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At least 775 records · Page 43Linked to original sources
PubMed1997

Differing mechanisms of stimulation of Na+ absorption in rabbit proximal colon.

Both alpha2-adrenergic agonists and decreased Na+ in the bathing fluids stimulate electroneutral Na+ absorption in rabbit proximal colon, but it is unclear whether they have similar modes of action. We sought to define regulatory events involved with stimulation of Na+ absorption by these two agonists. Transport parameters were assessed by ion flux studies under short-circuit and pH stat conditions, recordings of intracellular electrical potential difference (psi(mc)) with microelectrode impalements, and measurement of intracellular pH (pH(i)). Epinephrine elicited a yohimbine-inhibitable alkalinization of pH(i) but did not alter psi(mc) In contrast, lowered serosal Na+ concentration ([Na+]) did not significantly increase pH(i) but did depolarize psi(mc). Removal of serosal HCO(3)- stimulated Na+ absorption and reversed residual ion flux from secretion to absorption. pH stat studies demonstrated epinephrine-stimulated, amiloride-inhibitable serosal alkalinization. Serosal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid inhibited Na+ absorption. Epinephrine and lowered [Na+] have different effects on intracellular parameters associated with electroneutral Na+ absorption. Epinephrine stimulates an apical Na+/H+ exchanger. Lowered [Na+] elicits responses consistent with a coupled Na+-HCO(3x)- exit step. Coordinated function of apical Na+/H+ exchangers and a basolateral Na+-HCO(3)(x)- symport permit Cl(-)-independent electroneutral Na+ absorption while maintaining pH(i) homeostasis. Given the low [Cl-] environment of the colonic lumen, this transport pathway may be important for electroneutral Na+ absorption.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1998

Nonionic diffusion of short-chain fatty acids across rat colon.

Short-chain fatty acid (SCFA) transport across the colon may occur by nonionic diffusion and/or via apical membrane SCFA-/HCO3- exchange. To examine the relative importance of these processes, stripped segments of rat (Ratus ratus) proximal and distal colon were studied in Ussing chambers, and the unidirectional fluxes of radiolabeled SCFA butyrate, propionate, or weakly metabolized isobutyrate were measured. In N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) or 1 or 5 mM HCO3- Ringer, decreases in mucosal pH stimulated mucosal-to-serosal flux (Jm-->s) of all SCFA, decreases in serosal pH stimulated serosal-to-mucosal flux (Js-->m), and bilateral pH decreases stimulated both fluxes equally. These effects were observed whether the SCFA was present on one or both sides of the tissue, in both proximal and distal colon, in the absence of luminal Na+, and in the presence of either luminal or serosal ouabain. Changes in intracellular pH or intracellular [HCO3-] did not account for the effects of extracellular pH. Luminal Cl- removal, to evaluate the role of apical membrane Cl-/SCFA- exchange, had no effect on Jm-->s but decreased Js-->m 32% at pH 6.5 and 22% at 7.2. Increasing SCFA concentration from 1 to 100 mM, at pH 6.4 or 7.4, caused a linear increase in Jm-->s. We conclude that SCFA are mainly transported across the rat colon by nonionic diffusion.

Animals↗
PubMed2000

Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro.

The present study was conducted to elucidate the mechanisms by which Helicobacter pylori (HP)-derived ammonia causes gastric mucosal injury. Intact sheets of guinea pig gastric fundic mucosae were incubated in Ussing chambers. Both the luminal and the serosal pH were kept at 7.4. Transmucosal potential difference (PD) and electrical resistance (R) were monitored as indices of mucosal integrity. Restitution was evaluated by recovery of PD, R, and transmucosal [(3)H]mannitol flux after Triton X-100-induced mucosal injury. The effects of luminal or serosal NH(4)Cl on function and morphology of uninjured or injured mucosae were examined. In uninjured mucosae, serosal NH(4)Cl induced more profound decreases in PD and R and more prominent vacuolation in gastric epithelial cells than did luminal NH(4)Cl. In contrast, luminal NH(4)Cl markedly inhibited restitution in injured mucosae and caused an extensive vacuolation in gastric epithelial cells, as did serosal NH(4)Cl. Transmucosal ammonia flux was greater in the injured than in the uninjured mucosae. These results suggest that 1) basolateral membrane of gastric epithelial cells is more permeable to ammonia than apical membrane and 2) luminal ammonia, at concentrations detected in HP-infected gastric lumen, retards restitution in injured mucosae.

Ammonia↗
PubMed2001

Effect of E. coli heat-stable enterotoxin on colonic transport in guanylyl cyclase C receptor-deficient mice.

We studied the functional importance of the colonic guanylyl cyclase C (GCC) receptor in GCC receptor-deficient mice. Mice were anesthetized with pentobarbital sodium, and colon segments were studied in Ussing chambers in HCO3- Ringer under short-circuit conditions. Receptor-deficient mouse proximal colon exhibited similar net Na+ absorption, lower net Cl- absorption, and a negative residual ion flux (J(R)), indicating net HCO3- absorption compared with that in normal mice. In normal mouse proximal colon, mucosal addition of 50 nM Escherichia coli heat-stable enterotoxin (STa) increased the serosal-to-mucosal flux of Cl- (J(s-->m)(Cl)) and decreased net Cl- flux (J(net)(Cl)) accompanied by increases in short-circuit current (I(sc)), potential difference (PD), and tissue conductance (G). Serosal STa had no effect. In distal colon neither mucosal nor serosal STa affected ion transport. In receptor-deficient mice, neither mucosal nor serosal 500 nM STa affected electrolyte transport in proximal or distal colon. In these mice, 1 mM 8-bromo-cGMP produced changes in proximal colon J(s-->m)(Cl) and J(net)(Cl), I(sc), PD, G, and J(R) similar to mucosal STa addition in normal mice. We conclude that the GCC receptor is necessary in the mouse proximal colon for a secretory response to mucosal STa.

Animals↗
PubMed1991

Cardiovascular reflexes evoked by histamine stimulation of the stomach.

This study examined the potential for histamine to cause cardiovascular reflexes when applied to the serosal or mucosal surface of the stomach. Thus, in chloralose-anesthetized cats, histamine was applied to the serosal surface of the stomach in concentrations ranging from 0.5 to 1,000 micrograms/ml. This resulted in graded increases in mean arterial pressure (MAP), maximal left ventricular pressure over time (dP/dt), and heart rate ranging from 9 +/- 4 to 30 +/- 3 mmHg, 450 +/- 103 to 1,710 +/- 610 mmHg/s, and 2 +/- 1 to 13 +/- 4 beats/min, respectively. Histamine stimulation of the gastric serosa evoked a greater pressor response than that observed when the same concentration of histamine (100 micrograms/ml) was applied to the gastric mucosa (43 +/- 7 vs. 13 +/- 3 mmHg, respectively). In six cats, celiac ganglionectomy abolished the previously observed cardiovascular response to histamine stimulation of the serosal surface of the stomach. When the gastric serosa was treated with the H1-receptor antagonist diphenhydramine (1 mg/ml) (n = 5), the cardiovascular response to histamine was abolished. In five other cats, administration of the H2-antagonist ranitidine (1 mg/ml) had no effect on the histamine-induced responses. When indomethacin (2-5 mg/ml), was applied to the serosal surface of the stomach (n = 6), histamine-induced increases in MAP and dP/dt were attenuated. However, application of PGE2 (1 microgram/ml) restored these two responses. These results suggest that histamine stimulates H1-receptors in the gastric wall to cause reflex cardiovascular responses that are dependent, in part, on the local production of prostaglandins.

Animals↗
PubMed1975

Transport of H plus and other electrolytes across isolated gastric mucosa of the rabbit.

The relationship of transmural and cellular phenomena to the rate of spontaneous luminal HH+ secretion by short-circuited gastric mucosa bathed in HCO3- and CO2-free Ringer solution was studied by the pH-stat technique. The bulk of luminal acidification can be accounted for by the appearance of H+ and not by organic acids. Acid secretion requires the presence of O2 and exogenous substrate but is not limited by endogenous CO2 production. The rate of H+ secretion is matched by the serosal appearance of alkali. The greater appearance of CO2 on the serosal side of the mucosa is consistent with hydroxylation of CO2 and greater permeability of the serosal border to HCO3-. Luminal changes in H+ concentrations affect H+ secretion but serosal changes do not, suggesting that the gradient produced by H+ secretion is at the luminal border. Steady-state isotopic Na+ and Cl- fluxes indicate net secretion of both ions, but net K+ transport is negligible.

Animals↗
PubMed1975

Effects of bile salts on amphibian gastric mucosa.

The effect of five different bile salts on the mucosal or serosal surface of isolated bullfrog gastric mucosa was investigated. Serosal exposure (30 min) to 15-40 mM taurocholate (TCA) or taurodeoxycholate (TDCA), 10-40 mM deoxycholate (DCA), or 2.5-7.5 mM cholate (CA) typically produced a marked increase in resistance (R) and a decrease in potential difference (PD), short-circuit current (I-sc), and H+ secretion. Flux of 36Cl from serosal to mucosal solution decreased progressively. The flux of [14C]sucrose across the mucosa was slightly decreased. Microscopy showed condensation of the parietal cells. Mucosal exposure (30 min) at concentrations above 2.5 mM DCA or CA and 15 mM TCA and TDCA caused a marked decrease in R, PD, I-sc, and H+ secretion, and the flux of [14C]sucrose across the mucosa was increased. Extreme destruction of the surface mucous cells was the primary histologic finding. The effect of dehydrocholate was identical to that of TCA. Mucosal bile salts cause an increased permeability primarily by injury of the surface epithelium whereas serosal bile salts affected primarily the oxyntic cells.

Animals↗
PubMed2004

Bicarbonate secretion plays a role in chloride and water absorption of the European flounder intestine.

Experiments performed on isolated intestinal segments from the marine teleost fish, the European flounder (Platichthys flesus), revealed that the intestinal epithelium is capable of secondary active HCO3(-) secretion in the order of 0.2-0.3 micromol x cm(-2) x h(-1) against apparent electrochemical gradient. The HCO3(-) secretion occurs via anion exchange, is dependent on mucosal Cl(-), results in very high mucosal HCO3(-) concentrations, and contributes significantly to Cl(-) and fluid absorption. This present study was conducted under in vivo-like conditions, with mucosal saline resembling intestinal fluids in vivo. These conditions result in a transepithelial potential of -16.2 mV (serosal side negative), which is very different from the -2.2 mV observed under symmetrical conditions. Under these conditions, we found a significant part of the HCO3(-) secretion is fueled by endogenous epithelial CO2 hydration mediated by carbonic anhydrase because acetazolamide (10(-4) M) was found to inhibit HCO3(-) secretion and removal of serosal CO(2) was found not to influence HCO3(-) secretion. Reversal of the epithelial electrochemical gradient for Cl(-) (removal of serosal Cl(-)) and elevation of serosal HCO3(-) resulted in enhanced HCO3(-) secretion and enhanced Cl(-) and fluid absorption. Cl(-) absorption via an anion exchange system appears to partly drive fluid absorption across the intestine in the absence of net Na(+) absorption.

Acetazolamide↗
PubMed1982

PAH secretion in the urinary bladder of a crab Cancer borealis.

Uptake of 10 microM p-aminohippuric acid (PAH) by sections of Cancer borealis urinary bladder was concentrative, saturable (Km 67 microM, Vmax 1.7 nmol.mg tissue-1.h-1), inhibitable by other organic anions, and dependent on medium Na and glycolytic metabolism. Bladders mounted in flux chambers exhibited net secretory transport of PAH, with serosa-to-lumen fluxes (Js leads to l) being about 4 times lumen-to-serosa fluxes (Jl leads to s). In 60-min flux chamber studies, tissue-to-medium ratios exceeded unity with serosal, but not luminal, PAH. Initial (10 min) fluxes and tissue accumulations (Ac) were measured in the absence and presence of 1-5 mM BCG (bromocresol green; competitor organic anion). With serosal PAH, serosal BCG (1 mM) reduced serosa-to cell flux (Js leads to c), Ac, and Jc leads to l by 60-75%. With luminal PAH, luminal BCG (1 mM) had no effect on Jl leads to c, Ac, or Jc leads to s; increasing the luminal BCG concentration to 5 mM reduced Jl leads to c, Ac, and Jc leads to s by 40-50%. The data are consistent with a model featuring an inwardly directed pump on the serosal membrane, cellular accumulation, and a facilitated carrier on the luminal membrane.

Aminohippuric Acids↗
PubMed1984

Mechanisms of CO2 transport in rectal salt gland of aedes. I. Ionic requirements of CO2 secretion.

Rectal salt glands of Aedes dorsalis can be successfully isolated and microperfused in vitro. Microperfused salt glands maintain a large, stable transepithelial potential (-40 to -50 mV, lumen negative) and secrete total CO2 at high and stable rates [CO2 net flux ( JCO2net ) = 799 +/- 57 pmol . min-1 . mm-1]. Bilateral Na+ and K+ or serosal Cl- substitutions and serosal addition of 1.0 mM ouabain, 2.0 mM amiloride, or 0.5 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid had no effect on JCO2net . Removal of luminal Cl- inhibited JCO2net by 80%, whereas serosal addition of 1.0 mM acetazolamide or 0.5 mM 4,4'-diisothiocyano-2,2'-disulfonic acid inhibited JCO2net by 80 and 40%, respectively. Net Cl- reabsorption ( JClnet = -888 +/- 57 pmol . min-1 . mm-1) was equivalent to total CO2 secretion, suggesting that CO2 transport was mediated by a 1:1 exchange of luminal Cl- for serosal HCO-3.

Aedes↗
PubMed1994

cGMP and Ca2+ regulation of ion transport across the isolated porcine distal colon epithelium.

Intact epithelium from the porcine distal colon was stripped of serosal muscle and mounted in Ussing chambers to investigate the regulation of Na, Cl, and K transport by guanosine 3',5'-cyclic monophosphate (cGMP) and elevations in intracellular [Ca2+]. Under voltage-clamped conditions cGMP (250 microM) produced an increase in tissue short-circuit current (Isc) that reached a maximal value within 10-20 min and remained elevated > 40 min. This response was associated with an inhibition of NaCl absorption and stimulation of Cl and K secretion. In the absence of Cl the Isc also slowly increased but returned to baseline values within 20 min. Bicarbonate removal from both serosal and mucosal solutions or serosal bumetanide (20 microM) reduced the effect of cGMP on Isc by approximately 40%. When performed simultaneously, these conditions reduced the cGMP response by approximately 60%. Transepithelial Na and Cl flux measurements indicated that serosal bumetanide blocked increased Cl secretion without effecting changes in NaCl absorption. In contrast, mucosal amiloride blocked the effects of cGMP on NaCl absorption but not Cl secretion. The cGMP Isc response was potentiated in the presence of 1 mM, but not 10 microM, amiloride. Moreover, 1 mM amiloride inhibited Isc under control conditions but was ineffective in the presence of cGMP. The Ca2+ ionophore ionomycin (3 microM) produced a transient increase in the Isc that was also associated with a decrease in transepithelial NaCl absorption and an increase in Cl and K secretion. In contrast to cGMP, the ionomycin Isc response was eliminated after Cl removal from the bath.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1980

Osmolar influences on urinary acidification and metabolism in the Colombian toad bladder.

An increase in the osmolarity of the serosal fluid bathing the isolated toad bladder inhibits sodium transport across the preparation. Opposite effects occur with a decrease in serosal Ringer osmolarity. The present experiments investigate the specificity of these osmolar effects by examining the role of extracellular fluid tonicity on the acidification capacity of the isolated Colombian toad bladder. Acidification, estimated by the reversed short-circuit current (RSCC) developing across the Colombian toad bladder in the absence of sodium transport, was stimulated by serosal hypotonicity and inhibited by serosal hypertonicity of acetazolamide. Changes in the mucosal Ringer tonicity had no effect on RSCC. A direct correlation was found between the acidification process and the rate of oxidation of [14C]pyruvate by quarter-bladders exposed to changes in extracellular fluid osmolarity in the presence of amiloride. The osmolar effects on RSCC may result from changes in cell metabolism.

Acetazolamide↗
PubMed1983

Characteristics of NH4+ and NH3 transport across the isolated turtle urinary bladder.

To evaluate the contribution of NH+4 movement to net ammonia flux across the turtle urinary bladder, studies were designed to determine the individual permeabilities of NH3 and NH+4. In these studies we examined the effect of varying the NH+4 concentration gradient while holding that for NH3 constant or the opposite maneuver on the unidirectional flux of ammonia. It was demonstrated that the changes in the unidirectional flux of ammonia was a linear function of the change in the concentration of the varied species. From the slope of these relationships we estimated the NH+4 permeability (4.9 X 10(-6) cm . s-1) and the NH3 permeability (2.6 X 10(-4) cm . s-1). In the absence of H+ transport the unidirectional fluxes of NH+4 were equal, and these fluxes changed in a predictable manner with the application of transepithelial electrical potentials. In the presence of H+ transport there was net NH+4 secretion due to an increase in the serosal-to-mucosal flux. Net secretion could be abolished by inhibiting H+ transport with acetazolamide. The addition of NH4Cl to the serosal solution resulted in a decrement in the rate of mucosal acidification. The subsequent addition of nonvolatile buffer to the serosal solution restored H+ transport and reduced the secretory NH+4 flux to the same extent as that produced by acetazolamide. We conclude that the turtle bladder has a significant passive permeability to NH+4. There also is apparent coupling between H+ transport and ammonia secretion. This coupling may result from titration of NH+4 in the serosal solution to NH3 by alkali generated behind the H+ pump and the diffusion of NH3 into the mucosal solution.

Acetazolamide↗
PubMed1985

Anion transport inhibitors: effects on water and sodium transport in the toad urinary bladder.

Acidification of the medium bathing the serosal surface of the toad urinary bladder results in impairment of the water permeability response to vasopressin. The magnitude of the hydrosmotic response to a maximal concentration of either vasopressin or the cyclic nucleotide analogue 8-(p-chlorophenylthio)-cyclic 3',5'-adenosine monophosphate (C1PhS-cAMP) was progressively reduced when serosal bath pH was decreased from 8.5 to 6.5. The disulfonic stilbenes SITS and DIDS and the diuretic furosemide, agents known to interfere with anion transport and with the regulation of intracellular pH in other tissues, inhibited the water flow response to vasopressin and C1PhS-cAMP in a pH-dependent manner when added to the serosal bathing medium. Inhibition of the hydrosmotic response to 10(-5) M C1PhS-cAMP was estimated to be half-maximal at 1.5 X 10(-4) M SITS, 2 X 10(-5) M DIDS, and 1 X 10(-5) M furosemide. The degree of inhibition induced by the anion transport inhibitors varied inversely with the concentration of exogenous cyclic nucleotide. SITS, DIDS, and furosemide had no effect on either basal or vasopressin-stimulated short-circuit current at serosal pH 8.5; all three agents inhibited basal short-circuit current at pH 7.1 but had no effect on the natriferic response to vasopressin. These results are consistent with the view that changes in intracellular hydrogen ion and/or anion concentration can selectively inhibit the increase in water permeability elicited by vasopressin at a step(s) distal to the generation of cAMP.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1988

Regulation of ciliary beat frequency by autonomic mechanisms: in vitro.

The ciliated epithelium of the mammalian trachea separates the neurohumoral milieu of the tissue from that of the environment of the airway lumen. To determine whether specific autonomic receptors regulating ciliary beat frequency (CBF) were located on mucosal or serosal sides, we measured CBF by heterodyne mode correlation analysis laser light scattering in bovine tracheal tissues mounted in a two-sided chamber. A beta 2-adrenergic agonist, fenoterol, at 10(-7) M, stimulated serosal CBF from 7.9 +/- 1.3 to 20.2 +/- 5.8 Hz (P less than 0.01) and mucosal CBF from 6.6 +/- 0.9 to 14.7 +/- 4.6 Hz (P less than 0.01). A muscarinic cholinergic agonist, methacholine, at 10(-7) M, increased mucosal CBF from 8.4 +/- 1.0 to 19.5 +/- 5.5 Hz (P less than 0.01) and serosal CBF from 8.0 +/- 0.9 to 15.4 +/- 5.0 Hz (P less than 0.01). The differences in stimulation of CBF on the mucosal and serosal sides between fenoterol and methacholine were significant (P less than 0.01). Studies in which these autonomic agonist stimulating effects were inhibited by their respective antagonists, propranolol and atropine sulfate, demonstrated that CBF can be regulated independently by mediators both in the submucosa and within the mucus lining.

Animals↗
PubMed2001

Effects of SNP, ouabain, and amiloride on electrical potential profile of isolated sheep pleura.

The fluid and solute transport properties of pleural tissue were studied by using specimens of intact visceral and parietal pleura from adult sheep lungs. The samples were transferred to the laboratory in a Krebs-Ringer solution at 4 degrees C within 1 h from the death of the animal. The pleura was then mounted as a planar sheet in a Ussing-type chamber. The results that are presented in this study are the means of six different experiments. The spontaneous potential difference and the inhibitory effects of sodium nitroprusside (SNP), ouabain, and amiloride on transepithelial electrical resistance (R(TE)) were measured. The spontaneous potential difference across parietal pleura was 0.5 +/- 0.1 mV, whereas that across visceral pleura was 0.4 +/- 0.1 mV. R(TE) of both pleura was very low: 22.02 +/- 4.1 Omega. cm2 for visceral pleura and 22.02 +/- 3.5 Omega. cm2 for parietal pleura. There was an increase in the R(TE) when SNP was added to the serosal bathing solution of parietal pleura and to the serosal or mucosal bathing solution in visceral pleura. The same was observed when ouabain was added to the mucosal surface of visceral pleura and to either the mucosal or serosal surface of parietal pleura. Furthermore, there was an increase in R(TE) when amiloride was added to the serosal bathing solution of parietal pleura. Consequently, the sheep pleura appears to play a role in the fluid and solute transport between the pleural capillaries and the pleural space. There results suggest that there is a Na+ and K+ transport across both the visceral and parietal pleura.

Amiloride↗
PubMed1982

[In vitro studies on vitamin B6 serosa to mucosa flow in response to various concentrations of pyridoxine HCl in the serous solution].

In vitro experiments using everted sacs of the jejunum of rats weighing about 160 g were conducted to study the possibility of a flux of pyridoxine . HCl (PN . HCl) from the serosa to the mucosa. After an incubation of 45 min with 0, 2, 4, 10, 25, 50, 100, 200 or 500 micrograms PN . HCl per milliliter of serosal solution the transport of vitamin B6 into the intestinal wall and into the mucosal solution was measured. Between the concentration of PN . HCl of the serosal solution and the amount of vitamin B6 transported into the mucosal solution and into the intestinal wall, respectively, there existed a linear correlation in the tested range. In comparison to the serosal amount, the amount transported into the mucosal solution and into the intestinal wall, respectively, was constant when the concentration of PN . HCl in the serosal solution exceeded 25 micrograms PN . HCl per milliliter. Consequently a reflux of vitamin B6 from serosa to mucosa is principally possible, whereby this reflux would depend on a concentration gradient, however. THe possible role of this reflux in respect of maintaining homeostasis of vitamin B6 in the organism is discussed.

Animals↗
PubMed1994

Epithelial modulation of neonatal and fetal porcine bronchial contractile responses.

We tested the hypothesis that bronchial epithelium of newborn and fetal pigs exerts an inhibitory effect on bronchial contractile function. In vitro studies were performed on 13 isolated bronchial segments from seven neonatal pigs (12 h to 4 d old) and on 9 bronchial segments from five late-term pig fetuses (105 d gestation, term = 115 d). This preparation keeps the lumen of the airway physiologically intact and separate from the serosal aspect. Stem bronchi of the right and left lung were mounted horizontally at 6 cm H2O in a chamber containing oxygenated Kreb's solution. One bronchus was intact while the other had the epithelium removed with a cotton-tipped applicator soaked in Kreb's solution. Removal of epithelium was confirmed histologically. The lumen pressure of the mounted bronchi was measured at constant volume after the luminal application of acetylcholine (ACh) or K2SO4 (80 mM/L in place of NaCl), after serosal applications of these two substances at the peak of the luminal response, and after serosal application of ACh alone (newborn only). ACh (1, 10, and 100 microM) in the lumen of intact airways of neonatal pigs caused contractions of 0.1 +/- 0.07 (SEM), 0.4 +/- 0.14, and 0.9 +/- 0.18 cm H2O, respectively; in airways denuded of epithelium, ACh caused contractions of 3.9 +/- 1.1, 15.5 +/- 2.94, and 2.95 +/- 4.97 cm H2O (p < 0.001 versus intact airways). Luminal contractions were 2.9 +/- 2.2%, 2.6 +/- 0.9%, and 2.8 +/- 0.7% of the luminal+serosal values for intact segments, as compared with 65.5 +/- 4.6%, 58.8 +/- 7.7%, and 75.1 +/- 6.2% for denuded segments (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗