. Another effect of serosal BAY K 8644 (10(-5) M) was to induce oscillations in Pd. These Pd-oscillations had a frequency of about one per minute and an amplitude of 20-40 microV. The appearance of Pd-oscillations was dependent on the presence of Ca2+ in the serosal medium. The oscillations were abolished by 1-3 x 10(-5) M serosal nifedipine and by bilateral application of 3 mM barium (Ba2+) (a K+ channel blocker). In a sac preparation of the rabbit gall-bladder, spontaneous cyclic contractions of smooth muscle cells in the gall-bladder wall were observed as oscillations in the transmural pressure. These spontaneous contractions were not accompanied by oscillations in Pd. Serosal BAY K 8644 (10(-5) M) evoked oscillations in Pd in half of the sac preparations, but in each gall-bladder the frequencies of Pd-oscillations and pressure oscillations were different. Serosal nifedipine (2 x 10(-5) M) abolished both types of oscillation.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Requirement of HCO3- for Cl(-)-absorption in seawater-adapted eel intestine.

The role of HCO3-/CO2 buffer in Cl- absorption was examined in the in vitro perfused eel intestine adapted to seawater. Cl- absorption, expressed as short-circuit current (Isc), was measured in either 20 mM HCO3-/1% CO2 Ringer or HEPES Ringer, pH 8.0. Unilateral (mucosal or serosal) substitution of HCO3-/CO2 with HEPES/O2 was without effect on Isc and transepithelial voltage (Vt), whereas bilateral removal of HCO3-/CO2 reduced Isc and Vt by 50%, indicating that the presence of HCO3-/CO2 buffer at one side of the epithelium is sufficient to keep Cl- absorption at the maximum rate. We examined in further detail the individual components of the HCO3-/CO2 system that stimulates Cl- absorption. We found that, in tissues bathed with HEPES Ringer, addition of 1% CO2 to the luminal or serosal solution (final pH = 7.6 in the chamber) had no effect on Isc and Vt, while both electrical parameters could be restored to control values by unilateral (luminal or serosal) substitution of HEPES Ringer with 20 mM HCO3-/1% CO2 Ringer or 20 mM HCO3- alone. Stimulation of Isc induced by unilateral (luminal or serosal) HCO3-/CO2 was inhibited by luminal or serosal 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS) (0.25 mM) or by serosal Na+ removal, whereas amiloride (1 mM), luminal or serosal, had no effect. Acetazolamide (0.1 mM, both sides) inhibited stimulation of Isc induced by luminal addition of HCO3-/CO2, whereas it was without effect when HCO3-/CO2 was added serosally or bilaterally.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1984

Effect of external sodium on intracellular chloride activity in the surface cells of frog gastric mucosa. Microelectrode studies.

The intracellular chloride activity and its dependence on ionic substitutions in the bathing media was studied in individual surface cells of resting gastric mucosa using conventional and Cl- selective microelectrodes. When the tissue was perfused with control NaCl-Ringer the cell membrane p.d.'s, cell-lumen (psi cm) and cell-serosa (psi cs) were -40.9 +/- 0.6 mV and -66.8 +/- 0.5 mV (n = 175) respectively and the p.d. measured by the Cl- selective microelectrodes across the serosal membrane (psi csCl-) averaged -32.4 +/- 0.7 mV (n = 138). From these values an intracellular Cl- activity (acCl-) of 15.3 mmol/l can be estimated. The data indicate that chloride ion is distributed close to equilibrium at the luminal membrane while it is accumulated by an energy requiring step at the serosal membrane. Reduction (2 mmol/l) or absence of chloride from the luminal bath did not result in any detectable change of acCl-; on the other hand, after removal of Cl- from the serosal bath the intracellular Cl- activity fell to 7.1 mmol/l. When the tissue was exposed to serosal Na+-free Ringer (Na+ replaced by choline or TMA), although the acCl- remained unaffected, a marked reduction of the electrochemical gradient for Cl- at the serosal membrane was observed. These data indicate that: chloride is accumulated in the surface cells against its electrochemical potential difference at the serosal membrane; the luminal membrane has a negligible conductance to Cl-, while the serosal membrane represents a conductive pathway to chloride; the uphill entry of chloride at the serosal membrane seems to be, at least partially, Na+-dependent.

Animals↗
PubMed1989

Rapid decrease in electrical conductance of mammalian duodenal mucosa in vitro. Combined effects of prostaglandin E2 and bicarbonate.

The effects of HCO3- on transepithelial conductance of guinea pig (and, in some experiments, rabbit) duodenum have been investigated using stripped preparations in Ussing-type chambers. Initial conductance amounted to approximately 27 mS/cm2. In the presence of serosal or bilateral HCO3- (20 mM), it fell to approximately 15 mS/cm2 within 60 min. With mucosal HCO3- or HCO3- -free solutions, conductance decreased to only approximately 23 mS/cm2. In the absence of HCO3-, serosal but not mucosal addition of HCO3- prompted a steep conductance drop that was 50% complete within 6 min. These effects were the same in proximal and distal segments, whereas conductance levels in the latter were higher. The effects of HCO3- required serosal Na+; they were partly prevented or reversed by serosal ouabain (3 x 10(-5) M), furosemide (10(-3) M), and other loop diuretics, and indomethacin (10(-5) M). Serosal addition of prostaglandin E2 (10(-7) M, followed by 10(-6) M) reduced conductance from approximately 22 to approximately 17 mS/cm2. This effect required serosal HCO3- and the presence of indomethacin. 8-Br-cyclic adenosine monophosphate (10(-3)M, serosal side) mimicked the effects of prostaglandin E2. Indomethacin and prostaglandin E2 did not influence the secretory flux of HCO3- (approximately 0.5 mumol/cm2.h, pH-stat method). Our results assign a critical role to serosal HCO3- in the maintenance of a low tissue permeability, dependent on the availability of prostaglandins (cyclic adenosine monophosphate) and involving HCO3- access to the cell rather than secretion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1990

Influence of atrial natriuretic peptide on mammalian large intestine.

Atrial natriuretic peptide is distributed in a number of organs including the large intestine. Atrial natriuretic peptide has potent diuretic and natriuretic properties and appears to play a central role in fluid and electrolyte homeostasis by an action on the kidney. We examined the influence of atrial natriuretic peptide on mammalian colon because this organ is also intimately involved in homeostasis. Segments of the distal colons of male Sprague-Dawley rats were stripped of muscle layers and mounted in flux chambers. Atrial natriuretic peptide, when added to the serosal side of the mucosa, in concentrations ranging from 10(-8)-10(-5) M, caused a rapid, concentration-dependent increase in short-circuit current, transmucosal electrical potential difference, and conductance. The response to atrial natriuretic peptide was inhibited by (a) chloride-free solution on the serosal surface; (b) pretreatment of the tissues with the chloride channel blocker, diphenylamine-2-carboxylate (10(-3) M mucosally); (c) pretreatment with d,l-verapamil (10(-4) M mucosally and serosally); (d) calcium-free solution on the serosal surface; (e) pretreatment with tetrodotoxin (10(-7) M to serosal surface); and (f) pretreatment with atropine (10(-5) M serosally). However, the response to atrial natriuretic peptide was not influenced by pretreatment with amiloride (10(-4) M to mucosal and serosal surfaces) or piroxicam (10(-5) M serosally). Atrial natriuretic peptide did not elicit an increase in short-circuit current and potential difference across T84 cells derived from a human colonic carcinoma cell line, suggesting that the response to atrial natriuretic peptide is not due to a direct effect on colonocytes. These findings suggest that atrial natriuretic peptide acts by a calcium-mediated secretory mechanism involving cholinergic nerves and is likely to be involved in the endogenous neurohumoral regulation of ion transport in the mammalian colon.

Animals↗
PubMed1992

Intracellular pH in isolated Necturus duodenal mucosa exposed to luminal acid.

Regulation of intracellular pH (pHi) and its maintenance within physiological ranges during exposure to luminal acid was studied in isolated Necturus duodenal mucosa using liquid sensor microelectrodes. Exposure of the mucosa to luminal pH 2.7 caused significant intraepithelial acidification. Subsequent removal of HCO3-/CO2 (HEPES/O2 substitution) from the serosal perfusate caused a further decrease of pHi. Blocking of HCO3- transport across the basolateral cell membrane by addition of 4-acetamido-4,isothiosyanostilbene-2,2-disulfonic acid (SITS) to serosal perfusate also caused a slight but significant decrease of pHi. Removal of Na+ (choline substitution) from the serosal perfusate during acid exposure likewise caused a significant decrease in pHi, as did serosal addition of an inhibitor of Na+/H+ antiport, 1 mmol/L amiloride. When Na+ was removed from the serosal perfusate after HCO3- removal, pHi first rapidly acidified; this was followed after an initial 5-minute steady state by an uncontrolled progressive acidification at a rate of 0.33 pH unit/15 min without any further steady state. A similar but weaker effect could also be shown with amiloride addition. The epithelial surface pH was 7.13 +/- 0.08 at the apex of mucosal villus and 7.42 +/- 0.11 (n = 5) in the cryptal area between the villi, i.e., greater than 1 pH unit higher than that of the luminal bulk solution (pH 6), thus suggesting active alkalization of the epithelial surface. Removal of serosal HCO3-/CO2 decreased surface pH significantly both at the villus apex and at the cryptal area, suggesting that the surface alkalization is mediated by transport of serosal HCO3- to the epithelial surface. The data suggest that pHi in acid-exposed duodenal mucosa is primarily maintained within physiological range by an HCO3(-)-dependent mechanism, which, at least in part, exerts its action extracellularly by forming an alkaline buffer layer at the epithelial surface. If adequate serosal (or systemic) HCO3- is not available, a second-line Na(+)-dependent and amiloride-sensitive pHi-regulatory mechanism, presumably an Na+/H+ antiport, becomes the main regulator of pHi.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1995

Effects of pH on calcium transport in turtle bladder.

This study was designed to examine the effect of apical and basolateral (ie, mucosal and serosal) pH on calcium (Ca) transport in turtle bladder, a nonmammalian analog of the distal nephron. Unidirectional Ca45 fluxes were measured when serosal pH was 6.4, 7.4, or 8.4 (mucosal pH, 7.4) in the presence and absence of ouabain. When serosal pH was 8.4, M-->S Ca45 flux increased significantly, and when it was 6.4, M-->S Ca45 flux decreased markedly. Changes in serosal pH did not affect the S-->M Ca45 flux. When 5 x 10(-4) mol/L ouabain was added to inhibit sodium transport, M-->S Ca45 flux, at pH 7.4, was 221.6 +/- 27.4 pmol/mg/h (n = 10), and low pH again inhibited this flux (approximately 50%). Lowering mucosal pH (with serosal pH 7.4) also decreased M-->S Ca45 flux. In stripped bladders, Ca45 uptake increased linearly as medium pH was increased from 4.4 to 8.4. Total tissue Ca concentration did not change when serosal pH was varied, except at the extreme of pH 4.4, where tissue Ca decreased. By contrast, when apical pH was 6.4, tissue Ca rose substantially (approximately 1.5-fold). these results demonstrate that extracellular pH directly affects Ca homeostasis in the turtle bladder. Lowering the pH of either the serosal or mucosal medium directly inhibits apical Ca permeability. This change in Ca permeability is seen in the presence of ouabain. By contrast, alkalization of the serosal medium enhances apical permeability, but this effect is, in some manner, related to sodium transport.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

pH-Dependence of water and solute transport in toad urinary bladder.

Stimulation of urea and water transport by vasopressin (ADH) appears to occur via independent pathways. We examined the effects of altering serosal or mucosal bath pH on transport of water, urea, and sodium. Compared to bladders with a serosal bath pH of 7.4 to 8.0, reducing the serosal bath pH to 6.8 led to a 60% fall in ADH-stimulated osmotic water flow, without decreasing the permeability of urea. Raising the serosal pH to 9.5 had the opposite effect: urea permeability was inhibited by 40% without altering water flow. Exogenous cyclic AMP-stimulated water and urea permeabilities were not dissociated, but were changed in the same direction by alterations in serosal pH: serosal acidification enhanced the effect of exogenous cyclic AMP on both urea and water, whereas the cyclic AMP effect on both was diminished by serosal alkalinization. This was especially marked for urea, suggesting that an alteration in the urea response to cyclic AMP may be particularly important in defining vasopressin-stimulated urea permeability as the serosal bath pH is altered. Mucosal acidification increased short circuit current but decreased both the urea and water response to ADH and 8-bromo-cyclic AMP. The response to cyclic AMP was less consistent. Mucosal alkalinization did not cause significant changes in either basal or stimulated transport. The data demonstrate distinct and separable effects of bath pH alterations on each of the transport systems examined.

Animals↗
PubMed1988

Transport and metabolism of 6-thioguanine and 6-mercaptopurine in mouse small intestine.

1. The transport of 6-thioguanine and 6-mercaptopurine has been studied with isolated jejunal loops of mouse small intestine. H.p.l.c. was used to identify and quantify the thiopurines and their metabolites in the serosal secretions. 2. When the lumen of the intestinal loops contained either 6-thioguanine or 6-mercaptopurine at a concentration of 1 mmol/l, the concentration of unmetabolized drug in the serosal secretions reached a maximum of 0.13 +/- 0.02 mmol/l (mean +/- SEM). 3. Analysis of the serosal secretions from the perfusions with either of the drugs revealed the appearance of an unknown compound which had the characteristics of a thiopurine and the same time course of appearance as the unmetabolized drug. Thus 6-thioguanine and 6-mercaptopurine are significantly metabolized during absorption in mouse intestine. 4. The unknown compound was identified as 6-thiouric acid, and with 1 mmol/l 6-thioguanine or 6-mercaptopurine in the lumen the concentration of this metabolite in the serosal secretions rose to a maximum of 0.13 +/- 0.01 and 0.18 +/- 0.03 mmol/l, respectively. At luminal drug concentrations of 0.1 mmol/l, the metabolite accounted for approximately 90% of the serosal thiopurine. 5. After an initial lag period of 20 min, linear rates of appearance in the serosal secretions were obtained for both the unmetabolized drugs and 6-thiouric acid. 6. Addition of the xanthine oxidase inhibitor oxypurinol at a luminal concentration of 0.3 mmol/l prevented the formation of 6-thiouric acid from 6-thioguanine. However, the inhibitor reduced the rate of 6-thioguanine appearance in the serosal secretions by 50%. 7. The conversion of 6-mercaptopurine to 6-thiouric acid was prevented when allopurinol or oxypurinol were added to the lumen. At a luminal drug concentration of 1 mmol/l, allopurinol increased the rate at which 6-mercaptopurine appeared in the serosal secretions by 90% compared with an increase of only 50% with oxypurinol. 8. The transport of water and glucose by the mouse intestinal loops was unaffected by 6-thioguanine or the xanthine oxidase inhibitors. However, 6-mercaptopurine caused significant reductions in the rate of water transport (30%) and glucose transport (39%). These effects were observed at a luminal drug concentration of 0.1 mmol/l and there was no further increase at a drug concentration of 1 mmol/l.

Allopurinol↗
PubMed1991

Asymmetrical effects of increases in hydrostatic pressure on macromolecular movement across the airway mucosa. A study in guinea-pig tracheal tube preparations.

This study employed isolated guinea-pig tracheal tube preparations in order to examine effects of increases in hydrostatic pressure on the movement of macromolecular solutes (fluorescein isothiocyanate-conjugated dextran; FITC-D, MW 70 kD; kept either in serosal or mucosal bathing fluids) across the mucosa. An asymmetry of the mucosal barrier was demonstrated by the finding that under baseline zero-pressure difference conditions luminal entry of serosal FITC-D was greater than serosal entry of luminal FITC-D. Furthermore, an increased serosal pressure (5 cm H2O) moved significant amounts of serosal FITC-D into the lumen, whereas a corresponding pressure applied on the luminal side only marginally increased mucosal crossing of luminal FITC-D. By raising the luminal pressure to 10 and 20 cm H2O (which may be used as positive end-expiratory pressures (PEEP) in vivo in patients) mucosal penetration of luminal FITC-D was as marked as that induced in the opposite direction by the low (5 cm H2O) serosal pressure increase. Another aspect of the asymmetry of the airway mucosal barrier was evident from experiments examining the effect of a serosal pressure increase on mucosal penetration of luminal FITC-D. Neither during nor after the period of sustained serosal pressure increase was luminal FITC-D crossing the mucosa to a greater extent than under baseline zero-pressure conditions. This finding agrees with in-vivo data demonstrating that plasma exudation into the airway lumen may not be associated with an increased absorption of luminal solutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1958

Observations concerning the action of 5-hydroxytryptamine on the peristaltic reflex.

In isolated guinea-pig intestine 5-hydroxytryptamine increased the longitudinal muscle contractions in response to acetylcholine while the ganglionic action of nicotine was first facilitated and then blocked. Phenyldiguanide, veratrine, veratridine and protoveratrine, like 5-hydroxytryptamine, depressed the response to nicotine, leaving that to acetylcholine unaffected.The sensory stimulants, like 5-hydroxytryptamine, facilitated the peristaltic reflex when applied to the mucosa, and abolished it when applied to the serosa. Preceding the block, the initial effect of low concentrations of 5-hydroxytryptamine applied to the serosa was a short stimulation of peristalsis.Concentrations of 5-hydroxytryptamine which had an approximately equal stimulant action (mucosal 1 to 4 x 10(-6), serosal 2 to 8 x 10(-8)) were tested when various parts of the reflex arc were blocked. During block by procaine introduced into the lumen, mucosal application of 5-hydroxytryptamine re-established peristalsis, but serosal application of 5-hydroxytryptamine had no effect. During block by hexamethonium or atropine present in the bath, 5-hydroxytryptamine restored peristalsis more effectively by serosal application than by mucosal application. During block by serosal application of 5-hydroxytryptamine, morphine, phenoxybenzamine or dihydroergotamine, mucosal application of 5-hydroxytryptamine restored the peristaltic reflex while serosal application had no effect. During block by 2-bromo-lysergic acid diethylamide or lysergic acid diethylamide acting from the serosal surface, 5-hydroxytryptamine had no effect whether acting on the mucosal or on the serosal surface.It is concluded that 5-hydroxytryptamine facilitates the peristaltic reflex at two sites: when introduced into the lumen it stimulates mucosal sensory receptors; when acting from the serosal surface it sensitizes the muscle to the transmitter acetylcholine. There is also a transient stimulant action on the ganglia which is soon followed by inhibition; this indicates that 5-hydroxytryptamine applied to the serosa abolishes peristalsis by ganglion block.

Acetylcholine↗
PubMed1987

Effects of theophylline, choleragen and loperamide on rabbit ileal fluid and electrolyte transport in vitro.

1 The effects of theophylline and cholera toxin on water and anion movements across rabbit ileum in vitro and the reversal of these effects by the opiate action of loperamide have been investigated. Water movement across the mucosal and serosal surfaces of the tissue was measured continuously by a high resolution method. 2 Theophylline caused an increase in short circuit current and reversed the direction of net C1- movement, due mainly to a decrease in mucosal-serosal flux. It also caused a rapid, but transient, reversal in the direction of fluid movement across the mucosal surface. Fluid outflow across the serosal surface was decreased but not reversed. Cholera toxin caused a slow inhibition of water movement across both mucosal and serosal surfaces. 3 Theophylline increased the exit rate of 77Br across the mucosal surface and decreased the exit rate of 77Br across the serosal surface. Theophylline increased the exit rate of 3H-labelled mannitol across the mucosal surface. 4 Loperamide reversed the effects of theophylline and cholera toxin on water flow across the mucosal and serosal surfaces and on net transepithelial C1- flux; it also increased the rate of 77Br exit across the serosal surface of theophylline-treated tissue. These effects of loperamide could be reversed by naloxone. 5 The hydraulic conductivity, Lp of the serosal surface was measured directly by determining the osmotic flow generated by low concentrations of polyethylene glycol (mol. wt. 20,000 and 90,000). Theophylline reduced the Lp by 57%. Loperamide added to theophylline-treated tissues increased the Lp by 340%. This effect was reversed by naloxone. 6 These results indicate that modulation of intestinal smooth muscle tone affects transepithelial ion and water flows in vitro. The increase in tone induced by secretagogues increases ion and water reflux via wide shunt channels in the mucosa and thereby reduces net absorption. The increased net fluid and electrolyte absorption induced by loperamide results from the opiate-dependent inhibition of acetylcholine release from intrinsic ganglia which reduces smooth muscle tone and thereby enhances the fluid and electrolyte conductance of the submucosal layers.

Animals↗
PubMed1972

Ionic basis of membrane potentials of epithelial cells in rat small intestine.

1. Potentials across the mucosal and serosal membranes of the epithelial cells of rat jejunum together with transmural potentials were recorded using everted sac preparations.2. Ionic changes in either mucosal or serosal fluids affect mucosal or serosal membrane potentials respectively with comparable changes in the transmural potential. The contralateral membrane potential is relatively unaffected.3. Replacement of mucosal sodium chloride by potassium chloride or lithium chloride had little effect on potentials, but its replacement by mannitol or Tris chloride increased the negativity of the mucosal potential, giving linear relationships against log(10)[Na](m) with slopes of 41.4 and 30.7 mV respectively for tenfold change in [Na](m).4. At constant [Na](m), potassium or lithium increased the mucosal potential by 25.7 and 19.8 mV respectively for tenfold concentration changes.5. Qualitatively similar changes occurred in the serosal potential when the ionic composition of the serosal fluid was varied.6. Mucosal potential changes in response to modifications of the ionic composition of the mucosal fluid were the same in the presence and absence of galactose.7. Sodium and potassium diffusion potentials largely determine both the mucosal and serosal membrane potentials. For the mucosal membrane, P(K):P(Na) is 1.26:1, and is probably higher for the serosal membrane. Chloride makes no significant contribution to membrane potentials.8. Potentials generated by the electrogenic sodium pump are superimposed on diffusion potentials across the serosal membrane.

Animals↗
PubMed1987

Transmural calcium fluxes and role of mucins as cellular calcium-transport vehicles in chicken trachea in vitro.

1. Transmural Ca2+ fluxes in tracheal tissue under physiological [Ca2+] conditions and the effect of altered serosal and luminal [Ca2+] on Ca2+ movements were investigated using chicken tracheal preparations in vitro. 2. In the presence of physiological [Ca2+] (1.8 mM), there was unidirectional Ca2+ flux with a small but steady uptake of Ca2+ from the serosal side into the submucosa followed by Ca2+ transport into the mucosa and then Ca2+ efflux into the tracheal lumen. The Ca2+ uptake by the tracheal tissue was via a diffusion process. There was no evidence of Ca2+ uptake via slow Ca2+ channels or Na+-Ca2+ exchange pathways. On the other hand, Ca2+ uptake from the lumen into the mucosa and Ca2+ efflux from the submucosa into the serosal side were almost negligible. 3. High serosal [Ca2+] (18.0 mM) and/or low luminal [Ca2+] (0.18 mM) increased significantly both Ca2+ uptake by the tissue from its serosal side and Ca2+ efflux into the lumen. Directional Ca2+ effect appeared to increase Ca2+ uptake via a diffusion process. 4. Transport of Ca2+ from the mucosa into the lumen comprised efflux of both filterable and mucin-bound forms of Ca2+. Under physiological [Ca2+] conditions, whilst initial efflux rates of both filterable and mucin-bound Ca2+ were almost equal, the net efflux of Ca2+ in mucin-bound form after 10 min was about 33% higher than that of filterable Ca2+. Similarly, the increase in Ca2+ efflux as a result of high serosal [Ca2+] involved a significant increase in the efflux of mucin-bound Ca2+ only, whereas the increased Ca2+ efflux as a result of low luminal [Ca2+] involved a significant increase in efflux of both filterable and mucin-bound Ca2+. 5. The transport of Ca2+ from the mucosa into the lumen in the form of mucin-bound Ca2+ appeared to play a significant role in the regulation of Ca2+ efflux from the tissue under increased Ca2+ influx or efflux conditions resulting from interventions with serosal and luminal [Ca2+]. 6. A concurrent stimulation of secretion of unique low molecular weight sulphate-rich components and high molecular weight mucin complexes with increased Ca2+ influx into and efflux from the tracheal tissue in response to high serosal and low luminal [Ca2+] allude to a plausible role of these secretory macromolecular mucin complexes as cellular Ca2+ transport vehicles.

Animals↗
PubMed1993

Purine nucleoside transport and metabolism in isolated rat jejunum.

1. The absorption and metabolism of purine nucleosides and their constituent bases has been investigated by perfusion through the lumen of isolated loops of rat jejunum. In control perfusions and those with luminal purines or purine nucleosides, high-performance liquid chromatography (HPLC) revealed uric acid as the only detectable purine in the mucosal epithelial layer and the serosal secretions unless the xanthine oxidase inhibitor allopurinol was present. 2. Adenosine (0.5 mM) was quantitatively deaminated to inosine in the lumen after perfusion for 30 min. 3. Luminal inosine and hypoxanthine (0.15-1.0 mM) increased the serosal uric acid concentration significantly (P < 0.001); at 0.5 and 1.0 mM the nucleoside gave a significantly greater (P < 0.01) rate of serosal uric acid appearance than the base. 4. Luminal guanosine (0.05-0.50 mM) and guanine (0.05-0.15 mM) increased the serosal uric acid concentration significantly (P < 0.001); with 0.15 mM nucleoside the serosal uric acid appeared significantly faster (P < 0.01) than it did from the base. 5. Luminal allopurinol (0.3 mM) inhibited xanthine oxidase by 80% and reduced serosal purine appearance significantly (P < 0.01) from luminal guanine, hypoxanthine and inosine. With allopurinol, guanosine (0.1 and 0.15 mM) and inosine (0.1-1.0 mM) gave significantly higher (P < 0.01) total serosal purine concentrations than their respective bases. 6. Inosine and guanosine were cleaved to their respective bases plus ribose phosphate by the action of a cytoplasmic nucleoside phosphorylase, which was found to have widely different Michaelis constants (Km; 318 +/- 45 and 41.4 +/- 3.6 microM for inosine and guanosine, respectively) and maximum velocities (Vmax; 79.3 +/- 4.0 and 20.5 +/- 0.05 mumol min-1 (mg protein)-1 for inosine and guanosine, respectively). 7. We conclude that hypoxanthine and guanine absorbed by rat small intestine are oxidized to uric acid which is released in the serosa. The corresponding nucleosides are split by phosphorolysis after absorption and the resulting purine bases are converted to uric acid which appears on the serosal side with similar quantities of ribose phosphate.

Allopurinol↗
PubMed1985

Ammonia transport by the turtle bladder: relationship to H+ secretion.

The turtle bladder is apparently capable of transporting ammonia in the form of NH3 as well as NH+4. In the present study we examined the relationship of ammonia transport into the mucosal solution to H+ secretion and to chemical reactions in the unstirred layers. The relationship between ammonia transport and H+ secretion was examined before and after inhibition of H+ secretion by acetazolamide, SITS, and the putative inhibitor of the H+ pump dicyclohexylcarbodiimide. All these inhibitors caused a significant decrease in H+ secretion and led to a parallel decrease in the rate of ammonia transport with serosal pH at 6.4. Stimulation of H+ secretion by 1% CO2 increased both H+ secretion and ammonia transport at serosal pH 6.4. At serosal pH 6.4 the changes in H+ secretion were highly correlated with changes in ammonia transport. Ammonia transport at serosal pH 6.4 was electrogenic and inhibited by a low mucosal pH. In contrast, the diffusion of NH3 down an imposed concentration gradient was not correlated with changes in H+ secretion. Chemical reactions in the unstirred layers seem to influence ammonia transport in that increasing serosal nonvolatile buffer concentrations decreased the diffusion of NH3 down the concentration gradient from the serosal into the mucosal solution, probably by decreasing serosal NH3 concentration. Conversely, addition of uncouplers in the mucosal solution in an attempt to decrease the H+ concentration in the mucosal solution unstirred layer decreased the ammonia transport at serosal pH 6.4.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1987

Relationship of K and ammonia transport by the turtle bladder.

The relationship between K and ammonia transport was investigated in the turtle bladder. At serosal pH 6.4, ammonia transport is preferentially from serosa to mucosa and is, at least in part, mediated by NH4+ transport. Since K and NH4+ share similar features such as permeability and stimulation of Na-K-ATPase, we studied the interaction of transport of these ions by the turtle bladder. Removal of K from the mucosal solution inhibited partially ammonia transport from serosa to mucosa and the inhibition was reversible by restoration of K. In contrast, removal of serosal K failed to inhibit ammonia transport. Since NH4+ can replace K in the activation of Na-K-ATPase in turtle bladder plasma membrane fraction with similar K, we examined the effect of ouabain on ammonia transport. Ouabain added to the serosal solution failed to inhibit ammonia transport thus, suggesting that the Na-K-ATPase is not required for ammonia entry into the cell. Methylammonium (a competitive inhibitor of NH4+ transport in other systems) decreased both ammonia transport and the observed increase in short circuit current elicited by NH4Cl addition to the serosal solution. This finding suggests that NH4+ and methylammonium are transported through a common pathway in the serosal side. Since the permeability of the serosal side to K and NH4+ is similar, we evaluated the effect of serosal depolarization and the effect of barium, an inhibitor of K channels, on ammonia transport. Serosal depolarization inhibited ammonia transport but barium did not affect ammonia flux.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia↗
PubMed1983

Regulation of serotonin release from rabbit intestinal enterochromaffin cells.

Serotonin release from rabbit enterochromaffin cells located in the mucosal epithelium of the small intestine was studied in vitro. Serotonin release from both the serosal and mucosal sides of the small intestine was measured. The addition of muscarinic but not nicotinic cholinergic agonists to the serosal medium resulted in a large but transient increase in serotonin release from the serosal but not the mucosal side of the intestine. Mucosal addition of these agents was ineffective. Serotonin release stimulated by the cholinergic agonist carbachol appeared to be dependent upon influx of extracellular Ca++ for the following reasons: 1) depletion of serosal Ca++ inhibited carbachol-stimulated release; 2) carbachol-stimulated serotonin release was blocked by the inorganic calcium channel blockers Co++, Ni++, Cd++, La and Gd; and 3) serosal serotonin release was increased by the Ca++ ionophore, ionomycin, and by Ba++. The addition of 8-bromoadenosine cyclic AMP or the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, to the serosal medium produced a sustained elevation of serosal serotonin release. 8-bromoadenosine-cyclic AMP-stimulated release was not blocked by depleting extracellular Ca++. Forskolin, a compound which stimulates adenylate cyclase, also stimulated serosal serotonin release. 8-bromoadenosine-cGMP had no effect on serotonin release. Somatostatin (10(-8)-10(-6) M) caused a dose-dependent inhibition of carbachol-stimulated serotonin release. Somatostatin (10(-6) M) only partially inhibited serotonin release stimulated by 8-bromoadenosine-cyclic AMP, 3-isobutyl-1-methylxanthine and forskolin and had no effect on release stimulated by Ba++. The results suggest potential roles for both calcium and cyclic nucleotides in the regulation of serotonin release.

Animals↗