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PubMed1978

The relationship of phosphodiesterase and cyclic AMP to the process of fluid secretion in the salivary glands of the ixodid tick Amblyomma americanum.

Phosphodiesterase (PDE) activity in the salivary glands of the female. Amblyomma americanum decreased as the tick progressed from a slow to a rapid phase of feeding, while the rate of fluid secretion increased when glands were stimulated with cyclic AMP and theophylline. Dopamine stimulated PDE activity and an 'inhibitory' factor was found in glands obtained from rapidly engorging ticks which decreased PDE activity. These findings are discussed as they relate to the process of fluid secretion by salivary glands of feeding ixodid ticks.

Animals↗
PubMed1991

Developing fetal alveolar epithelial cells secrete fluid in primary culture.

The developing pulmonary epithelium secretes a Cl(-)-rich fluid during fetal life by a process involving active transport. To determine if alveolar cells contribute to this fluid production, we studied developing fetal rat alveolar epithelial cells (18-day gestation) in primary culture. Fetal alveolar epithelial cells aggregated to form cystic, alveolar-like structures with a fluid-filled lumen. On light and transmission electron microscopy, the cells were polarized with microvilli facing the lumen. Dexamethasone and triiodothyronine stimulated lamellar body production in many of the epithelial cells of the cyst wall. The transepithelial voltage in the cyst was -2.4 +/- 0.4 mV (lumen negative), suggesting the presence of active electrolyte transport. Bumetanide, an inhibitor of Cl- secretion in other systems, decreased the size and number of cysts. A membrane-permeant analogue of adenosine 3',5'-cyclic monophosphate (cAMP) and 3-isobutyl-1-methylxanthine increased the size of cysts, an effect that was blocked by coincubation with bumetanide. The increased size of the cysts did not result from stimulation of cell growth; in fact, [3H]thymidine incorporation was inhibited to 40% control values by cAMP, suggesting that growth was inhibited rather than stimulated. These results suggest that fetal alveolar epithelial cells secrete fluid via a cAMP-mediated Cl(-)-secretory process. Secretion of fluid by the developing alveolar epithelium may play an important role in lung development.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Mechanisms underlying the small intestinal fluid secretion caused by arachidonic acid, prostaglandin E1 and prostaglandin E2 in the rat in vivo.

Prostanoids were given intraluminally (PGE2) or infused close intra-arterially (PGE1 and PGE2) or arachidonic acid was administered intraluminally to denervated jejunal segments of the rat in vivo. These experimental manoeuvres caused a net fluid secretion, although a 1,000-fold higher concentration of the prostanoids was needed from the luminal than from the vascular side. I.v. hexamethonium or serosally applied lidocaine diminished the induced fluid secretion suggesting that the prostanoids act mainly by eliciting local secretory reflexes in the enteric nervous system. This nerve-mediated secretion is not accompanied by any increase in tissue cAMP. However, at higher i.a. concentrations of PGE2 there seems to be a non-neurogenic effect on the enterocytes associated with an increase in tissue cAMP.

Alprostadil↗
PubMed1990

[Ca2+]i modulation of Cl- content controls cell volume in single salivary acinar cells during fluid secretion.

Differential interference contrast microscopy and low-light-level digital imaging of the fluorescent chloride indicator dye 6-methyl-1-(3-sulfonatopropyl)quinolinium (SPQ) were performed simultaneously in single mammalian salivary gland acinar cells to examine the relationship between cytoplasmic chloride concentration [( Cl-]i) and cell volume during stimulus-secretion coupling. Agonist stimulation of Cl(-)-driven fluid secretion is associated with rapid, Ca2(+)-dependent changes of cell volume, which are temporally coupled to changes of [Cl-]i. The agonist-induced changes in [Cl-]i, if accompanied by cations and water, quantitatively account for the cell volume changes, demonstrating in a single cell that cell volume is determined by cell solute content. Agonist-induced modulation of cell volume appears to be a consequence of the requirement to develop appropriate ion gradients necessary for vectorial salt (and fluid) transport.

Animals↗
PubMed2003

Acid challenge delays gastric pressure adaptation, blocks gastric emptying and stimulates gastric fluid secretion in the rat.

Functional dyspepsia can be associated with impaired gastric relaxation in response to food intake and delayed gastric emptying. In this study, we investigated whether luminal hydrochloric acid (HCl) may reproduce these motor alterations in phenobarbital-anaesthetized rats via activation of extrinsic neural pathways. Intragastric pressure (IGP) changes induced by a 2-mL fluid bolus were recorded with an oesophageal catheter, and gastric emptying was determined via the fluid volume recovered from the stomach 30-min post-bolus. Experiments involving acute nerve transections or pharmacological blockade of nitric oxide synthesis revealed that the initial increase of IGP after a 0.35 mol L(-1) HCl bolus is dampened by duodenogastric and gastrogastric relaxation reflexes depending on vagal and splanchnic pathways as well as nitric oxide. Compared with saline, HCl (0.15-0.5 mol L(-1)) delayed the subsequent decrease (adaptation) of IGP, inhibited gastric emptying and stimulated gastric fluid secretion as seen in stomachs with ligated pylorus. The acid-evoked delay in IGP adaptation and inhibition of gastric emptying involved duodenogastric and duodenopyloric extrinsic nerve reflexes, whereas the gastric fluid secretion was independent of the extrinsic innervation. It is proposed that the gastropyloric motor changes induced by luminal acid challenge have a bearing on the motor disturbances underlying functional dyspepsia.

Animals↗
PubMed2004

A model for fluid secretion in Rhodnius upper Malpighian tubules (UMT).

We have measured fluid secretion rate in Rhodnius prolixus upper Malpighian tubules (UMT) stimulated to secrete with 5-OH-tryptamine. We used double perfusions in order to have access separately to the basolateral and to the apical cell membranes. Thirteen pharmacological agents were applied: ouabain, Bafilomycin A(1), furosemide, bumetanide, DIOA, Probenecid, SITS, acetazolamide, amiloride, DPC, BaCl(2), pCMBS and DTT. These agents are known to block different ion transport functions, namely ATPases, co- and/or counter-transporters and ion and water channels. The basic assumption is that water movement changes reflect changes in ion transport mechanisms, which we localize as follows: (i) At the basolateral cell membrane, fundamental are a Na(+)-K(+)-2Cl(-) cotransporter and a Cl(-)-HCO(3) (-) exchanger; of intermediate importance are the Na(+)-K(+)-ATPase, Cl(-) channels and Rp-MIP water channels; K(+) channels play a lesser role: (ii) At the apical cell membrane, most important are a K(+)-Cl(-) cotransport that is being located for the first time, a V-H(+)-ATPase; and a Na(+)-H(+) exchanger; a urate-anion exchanger and K(+) channels are less important, while Cl(-) channels are not important at all. A tentative model for the function of the UMT cell is presented.

Animals↗
PubMed1990

5-HT2 and 5-HT3 receptor subtypes mediate cholera toxin-induced intestinal fluid secretion in the rat.

The mechanisms of diarrhea in Asiatic cholera have been studied extensively. Cyclic adenosine monophosphate, 5-hydroxytryptamine (5-HT), prostaglandins, and the function of neuronal structures have been implicated in the pathogenesis of cholera. To elucidate the action of 5-HT in mediating cholera secretion, in vivo experiments were performed in the rat jejunum. The inhibitory effects of the 5-HT2 receptor antagonist ketanserin and the 5-HT3 receptor antagonist ICS 205-930 were studied in cholera toxin- and 5-HT-induced fluid secretion. Both ketanserin and ICS 205-930 dose-dependently but only partially reduced the secretory effect of cholera toxin. The combination of the two blockers totally abolished cholera toxin-induced secretion without any influence on cholera toxin-induced increase in cyclic adenosine monophosphate. Prostaglandin E2- and bisacodyl-induced secretion was not affected by the combined administration of 5-HT2 and 5-HT3 antagonists. The present results provide evidence for an important role of 5-HT in cholera toxin-induced secretion. The data suggest a model in which cholera toxin may initiate the release of 5-HT from enterochromaffin cells. 5-Hydroxytryptamine may then cause prostaglandin E2 formation via 5-HT2 receptors and activation of neuronal structures via 5-HT3 receptors. These two effects may finally lead to the profuse fluid secretion which can be totally blocked by the combination of a 5-HT2 blocker and a 5-HT3 blocker.

Animals↗
PubMed1997

Role of kinases and phosphatases in the regulation of fluid secretion and Cl-/HCO3- exchange in cholangiocytes.

The role of protein kinase A (PKA), protein kinase C (PKC), and protein phosphatases in the process of secretin stimulation of fluid and bicarbonate secretion from biliary epithelium was examined using a novel isolated bile duct unit (IBDU) model from rat liver. Sp-adenosine 3',5'-cyclic monophosphothiolate (Sp-cAMPS), 100 microM, a PKA-specific agonist, significantly increased secretion during a 30-min perfusion (+61%, P < 0.01). In contrast, preincubation and perfusion of Rp-cAMPS, 100 microM, a specific PKA inhibitor, reduced the ability of secretin to stimulate both fluid secretion (111 vs. 25%; P < 0.01) and Cl-/HCO3- exchanger activity (80 vs. 28%). Neither the PKC agonist phorbol 12-myristate 13-acetate, 10 microM, nor the PKC antagonist staurosporine showed any effect on either basal or secretin-stimulated fluid secretion or Cl-/HCO3- exchange activity in IBDU. Okadaic acid, a specific inhibitor of protein phosphatases 1 and 2A, also had no effect on basal fluid secretion or on the basal activity of the Cl-/HCO3- exchanger. However, okadaic acid resulted in persistence of secretion after removal of secretin, in contrast to the reduction in secretion observed in controls. These findings indicate that PKA but not PKC is involved in the signal transduction of secretin-stimulated fluid secretion and Cl-/HCO3- exchange activity in rat bile duct epithelium, a process inactivated by dephosphorylation by protein phosphatases 1 and/or 2A.

Animals↗
PubMed2002

Role of gap junctions in fluid secretion of lacrimal glands.

In glands such as the liver and pancreas, gap junctions containing connexin 26 and 32 (Cx26 and Cx32, respectively) couple the secretory cells. Uncoupling these junctions compromises the secretory function of these glands. Lacrimal glands also contain extensive arrays of gap junctions consisting of Cx26 and Cx32. We wanted to determine the role of these junctions in fluid secretion. In Cx32-deficient mice, immunocytochemistry showed that, in the male lacrimal gland, the remaining Cx26 was found evenly distributed in the membrane whereas there was little in the membranes of female glands. Western blot analysis of Cx26 showed that female Cx32-deficient mice expressed Cx26. Patch-clamp analyses of acinar cell coupling showed that the cell pairs from male glands were coupled whereas those from female glands were not. Stimulated fluid production by the glands from Cx32-deficient mice was abnormally low in female glands compared with controls at low topical doses of carbachol. The protein secretory response to different doses of carbachol was the same in all animals. These data suggest that gap junctions are essential for optimal fluid secretion in lacrimal glands.

Analysis of Variance↗
PubMed2006

Bacteroides fragilis enterotoxin induces cyclooxygenase-2 and fluid secretion in intestinal epithelial cells through NF-kappaB activation.

Bacteroides fragilis produces an approximately 20-kDa heat-labile toxin (B. fragilis enterotoxin, BFT) which is known to be associated with diarrhea. To determine whether cyclooxygenase (COX)-2, via NF-kappaB activation, can contribute to BFT-induced diarrhea, the relationship between COX-2 expression and fluid secretion in BFT-stimulated human intestinal epithelial cells was examined. BFT stimulation increased the expression of COX-2, but not COX-1, in human intestinal epithelial cells. Suppression of the NF-kappaB signal significantly decreased COX-2 expression in response to BFT stimulation. Prostaglandin E2 (PGE2) levels were increased in parallel with COX-2 expression, and, conversely, PGE2 production was significantly inhibited when COX-2 or NF-kappaB activities were suppressed using COX-2 small interfering RNA (siRNA), p65 NF-kappaB subunit siRNA, or a retrovirus encoding the IkappaBalpha superrepressor. In addition, a selective COX-2 inhibitor, NS-398, significantly inhibited the increased cAMP level induced by BFT stimulation. Furthermore, a selective COX-2 inhibitor prevented BFT-induced PGE2 production and ileal fluid secretion in a mouse ileal loop model. These results suggest that the secretory response to BFT stimulation may be mediated by the production of PGE2, through NF-kappaB activation and the up-regulation of COX-2 in intestinal epithelial cells.

Animals↗
PubMed1997

A single cDNA encodes all three Aedes leucokinins, which stimulate both fluid secretion by the malpighian tubules and hindgut contractions.

A cDNA encoding preproleucokinin was isolated from a cDNA library of the mosquito Aedes aegypti. The deduced amino acid sequence of Aedes preproleucokinin contains a putative signal peptide of 18 amino acid residues and a 210-amino acid residue proleucokinin. Within the proleucokinin are encoded one copy each of the Aedes leucokinins 1, 2, and 3 isolated previously from this species (Veenstra, J. A. (1994) Biochem. Biophys. Res. Commun. 202, 715-719). All three Aedes leucokinins depolarize the transepithelial voltage of the malpighian tubule in concentrations of less than 10(-9) M and increase the frequency of hindgut contractions at concentrations above 10(-8) M. At higher concentrations the Aedes leucokinins 1 and 3 but not Aedes leucokinin 2 are also able to increase the rate of fluid secretion by the malpighian tubules. The differences of the three Aedes leucokinins in their potencies to induce fluid secretion or depolarizations in the malpighian tubules suggest that there may be more than one type of leucokinin receptor in this tissue.

Aedes↗
PubMed2002

NaCl and fluid secretion by the intestine of the teleost Fundulus heteroclitus: involvement of CFTR.

Sections of posterior intestine of the euryhaline killifish Fundulus heteroclitus adapted to sea water were stimulated by the calcium ionophore ionomycin (1 micromol l(-1)) in combination with agents to elevate intracellular cyclic AMP levels, 0.5 mmol l(-1) dibutyryl-cyclic AMP (db-cAMP) with 0.1 mmol l(-1) 3-isobutyl-1-methylxanthine (IBMX). Intestinal bag preparations from recently fed animals (but not from overnight unfed animals) changed from fluid absorption (+18.9+/-8.30 microl cm(-2) h(-1), N=8) in the untreated control period to net fluid secretion after stimulation (-7.43+/-1.30 microl cm(-2) h(-1), N=8, P<0.01; means +/- S.E.M.), indicative of the capacity of teleost intestine to undergo secretion. Posterior intestinal pieces mounted in vitro in Ussing-style membrane chambers showed net Cl(-) uptake (+2.245+/-0.633 microequiv cm(-2) h(-1), N=7) that turned to net secretion following stimulation by ionomycin + db-cAMP + IBMX (-3.809+/-1.22 microequiv cm(-2) h(-1), N=7, P<0.01). Mucosal application of the anion channel blocker 1 mmol l(-1) diphenylamine-2-carboxylate (DPC) after ionomycin + db-cAMP + IBMX treatment significantly reduced serosal-to-mucosal unidirectional Cl(-) flux (P<0.001), net Cl(-) flux (P<0.05), short-circuit current (I(sc), P<0.001) and tissue conductance (G(t), P<0.001), while 0.1 mmol l(-1) 4,4'-diisothiocyano-2,2'-stilbene-disulphonic acid (DIDS, a blocker of anion exchange) was without effect. Stimulation by db-cAMP + IBMX (no ionomycin) significantly increased unidirectional fluxes, I(sc) and G(t) but did not produce net Cl(-) secretion. Ionomycin alone produced a transient increase in I(sc) but had no effect on G(t) and caused no significant changes in unidirectional or net Cl(-) fluxes. Addition of db-cAMP + IBMX after ionomycin treatment produced net secretion of Cl(-) and large increases in unidirectional fluxes and G(t). Cystic fibrosis transmembrane conductance regulator (CFTR) was immunocytochemically localized with a monoclonal mouse antibody to the carboxy terminus and found to be present in the cytoplasm and basolateral membranes of all enterocytes and in the brush-border membrane of some cells, whereas NKCC immunofluorescence, demonstrating the presence of the Na(+)/K(+)/2Cl(-) cotransporter, was present in the cytoplasm and brush-border membrane. We conclude that the teleost intestine is capable of salt and fluid secretion only if intracellular Ca(2+) and cyclic AMP pathways are stimulated together and that this secretion appears to involve activation of CFTR ion channels in the apical membrane of a subpopulation of enterocytes.

1-Methyl-3-isobutylxanthine↗
PubMed1976

Studies on the mechanism of fluid secretion by isolated salivary glands of Calliphora.

1. Potassium is the major cation in the secretion of the salivary glands of Calliphora and is necessary for full secretory rates. 2. Other ions (rubidium and sodium) can support secretion in the absence of potassium. 39. During stimulation with 5-HT a Nernst plot of the basal membrane potential has a slope of 53 mV for a tenfold change in external potassium concentration and the slope at rest deviates from this over the range I-20 mM external potassium. 4. Hyperpolarization of the basal membrane by 5-HT is abolished if the chloride in the bathing medium is replaced by isethionate. 5. The diuretic agent amiloride inhibits fluid secretion by a mechanism which may include a reduction in calcium entry in addition to its recognized effect on sodium permeability. 6. A model is proposed in which fluid secretion is driven by the active transport of potassium across the apical membrane with chloride following passively.

Amiloride↗
PubMed1984

Electrical potential, resistance, and fluid secretion across isolated ciliary body.

Rabbit ciliary epithelium was mounted with the sclera and lens still attached. The potential measured in physiological bathing medium was 1.29 +/- 0.18 mV initially, but dropped to 0.66 +/- 0.34 mV, then became stable for 2 hr or more. The resistance of the epithelium was measured by comparing total trans-tissue resistance before and after treatment with Triton X-100, ethanol, or distilled water. The calculated resistance with correction for epithelial surface area was found to be 1504 +/- 452 omega, in six experiments. Fluid secretion was measureable against a hydrostatic gradient when identical solutions bathed both sides of the preparation. Ouabain caused opposite responses when applied to either side of the preparation, indicating that it does not readily cross the epithelial barrier. The evidence presented suggests that the ciliary epithelium is a 'tight' rather than a 'leaky' epithelium, and that fluid secretion in the normal ciliary epithelium occurs by active transport rather than by ultrafiltration.

Animals↗
PubMed2001

Rubidium reduces potassium permeability and fluid secretion in Malpighian tubules of Locusta migratoria, L.

The basal membrane potential (V(b)) of Locusta Malpighian tubule cells in control saline results from its relatively high permeability to potassium. In the presence of 1 mM barium added to the control saline V(b) hyperpolarized from a mean resting potential of -72.1 mV to -90.1 mV. On substituting rubidium for potassium in the control saline, V(b) also hyperpolarized to a value of -91.4 mV. Rubidium was also similarly effective in hyperpolarizing the basal membrane even in the presence of control concentrations of potassium in the bathing medium. Substitution of rubidium for potassium also effected a approximately 50% reduction in the rate of fluid secretion. The action of inhibitors on V(b) in the presence of rubidium showed that V(b) under these conditions probably originated from the bafilomycin-sensitive electrogenic potential generated across the apical membrane by a V-type ATPase. The responses of V(b) to potassium, barium and rubidium and their inhibition of fluid secretion suggest the presence of a substantial rubidium-blockable potassium conductance located on the basal membrane of Locusta Malpighian tubule cells.

Journal Article↗
PubMed1981

Epidemiology of breast fluid secretion: association with breast cancer risk factors and cerumen type.

The epidemiology of breast fluid secretion was studied on the basis of nipple aspirates of breast fluid obtained from 3,929 nonlactating women of various racial groups. The results confirmed and extended earlier findings by our group: Variation in the proportion of secretors was related to most breast cancer risk factors, including age, race, age at menarche, age at first pregnancy, age at menopause, clinically diagnosed fibrocystic disease, menopausal estrogen use, and cerumen phenotype. Secretory activity as measured by nipple aspiration appeared to reflect hormonal and genetic effects on breast epithelium.

Adolescent↗
PubMed1981

A possible role for calcium in cyclic nucleotide mediated fluid secretion.

This article suggests that calcium acts as an intermediate for intestinal fluid secretion mediated by adenosine-3':5'-cyclic monophosphoric acid (cAMP) and guanosine -3':5-'cyclic monophosphoric acid (cGMP). It is hypothesized that microbial enterotoxins disrupt the normal interrelationships between calcium and cyclic nucleotides, thereby leading to adverse biological effects. It is further proposed that the inhibitory effect of chlorpromazine on calmodulin accounts for the ability of this drug to inhibit enterotoxins which separately elevate cAMP or cGMP concentrations.

Adenylyl Cyclases↗
PubMed1991

A capacitative Ca2+ influx is required for sustained fluid secretion in sublingual mucous acini.

The Ca2+ dependence of muscarinic-induced fluid and electrolyte secretion was studied using rat sublingual mucous gland preparations. During stimulation, secretions from vascularly perfused glands were totally inhibited when perfused with a Ca(2+)-free medium. Fluid secretion correlated with sustained losses of 42K+ and 36Cl- content and sustained increases in 22Na+ content and the intracellular free Ca2+ concentration ([Ca2+]i) in fura-2-loaded acini. The magnitudes of the initial agonist-induced changes in Na+, K+, and Cl- content and [Ca2+]i were unaltered in a Ca(2+)-free medium, whereas extracellular Ca2+ removal resulted in the recovery of these ions during the sustained phase to pre-stimulation levels. The recovery of Cl- content induced by Ca2+ depletion was totally blocked in the presence of bumetanide, an inhibitor of Na(+)-K(+)-2Cl- cotransport, while 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), an inhibitor of anion exchange, did not influence Cl- recovery in a HCO(3-)-containing solution (25 mM NaHCO3, 5% CO2). The stimulated increase in [Ca2+]i was not inhibited by the addition of voltage-activated Ca2+ channel blockers (D 888, nifedipine, and diltiazem) or in a Na(+)-free medium. Studies using the quench of fura-2 by Mn2+ as an index of Ca2+ influx and thapsigargin, an inhibitor of microsomal Ca(2+)-ATPase, indicate that a capacitative Ca2+ entry pathway mediates Ca2+ entry during stimulation. The above data demonstrate that Ca2+ uptake, which is dependent on the refill status of the agonist-sensitive intracellular Ca2+ pool, is a prerequisite for sustained muscarinic-induced fluid and electrolyte secretion in the rat sublingual mucous gland.

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