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Results for “Fluids and Secretions”

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At least 55 records · Page 3Linked to original sources

PubMed1996

Suppression of enterotoxin-induced intestinal fluid secretion by wood creosote.

Wood creosote suppresses intestinal fluid secretion induced by heat-labile enterotoxin (LT) of enterotoxigenic Escherichia coli (ETEC). When rabbit jejunum is ligated into a 5-cm segment and LT is administered locally, it actively induces intestinal fluid secretion in a dose-dependent manner. Local administration of wood creosote together with a fixed dose of LT suppressed the LT-induced fluid secretion in a dose-dependent manner. At a 50-ng/segment dose of LT, 7.4 +/- 1.1 ml (n = 5) of fluid is secreted into an intestinal segment; coadministration of wood creosote (150 micrograms/segment) significantly (p < 0.01) suppressed the fluid secretion to 2.4 +/- 2.3 ml. Based on these results, we conclude that the antidiarrheal activity of wood creosote is attributable to its antisecretory or proabsorptive effect (or both) on the intestine.

Animals↗

PubMed1995

Influence of adrenoceptor agonists and antagonists on fluid secretion in small bowel obstruction.

OBJECTIVES: To investigate the importance of adrenoceptors on fluid losses in small bowel obstruction. DESIGN: Evaluation of the effects of adrenergic agonists and antagonists on in-vivo net fluid secretion in chronic small bowel obstruction in rats. METHODS: Net fluid transport in a jejunal segment was continuously registered in vivo after 18 h of mechanical obstruction of the small bowel in anaesthetized rats. The effect on net fluid transport of adrenoceptor agonists and antagonists and of isotonic saline was quantified. RESULTS: Clonidine, an alpha 2-agonist, had a significant (P < 0.05) anti-secretory effect, while yohimbine, an alpha 2-antagonist, significantly (P < 0.05) increased net fluid secretion. Phenylephrine, an alpha 1-agonist, and prazosin, an alpha 1-antagonist, lacked significant effects on net fluid transport. Similarly, prenalterol, a beta 1-agonist, and metoprolol, a beta 1-antagonist, had no significant effect on the net fluid transport. The beta 2-agonist salbutamol significantly (P < 0.001) decreased net fluid secretion, while the beta-antagonist propranolol significantly (P < 0.001) decreased net fluid secretion. CONCLUSION: Activation of alpha 2-adrenoceptors and blockade of beta 2-adrenoceptors significantly reduce net fluid secretion in small bowel obstruction. Results also demonstrate a continuous stimulatory effect on fluid secretion mediated by beta 2-receptors and a continuous inhibitory effect mediated by alpha 2-receptors.

Adrenergic Agonists↗

PubMed2005

Dual effects of n-alcohols on fluid secretion from guinea pig pancreatic ducts.

Ethanol strongly augments secretin-stimulated, but not acetylcholine (ACh)-stimulated, fluid secretion from pancreatic duct cells. To understand its mechanism of action, we examined the effect of short-chain n-alcohols on fluid secretion and intracellular Ca(2+) concentration ([Ca(2+)](i)) in guinea pig pancreatic ducts. Fluid secretion was measured by monitoring the luminal volume of isolated interlobular ducts. [Ca(2+)](i) was estimated using fura-2 microfluorometry. Methanol and ethanol at 0.3-10 mM concentrations significantly augmented fluid secretion and induced a transient elevation of [Ca(2+)](i) in secretin- or dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP)-stimulated ducts. However, they failed to affect fluid secretion and [Ca(2+)](i) in unstimulated and ACh-stimulated ducts. In contrast, propanol and butanol at 0.3-10 mM concentrations significantly reduced fluid secretion and decreased [Ca(2+)](i) in unstimulated ducts and in ducts stimulated with secretin, DBcAMP, or ACh. Both stimulatory and inhibitory effects of n-alcohols completely disappeared after their removal from the perfusate. Propanol and butanol inhibited the plateau phase, but not the initial peak, of [Ca(2+)](i) response to ACh as well as the [Ca(2+)](i) elevation induced by thapsigargin, suggesting that they inhibit Ca(2+) influx. Removal of extracellular Ca(2+) reduced [Ca(2+)](i) in duct cells and completely abolished secretin-stimulated fluid secretion. In conclusion, there is a distinct cutoff point between ethanol (C2) and propanol (C3) in their effects on fluid secretion and [Ca(2+)](i) in duct cells. Short-chain n-alcohols appear to affect pancreatic ductal fluid secretion by activating or inhibiting the plasma membrane Ca(2+) channel.

1-Propanol↗

PubMed2000

Relationship between amylase and fluid secretion in the isolated perfused whole parotid gland of the rat.

Whole gland perfusion technique was applied to rat parotid glands to assess whether amylase affects fluid secretion. Control perfusion without any secretagogue evoked no spontaneous secretion. Carbachol (CCh 1 microM) induced both amylase and fluid secretion with distinctive kinetics. Fluid secretion occurred constantly at 40-120 microliter/g-min (average plateau was 60 microliter/g-min), whereas amylase secretion exhibited an initial peak (10 mg maltose/30 s per g wet w. of the gland), followed by a rapid decrease to reach a plateau level of 1 mg maltose/30 s later than 1.5-2 min. Isoproterenol (Isop 1 microM) alone did not induce fluid secretion although it evoked amylase secretion as measured in isolated perfused acini. Addition of Isop during CCh stimulation evoked a rapid and large rise in amylase secretion to 15 mg maltose/30 s accompanied by the increase in oxygen consumption. However, the fluid secretion exhibited a rather gradual decrease. These findings suggest that control of salivary fluid secretion is independent of the amylase secretion system induced by CCh and/or Isop. Morphological observations carried out by HR SEM and TEM revealed exocytotic profiles following Isop stimulation. CCh stimulation alone seldom showed -exocytotic profiles, suggesting a low incidence of amylase secretion during copious fluid secretion. Combined stimulation of CCh and Isop induced both vacuolation and exocytosis along intercellular canaliculi. During washout of secretagogues, lysosomal digestion of excess membrane took place.

Amylases↗

PubMed2001

cAMP-dependent fluid secretion in rat inner medullary collecting ducts.

We used an unambiguous in vitro method to determine if inner medullary collecting ducts (IMCD) have intrinsic capacities to absorb and secrete solutes and fluid in an isotonic medium. IMCD(1), IMCD(2), and IMCD(3) were dissected from kidneys of young Sprague-Dawley rats. 8-Bromo-3',5'-cyclic monophosphate (8-BrcAMP) stimulated lumen formation and progressive dilation in all IMCD subsegments; lumen formation was greatest in IMCD(1.) Benzamil potentiated the rate of lumen expansion in response to 8-BrcAMP. Fluid entered tubule lumens by transcellular secretion rather than simple translocation of intracellular fluid. Secreted lumen solutes were osmometrically active. Inhibition of protein kinase A with H-89 and Rp diastereomer of adenosine 3',5'-cyclic monophosphorothioate blocked fluid secretion. The rate of lumen expansion was reduced by the selective addition of ouabain, barium, diphenyl-2-carboxylate, bumetanide, glybenclamide, or DIDS, or reduction of extracellular Cl(-). We conclude that IMCD absorb and secrete electrolytes and fluid in vitro and that secretion is accelerated by cAMP. We suggest that salt and fluid secretion by the terminal portions of the renal collecting system may have a role in modulating the composition and volume of the final urine.

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

PubMed2001

Salivary fluid secretion in the ixodid tick Rhipicephalus appendiculatus is inhibited by Thogoto virus infection.

Adult Rhipicephatus appendiculatus ticks, infected with Thogoto (THO) virus or control, were fed on guinea pigs and removed at intervals throughout the feeding cycle. Salivary fluid secretion was measured by an in vitro technique. The salivary glands of infected, partially-fed ticks secreted fluid in vitro at about 75% the rate of controls, but the difference between infected and controls among engorged ticks was not statistically significant. Basal and DA-stimulated levels of cyclic AMP (cAMP) were determined in isolated glands and were significantly affected by THO virus infection. The differences in secretory rate among control and infected ticks could not be explained in terms of altered cAMP levels. Haemolymph volume was measured by a tracer-dilution technique using 3H-inulin. The mean haemolymph volume for both THO-infected and control groups was between 23-24% body weight throughout the feeding cycle, indicating that infection by this arbovirus did not influence salivary fluid secretion via altered haemolymph volume. The mechanism by which THO virus affects secretory activity of its tick vector remains unknown.

Animals↗

PubMed1984

Gossypol does not affect testicular fluid secretion in rats.

Male rats fed with gossypol acetic acid at a dose rate of 20 mg/kg/day for 16 weeks were rendered infertile. Spermatozoa flushed out from the cauda epididymides completely lost their capacity to initiate forward motility. However, the rate of testicular fluid secretion measured by the efferent duct ligation technique was not affected by gossypol treatment. The sodium and potassium concentrations of the secreted fluid were found to be unchanged. It is concluded that at low antifertility doses, gossypol disrupts spermatogenic elements in the testis without affecting fluid secretion by the Sertoli cells.

Animals↗

PubMed2004

Adrenergic regulation of salt and fluid secretion in human medullary collecting duct cells.

Transepithelial salt and fluid secretion mediated by cAMP in initial inner medullary collecting ducts (IMCDi) may be important for making final adjustments to urine composition. We examined in primary cultures of human IMCDi cells the effects of adrenergic receptor (AR) agonists and antagonists on intracellular cAMP levels, short-circuit current (I(SC)), and fluid secretion. Epinephrine (1 microM), norepinephrine (1 microM), and isoproterenol (10 nM) individually increased intracellular cAMP levels 57-, 2-, and 25-fold, respectively, and stimulated I(SC) 3.3-, 2.9-, and 3.4-fold, respectively. beta-AR activation increased net fluid secretion by cultured human IMCDi cell monolayers from 0.09 +/- 0.04 to 0.26 +/- 0.05 microl x h(-1) x cm(-2) and freshly isolated rat IMCDi from 0.02 +/- 0.01 to 0.09 +/- 0.02 nl x h(-1) x mm(-1). In monolayers, these effects were eliminated by blocking beta2-AR, but not beta1-AR. Activation of alpha2-AR with guanabenz inhibited isoproterenol-induced I(SC) by 37% in human IMCDi monolayers and fluid secretion by 91% in rat IMCDi. Immunohistochemistry of human medullary tissue sections revealed greater expression of beta2-AR than beta1-AR; beta2-AR was localized to the basolateral membranes of human IMCDi. Immunoblots identified alpha2A-AR and alpha2B-AR in cultured human IMCDi cell monolayers. We conclude that 1) catecholamines stimulate cAMP-dependent anion and fluid secretion by IMCDi cells primarily through beta2-AR activation and 2) alpha2-AR activation attenuates cAMP-dependent anion secretion.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Role of cyclooxygenase-2 for fluid secretion by the inflamed gallbladder mucosa.

Inflammatory fluid secretion by the gallbladder mucosa in experimental cholecystitis is induced by activation of cyclooxygenase, which leads to an increase in prostaglandin formation. Cyclooxygenase exists as a constitutive (cyclooxygenase-l) and an inducible (cyclooxygenase-2) isoform. The aim of this study was to demonstrate the role of cyclooxygenase-2 in inflammatory fluid secretion of the feline gallbladder. Experiments were performed 10 weeks after a surgical procedure in which chronic cholecystitis was induced in cats by ligation of the cystic duct and implantation of a gallstone in the gallbladder. Gallbladder fluid transport was continuously monitored via a perfusion system. In inflammed gallbladders the continuous fluid secretion was reversed to absorption by intravenous injection of the selective cyclooxygenase-2 blocker, NS 398 (P <0.001). Increased levels of the inducible cyclooxygenase-2 were shown by immunoblotting in inflamed gallbladders. Selective pharmacologic blockage of cyclooxygenase-2 reduced the prostaglandin E2 release to the inflamed gallbladder lumen (P <0.01). These data suggest that cyclooxygenase-2 is involved in the inflammatory response during chronic cholecystitis. Selective cyclooxygenase-2 blockers may offer an alternative to traditional nonsterodial anti-inflammatory drugs with fewer side effects in patients with cholecystitis who are awaiting operation.

Animals↗

PubMed1993

Regulation of fluid secretion and intracellular messengers in isolated rat pancreatic ducts by acetylcholine.

1. We have studied the effects of acetylcholine (ACh) on fluid secretion and intracellular messengers in interlobular ducts isolated from the rat pancreas and maintained in short-term tissue culture. 2. Ductal fluid secretion was measured using micropuncture techniques. Intracellular free calcium ([Ca2+]i) and cyclic AMP concentrations were measured in single ducts using fura-2 microspectrofluorimetry and radioimmunoassay techniques respectively. Changes in the levels of these intracellular messengers were correlated with fluid secretion. 3. ACh stimulated ductal fluid secretion. The dose required for a half-maximal response was about 0.4 microM and maximal secretion was achieved with 10 microM ACh. These effects of ACh were blocked by atropine and by removal of extracellular Ca2+. 4. ACh was about four orders of magnitude less potent as an activator of ductal fluid transport than the hormone secretin; however, the maximal rates of fluid secretion evoked by these two agonists were similar. 5. ACh caused a dose-dependent rise in duct cell [Ca2+]i, but had no effect on cyclic AMP. In contrast, secretin increased duct cell cyclic AMP, but had no effect on [Ca2+]i. 6. The [Ca2+]i response evoked by ACh resulted from both mobilization of intracellular Ca2+ stores and influx of Ca2+ from the extracellular space. 7. The Ca2+ ionophore, ionomycin, mimicked the effect of ACh on ductal [Ca2+]i and fluid secretion. 8. We conclude that ACh stimulates fluid secretion from rat pancreatic duct cells by activating a 'Ca2+ pathway' which is distinct from the well documented 'cyclic AMP pathway' utilized by secretin.

Acetylcholine↗

PubMed1997

Cystic fibrosis transmembrane conductance regulator mediates the cyclic adenosine monophosphate-induced fluid secretion but not the inhibition of resorption in mouse gallbladder epithelium.

We have studied the physiological role of the cystic fibrosis (CF) gene product (cystic fibrosis transmembrane conductance regulator [CFTR]) in gallbladder epithelium using a knockout mouse model for CF. We found that normal mouse gallbladder epithelium expresses functional CFTR as shown by reverse-transcription polymerase chain reaction (RT-PCR) analysis and Ussing chamber experiments. Gallbladders from Cftr -/- mice were structurally intact as shown by microscopic and physiological parameters but lacked the cyclic adenosine monophosphate (cAMP)-induced chloride current observed in normal gallbladders. In fluid transport measurements, normal and Cftr -/- gallbladders were equally active in basal resorption. The addition of forskolin, which activates CFTR anion channel activity through the cAMP system, resulted in net fluid secretion in normal gallbladders. In contrast, Cftr -/- gallbladders were unable to secrete fluid while a complete inhibition of resorption by forskolin was observed. We conclude that, in normal mouse gallbladder epithelium, cAMP-induced fluid secretion involves simultaneous inhibition of apical sodium chloride resorption and activation of CFTR. Our data support the hypothesis that gallbladder disease in CF is at least in part caused by a deficient secretory response to the endogenous cAMP-linked hormones VIP and secretin.

Animals↗

PubMed1979

Involvement of calcium and cyclic AMP in controlling ixodid tick salivary fluid secretion.

Catecholamine-stimulated salivary fluid secretion (in vitro) by ixodid ticks is reduced by deletion or lowering the concentration of exogenous bathing medium Ca++. The Ca++ antagonist, verapamil, reversibly inhibits dopamine-stimulated secretion. Ionophore A-23187 is unable to induce glands to secrete. Studies in which labeled and unlabeled Ca++ flux were measured indicate that catecholamines induce release of calcium from intracellular stores during secretion. Cyclic AMP/theophylline-stimulated secretion is inhibited by verapamil, and the exclusion of calcium from the support medium. It is concluded that the primary catecholamine stimulus induces cyclic AMP formation and mobilization of Ca++ (intra- and extracellular). Cyclic AMP and calcium are thought to interact to control secretion within the fluid transporting cells of types II and III alveoli.

Animals↗

PubMed1984

5-Hydroxytryptamine stimulates fluid secretion in locust malpighian tubules independently of cAMP.

5-Hydroxytryptamine (5-HT) stimulates fluid secretion by semi-isolated Malpighian tubules of Locusta in a dose-dependent manner. The threshold of stimulation is between 10(-8) and 10(-7) M 5-HT; maximal activation occurs at doses greater than 10(-6) M. Relative to the activation induced by diuretic hormone (storage lobe extracts), 5-HT increases the rate of fluid secretion by only 65%. Phentolamine, the alpha-adrenergic blocker, failed to inhibit either DH or 5-HT stimulated secretion. Diuretic hormone raises the levels of intracellular of cAMP, and activates adenylate cyclase in plasma membrane preparations of Locusta Malpighian tubules. 5-HT (10(-4) M) has no effect in either assay system. Thus 5-HT can stimulate fluid secretion independently of cAMP. A hypothetical model for hormone stimulated fluid secretion by Locusta Malpighian tubules, involving dual-receptor activation, is proposed. Other biogenic amines, including octopamine, adrenalin, dopamine, synephrine and the formamidine chlordimeform were tested for their ability to stimulate fluid secretion. Only dopamine showed a weakly stimulatory effect.

Animals↗

PubMed2004

A small molecule CFTR inhibitor produces cystic fibrosis-like submucosal gland fluid secretions in normal airways.

Airway submucosal glands have been proposed as a primary site for initiating and sustaining airway disease in cystic fibrosis (CF). However, it has been difficult to define the role of CFTR in gland fluid secretion because of concerns in interpreting experiments on diseased CF human airways subjected to chronic infection and inflammation. Here, we test the role of CFTR in gland fluid secretion by using a selective CFTR inhibitor (CFTRinh-172) in pig and human airways. Measurements of single-gland fluid secretion rates showed inhibition of both cholinergic and cAMP-stimulated fluid secretion by CFTRinh-172. Secreted fluid [Na+] and [Cl-] measured by fluorescence ratio imaging were 101 and 116 mM, respectively, and not significantly altered by secretory agonists or CFTR inhibition. Gland fluid pH was 7.1 and reduced by 0.4 units after CFTR inhibition. Gland fluid viscosity, determined by photobleaching of FITC-dextran, was threefold increased in pilocarpine-stimulated gland fluid after CFTR inhibition, and protein concentration was increased from 12 to 20 mg/ml. Our data provide strong evidence that gland fluid secretion is CFTR-dependent. The relatively hyper-viscous and acidic fluid secretions produced by acute CFTR inhibition support a role for defective gland function in CF lung disease and provide a rational basis for pharmacological creation of a large animal model of CF.

Animals↗

PubMed2003

Inhibition of the SAPK/JNK pathway blocks the stimulatory effects of glutamine on fluid secretion by the Malpighian tubules of Rhodnius prolixus.

Physiological levels of amino acids such as glutamine, glutamate, aspartate and proline increase the rates of fluid secretion and ion transport by serotonin-stimulated Malpighian tubules (MTs) of Rhodnius prolixus. Here, we examine the proposal that the effects of glutamine are mediated through activation of specific kinases to produce the observed increases in fluid secretion. The glutamine-dependent increase in MT fluid secretion rate was blocked by two chemically unrelated inhibitors of the stress activated protein kinase (SAPK) pathway, SP600125 and dicumarol. Inhibitors of phosphatidyl inositol-3 kinase, p38 mitogen activated protein kinase (MAPK), extracellular-signal regulated kinases and MAPK kinase did not block glutamine's effects on fluid secretion rate when applied at commonly used concentrations. Inhibitors of protein kinase A or C reduced fluid secretion rates of serotonin-stimulated MTs, but did not block the response to glutamine. The glutamine-dependent increase in fluid secretion was also insensitive to cytoskeletal disrupting agents and protein synthesis inhibitors. Results of this study are the first to suggest a role for the SAPK pathway in the control of fluid secretion rates by insect MTs.

Animals↗

PubMed1998

Gastric cytoprotection is secondary to increased mucosal fluid secretion: a study of six cytoprotective agents in the rat.

We tested the hypothesis that rapidly developing gastric cytoprotection produced by topical application of exogenous compounds is a result of increased gastric mucosal fluid secretion. Ex vivo gastric chambers were prepared in rats which were subsequently exposed topically to one of the prostaglandin (PG) E1 analogues misoprostol or rioprostil, PGE2, nicotine, N-ethylmaleimide (NEM), 0.25 M HCl, or to their respective vehicles. All agents were added to empty chambers to avoid complications resulting from dilution by gastric contents. Effects of these agents on intraluminal volume changes, blood flow, juxtamucosal pH, histology, and on the mucosal damage resulting from necrotizing agents were studied. All six agents were cytoprotective and each increased net secretion of fluid by the chambered mucosae. Gastric blood flow was not significantly increased by NEM, by 0.25 M HCl, or by nicotine compared to controls, and the juxtamucosal pH was not significantly increased by any of the three agents for which this was studied. Vacuole formation in surface epithelial cells and subepithelial edema were seen after exposure to some agents, but none of the agents led to formation of a thick barrier of exfoliated cells and mucus. Ablation of primary afferent nerves with capsaicin abolished both protection by 0.25 M HCl and the net increase in fluid secretion by the mucosae. Capsaicin ablation did not alter either the protection afforded by NEM or the increase in volume of secretion. We conclude that increased mucosal fluid secretion is the common factor present with all six cytoprotective agents and hence may be the predominant mechanism of cytoprotection against topically applied necrotizing agents.

Animals↗

PubMed1988

Fluid secretion in glomerular renal proximal tubules of freshwater-adapted fish.

Tubular secretion by renal proximal tubules, as a mechanism for delivering fluid and electrolytes to the urine, has received little attention in modern conceptions of renal function in vertebrates even though it is the mechanism for urine production in aglomerular fish. This report demonstrates that some proximal tubules of glomerular kidneys of freshwater-adapted euryhaline fish spontaneously secrete fluid. The fluid consists primarily of Na (138 mM) and Cl (160 mM). NaCl and fluid secretion can be stimulated by adenosine 3',5-cyclic monophosphate, suggesting that tubular fluid secretion is under hormonal control. Fluid secretion driven by NaCl secretion in glomerular proximal tubules of fish that already filter NaCl and water suggests that secretion of fluid and NaCl may play a fundamental role in vertebrate renal function beyond a preadaptation for aglomerular urine formation.

Animals↗

PubMed1986

Calcium-activated potassium channels and fluid secretion by exocrine glands.

Fluid secretion by exocrine glands is regulated by neurotransmitters and hormones. The secretagogues act on the acinar cells by switching on two types of conductance pathways: K+-selective channels in the basolateral membrane and Cl(-)-selective channels localized to the luminal membrane. The K+ channels have been quantitatively characterized in patch-clamp single-channel and whole-cell current-recording studies. Opening of the K+ channels is determined by the membrane potential (depolarization enhances the probability of channel opening), and the intracellular free Ca2+ concentration ([Ca2+]i) (a rise in [Ca2+]i increases the open-state probability). The Cl- channels are also controlled by internal Ca2+ in such a way that an elevation of [Ca2+]i favors opening. Secretagogues evoking an increase in [Ca2+]i activate both sets of channels causing a substantial loss of cellular KCl. KCl is taken up via a Na+-K+-2Cl- cotransport mechanism in the basolateral membrane and the Na+ uptake activates the Na+-K+ pump. In the steady-state stimulated situation the three basolateral transport proteins, the K+ channels, the Na+-K+ pump, and the Na+-K+-2Cl- cotransporter operate together as an electrogenic Cl- pump. Cl- exits into the lumen via the Ca2+-activated Cl- channels and Na+ follows through the paracellular shunt pathway. When stimulation of the acinar cells ceases the K+ and Cl- conductance pathways close and the Na+-K+ pump together with the Na+-K+-2Cl- cotransporter operate as a KCl pump, restoring the intracellular KCl lost initially after start of stimulation and secretion stops.

Animals↗