Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Fluids and Secretions”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources

Interrelationships of chloride, bicarbonate, sodium, and hydrogen transport in the human ileum.

Using a triple-lumen constant perfusion system, the following observations were made in normal subjects. First, chloride, bicarbonate, and sodium were found to exhibit net movement across ileal mucosa against electrochemical gradients. Second, during perfusion with a balanced electrolyte solution simulating plasma, the ileum generally absorbed, but sometimes secreted fluid. A reciprocal net movement of chloride and bicarbonate was noted when sodium movement was zero. Increasing rates of sodium absorption were associated with decreasing bicarbonate secretion rates and finally bicarbonate absorption. Even when bicarbonate was absorbed ileal contents were alkalinized (by contraction of luminal volume). Third, net chloride movement was found to be sensitive to bicarbonate concentration in ileal fluid. For instance, chloride was absorbed from solutions containing 14 or 44 mEq/liter of bicarbonate, but was secreted when ileal fluid contained 87 mEq/liter of bicarbonate. Fourth, when chloridefree (sulfate) solutions were infused, the ileum absorbed sodium bicarbonate and the ileal contents were acidified. Fifth, when plasma-like solutions were infused, the potential difference (PD) between skin and ileal lumen was near zero and did not change when chloride was replaced by sulfate in the perfusion solution. These results suggest that ileal electrolyte transport occurs via a simultaneous double exchange, Cl/HCO2 and Na/H. In this model neither the anion nor the cation exchange causes net ion movement; net movement results from the chemical reaction between hydrogen and bicarbonate. No other unitary model explains all of the following observations: (a) human ileal transport in vivo is essentially nonelectrogenic even though Na, Cl, and HCO3 are transported against electrochemical gradients, (b) the ileum can secrete as well as absorb, (c) ileal contents are alkalinized during absorption of or during secretion into a plasma-like solution, and (d) the ileum acidifies its contents when sulfate replaces chloride. Data obtained with a carbonic anhydrase inhibitor support the proposed model.

Acetazolamide↗

Ultrastructural, histochemical and electrophysiological study of calf gallbladder epithelium.

Calf (Bos taurus) gallbladder, contrary to that of most mammalian, does not concentrate bile. It is to be ascertained whether this phenomenon is the result of a lack of fluid absorption or a balance between the latter and fluid secretion. To this end we began a characterization of bovine gallbladder epithelium by means of electron microscopy, immunocytochemistry, enzymatic activity and electrophysiological measurements. We also partially characterized bile content. The ultrastructural examination showed that surface epithelial cells have the general structure that is observed in absorptive epithelia. Mucous secretory activity is also evident. Moreover, two distinct types of secreting cells line the glands in the lamina propria and contribute to the production of an abundant secretion. The cell surface shows a marked reactivity with the anti-alkaline phosphatase serum. Most of the activity of alkaline phosphatase and L-gamma-glutamyltransferase is found at the apical side of the epithelium. Electrophysiological parameters indicate that this is a low resistance epithelium. Therefore, coexistence of features typical of absorptive epithelia and the inability of concentrating bile suggest that, in this organ, fluid absorption and secretion are both present.

Alkaline Phosphatase↗

Effect of alpha- and beta-adrenergic agonists on fluid and calcium secretion by rat salivary glands.

The separate roles of alpha- and beta-adrenergic receptors in regulating fluid and calcium (Ca) secretion by rat salivary glands were examined using phenylephrine (PE), an adrenergic agonist that acts predominantly on alpha-receptors, isoproterenol (ISO), an adrenergic agonist that acts predominantly on beta-receptors, and PE and ISO in combination with beta-adrenergic antagonist propranolol (PROP) and alpha-adrenergic antagonist phentolamine (PHENTO), respectively. PE evoked a greater volume of saliva from submandibular (SM) gland than from parotid (PA) gland, whereas ISO evoked a similar volume of saliva from both glands during 60-min of drug stimulation. PE even at a low dose had beta-adrenergic effects on flow rate of salivary glands because pretreatment of rats with PROP (1 mg/kg) 20 min before PE (5 mg/kg, i.p.) stimulation resulted in a 4-fold reduction in total volume of PE-evoked PA saliva. Thus alpha-adrenergic receptors play a major role in fluid secretion by SM glands but play only a minor role in PA glands. ISO evoked SM and PA saliva with Ca concentration higher than that evoked by PE. ISO (25 mg/kg, i.p.) also had an effect on alpha-adrenergic receptors as well as beta-adrenergic receptors. Although PHENTO did not significantly alter flow rate and volume of ISO-evoked PA or SM saliva, Ca concentration of ISO-evoked saliva was greatly potentiated by PHENTO. Total Ca output of ISO-evoked saliva from either gland was not significantly altered by PHENTO. Thus, in both salivary glands, activation of beta-adrenergic receptors evoked saliva with a high concentration of Ca.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Excretion in the house cricket: stimulation of rectal reabsorption by homogenates of the corpus cardiacum.

1. We describe an in vitro perfused preparation of Acheta domesticus rectum which allows direct comparison of Malpighian tubule secretion and rectal absorption under identical conditions. Rectal absorption is stimulated four- to sixfold by corpora cardiaca (CC) homogenates and the stimulated rate is sufficiently rapid to account for all the fluid secreted by the tubules. 2. The time course for increased fluid absorption is similar to that required to stimulate electrogenic chloride transport in locusts and grasshoppers. Chloride is rapidly absorbed by the rectum under all conditions, along with lesser amounts of Na+ and K+. Unlike the situation in locusts, K+ uptake is unaffected by CC homogenates and the stimulated absorbate is NaCl-rich, similar in composition to the NaCl-rich tubule fluid produced under stimulated conditions. The absorbate is always slightly hypo-osmotic to the perfusate, reaching a maximum differential of approximately 15 mosmol l-1 following CC stimulation. 3. The antidiuretic factor that reduces tubule secretion does not promote fluid reabsorption by the rectum.

Absorption↗

Role of the W07-toxin on Vibrio cholerae-induced diarrhoea.

Vibrio cholerae W07 strain isolated from a cholera epidemic in South India, lacked the ctx gene but could still secrete a novel toxin, the W07-toxin that could cause fluid accumulation in ligated rabbit ileal loop. The important intracellular messengers implicated in this study were Ca(2+), cyclic AMP, inositol triphosphate and protein kinase C (PKC). A number of inhibitors/channel blockers have further shown the major role of [Ca(2+)](i) in modulation of the toxin-induced cellular response. An increase in the level of reactive oxygen species (ROS) in the W07-toxin-stimulated enterocytes correlated with the decrease in the levels of antioxidant enzymes, catalase and superoxide dismutase (SOD). The reactive nitrogen intermediates (RNI) detected by measuring the levels of nitrite and citrulline, were found to be high in the enterocytes triggered with the W07-toxin, thereby indicating their role in toxin-mediated change in mucosal permeability. The precise role of the toxin has also been authenticated by conducting the experiments with W07-toxin preincubated in the presence of IgG(WT) (IgG isolated from antitoxin sera) or GM(1). Thus, a significant increase in the levels of second messengers and a decrease in antioxidant defenses appear to be important in mediating the fluid secretion caused by this novel toxin from V. cholerae W07.

Animals↗

Glycoprotein 340 in normal human ocular surface tissues and tear film.

The tear film is a complex mixture of secreted fluid, ions, proteins, glycoproteins, and lipids that lubricates and protects the ocular surface. Recently, several antimicrobial peptides have been described in the tear fluid. In this study, we describe the presence of the large secreted glycoprotein gp340 in the tear film. Western blot analysis showed that gp340 is abundant in secreted tears and in the lacrimal glands. Lesser amounts of gp340 were detected in the cornea and conjunctiva. Consistent with Western blot data, reverse transcription-PCR and real-time quantitative PCR showed that gp340 transcripts were abundant in lacrimal gland tissue and were also present in the cornea and conjunctiva. Immunohistochemistry localized gp340 to the acinar cells of the lacrimal gland and the deeper layers of the conjunctival epithelium. gp340 was not detected in conjunctival goblet cells. In the cornea, gp340 was present only in a peripheral band of basal epithelial cells, suggesting that gp340 may play a role in the cycle of corneal epithelial renewal. To determine if tear film gp340 may function as a bacterial agglutinin as it does in saliva, tears were incubated with streptococcal cells and the formation of bacterial aggregates was monitored. Addition of tears to late-exponential-phase Streptococcus mutans cells resulted in time- and dose-dependent aggregation of the bacteria. Furthermore, Western blot analysis confirmed the presence of cell-associated gp340 in isolated bacterial aggregates. The ocular pathogen Staphylococcus aureus, but not Pseudomonas aeruginosa, also aggregated when incubated with tears. These results suggest that gp340 is a normal component of the tear film and that the glycoprotein may function as a bacterial agglutinin.

Adult↗

Altered ion transport by tracheal glands in cystic fibrosis.

Acini of tracheal glands from 12 humans without cystic fibrosis (CF) and from two CF patients were isolated by enzymatic digestion. They were plated on flasks coated with human placental collagen (HPC) in media containing Ultroser G serum substitute and a variety of growth factors. Confluent cell sheets formed after 20 days. Cells were then isolated by trypsinization and replated at 10(6) cells/cm2 onto porous-bottomed inserts coated with HPC. Confluent sheets formed on day 1 after replating and were studied on day 10 in Ussing chambers. Transepithelial resistance (Rte) and baseline short-circuit current (Isc) of CF cultures (171 +/- 67 omega.cm2, 3.8 +/- 0.8 microA/cm2; n = 5) were significantly less than non-CF (541 +/- 116 omega.cm2, 9.9 +/- 2.3 microA/cm2; n = 14). Responses in Isc to mediators were also significantly reduced in CF: isoproterenol (10(-5)M) = 0.04 +/- 0.04 vs. 1.9 +/- 0.6; methacholine (10(-5)M) = 0.2 +/- 0.1 vs. 7.1 +/- 1.7; bradykinin (10(-6)M) = 0.4 +/- 0.1 vs. 5.0 +/- 1.0 microA/cm2; n = 5 for CF, n = 14 for non-CF. When CF and non-CF cells were matched for baseline Isc and Rte, the responses of CF cells to mediators still remained statistically lower than normal. The reduced responses of CF cells to bradykinin and methacholine, in addition to isoproterenol, suggest that both Ca-dependent and adenosine 3',5'-cyclic monophosphate-dependent regulation of Cl secretion are defective in CF tracheobronchial glands. The resulting reduction in fluid secretion by glands may contribute to the accumulation of airway mucus in CF.

Adult↗

Heterogeneity of 5-HT receptors mediating secretion in the human intestine.

In conclusion, application of 5-HT has been shown to induce fluid secretion in both the small and large intestine of man. By the use of selective antagonists, the receptors mediating these effects have been identified and characterized. 5-HT induces secretion across human ileal mucosa via a receptor of the 5-HT4 sub-type, whereas a receptor of the 5-HT2A sub-type appears to mediate the effect in human sigmoid colon. The response in human ascending colonic mucosa cannot be definitively classified at this time, but may reflect the presence of a heterogenous receptor population.

Humans↗

Capsaicin evokes secretion of nasal fluid and depletes substance P and calcitonin gene-related peptide from the nasal mucosa in the rat.

1. The secretion of nasal fluid was studied in anaesthetized rats after topical application of capsaicin, and of calcitonin gene-related peptide (CGRP) alone or CGRP in combination with substance P (SP). The flow of nasal fluid was stimulated and the secretions collected by a filter paper technique. The concentrations of SP and CGRP in nasal biopsies were determined after topical or systemic administration of capsaicin. 2. Capsaicin (single dose administration) stimulated nasal secretion in a dose-dependent manner. The effect was inhibited by hexamethonium, lignocaine, or by the tachykinin antagonist (D-Pro2, D-Trp7,9)-SP, but not by atropine, or by a combination of the histamine H1-receptor antagonist chlorpheniramine and the H2-receptor antagonist ranitidine. 3. When applied cumulatively, capsaicin rapidly produced desensitization. The concentrations of SP and CGRP in the nasal mucosa were reduced by capsaicin 6 days after topical or s.c. administration but not 15 min after topical application of desensitizing doses. 4. CGRP did not stimulate the secretion of nasal fluid and did not alter SP-evoked nasal secretion. 5. The inhibition by hexamethonium of the capsaicin-evoked nasal secretion suggests the involvement of ganglionic reflexes. In addition, the inhibition of the response to capsaicin by (D-Pro2,D-Trp7,9)-SP and lidocaine and the depletion of SP and CGRP after capsaicin indicate the involvement of tachykinin-mediated axon reflexes.

Animals↗

Human mammary gland and breast carcinoma contain immunoreactive inhibin/activin subunits: evidence for a secretion into cystic fluid.

OBJECTIVE: Inhibins and activins are members of the transforming growth factor beta superfamily and are known to modulate the growth and differentiation of several cell types. The present study investigated the localization of inhibin and activin subunits in human normal and pathological breast tissues. DESIGN: A cross-sectional study comparing the expression of inhibin/activin subunits alpha, betaA and betaB in surgical specimens from women undergoing reductive mammoplasty (classified, according to the phase of the menstrual cycle, as follicular, luteal, or postmenopausal), and patients submitted to lumpectomy for fibrocystic disease, benign (intraductal papilloma, adenomyoepithelioma, and hamartoma) or malignant breast neoplams (intraductal, intralobular, and invasive carcinoma). METHODS: Immunohistochemistry was used to localize inhibin alpha and activin betaA and betaB subunits in the cytoplasm of epithelial cells of mammary glands. Dimeric activin A, inhibin A and inhibin B were measured by specific two-site enzyme immunoassay in the cystic fluid collected from patients with fibrocystic disease. RESULTS: An intense staining for the alpha inhibin subunit and a mild staining for betaA and betaB subunits were present in samples obtained from normal breast tissue regardless of menstrual cycle phase, and in fibrocystic disease and benign neoplasms. Carcinoma cells stained weakly to moderately for alpha subunit and were negative for betaA and betaB subunits. Fibrocystic disease was associated with absence of betaA subunit expression in normal epithelial cells and intense staining for all subunits in the apocrine cells. Immunoreactive inhibin A, inhibin B, and activin A were also present in cystic fluid, suggesting a local secretion of these proteins. CONCLUSION: These data suggest a local expression and secretion of inhibin and activin in human normal, fibrocystic disease and neoplastic breast tissues. The low expression of these proteins may facilitate abnormal cell proliferation in breast carcinoma.

Activins↗

Functional characterization of the adenosine receptor mediating inhibition of intestinal secretion.

1. Previous studies have shown that the mixed A1/A2 adenosine agonist 5'-N-ethylcarboxamido-adenosine (NECA) inhibits intestinal fluid secretion which is thought to contribute to its antidiarrhoeal effect in the rat. The aim of this study was to characterize the adenosine receptor mediating this antisecretory effect via functional studies using a range of selective agonists and antagonists and by applying the pharmacological criteria of relative agonist and antagonist potencies. 2. Adenosine agonists and antagonists were administered i.v. to anaesthetized rats. Intestinal secretion was then stimulated by i.a. infusion of vasoactive intestinal peptide (VIP, 0.8 microgram min-1) and the net fluid transport across the wall of the jejunum was measured by a recirculation technique. 3. The rank order of agonist potency to reduce the response to VIP was: NECA > N6-cyclopentyladenosine (CPA) > R-N6-(2-phenylisopropyladenosine) (R-PIA) > S-PIA > chloroadenosine (2-CADO) > 2-phenylaminoadenosine (CV-1808). This order best complies with the rank order of agonist potency that represents activation of the recently described A2B receptor: NECA > 2-CADO > R-PIA = CHA > S-PIA > = CV-1808 > = CGS-21680. The most potent agonists (NECA, CPA and RPIA) had ED50 values in the low microgram range. 4. The anitsecretory action of NECA (submaximal dose of 40 micrograms kg-1) was antagonized equally (approximately 50%) by the selective adenosine antagonists 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 0.1 mg kg-1) and 8-phenyltheophylline (8-PT, 0.1 mg kg-1). This equipotent activity indicates the presence of an A2 and not an A1 receptor. 5. It is suggested that adenosine A2B receptor agonists could be evaluated for potential use as antidiarrhoeal drugs.

Adenosine↗

Constitutive secretion of immunoglobulin A and other proteins into lumina of unstimulated submandibular glands in anaesthetised rats.

Salivary fluid secretion is dependent upon reflex stimuli mediated by autonomic nerves. In order to determine if immunoglobulin A (IgA) and salivary proteins are secreted in the absence of nerve stimulation, small volumes (< 2 microl) of saliva were consecutively collected from the submandibular duct of anaesthetised rats following rest pauses in order to sample the protein contents of the ductal system. Within the first 5 microl of such saliva collected by parasympathetic nerve stimulation, IgA and other salivary proteins reached peak concentrations that were over 20-fold greater than levels in parasympathetically stimulated saliva subsequently collected during a 5 min period of stimulation. Confocal microscopy of TRITC-labelled IgA added to live, acutely isolated submandibular acini indicated that it did not enter the lumina by paracellular leakage. IgG is thought to enter saliva by paracellular leakage but did not accumulate in luminal saliva in the present study. Electrophoresis suggested that the major proteins secreted in the absence of stimulation were the same as those present in subsequently stimulated saliva. It can be concluded that IgA and other major submandibular proteins are secreted into glandular lumina in the absence of nerve stimulation. The functional significance of such unstimulated protein secretion is at present unclear.

Anesthesia↗

Inhibition of rat intestinal Cl- secretion by 4,5-dimethylresorcinol.

Wood creosote, a mixture of phenolic compounds, inhibits enterotoxin-induced intestinal fluid secretion, suggesting that one of its constituents suppresses transepithelial Cl- secretion from the intestinal mucosa. To identify an active constituent in wood creosote that inhibits intestinal Cl- secretion through Cl- channels, we first examined its effect on Cl- secretion using a cultured cell line transfected with complementary DNA encoding a Cl- channel and a Cl- -sensitive fluorescent dye. We next assayed chromatographic fractions of wood creosote for the inhibitory activity on Cl- secretion using a Ussing chamber. We found that 4,5-dimethylresorcinol, identified by gas chromatography-mass spectrometry, inhibited intestinal Cl- secretion dose-dependently when added to a serosal, but not mucosal, surface of rat jejunum, a half-inhibitory concentration being 3.8 microg/ml (28 micromol/l). It was strongly suggested that this effect was due to inhibition of Cl- channels.

Animals↗

Reversal of cyclic AMP-mediated intestinal secretion by ethacrynic acid.

Ethacrynic acid (EA) has been reported to reduce cholera toxin-induced intestinal fluid secretion in the intact animal. We explored the nature of this inhibition in vitro by measuring unidirectional, transmural fluxes of (22)Na and (36)Cl across isolated rabbit ileal mucosa. Under control conditions (short-circuited mucosa bathed in bicarbonate-Ringer), there was net absorption of Na and Cl. Theophylline (10 mM), cyclic AMP (5 mM), and cholera toxin (added in vivo) abolished net Na flux and produced net Cl secretion. In the presence of either theophylline or cAMP, addition of 0.1 mM EA to the serosal bathing solution abolished net Cl secretion and restored net Na absorption. Cholera toxin-treated mucosa was exposed to 0.05 and 1.0 mM EA. The lower concentration restored net Na absorption but did not significantly reduce Cl secretion. The higher concentration abolished net transport of both Na and Cl. Short-circuit current and Na flux measurements in the presence and absence of glucose indicated that 0.1 mM EA does not inhibit glucose-coupled Na transport. Short-circuit current measurements in the presence of 1.0 mM EA suggested that even this concentration of EA does not inhibit glucose-coupled Na transport. Thus EA appears to specifically inhibit Cl (or NaCl) secretion without inhibiting the absorptive Na "pump." The anti-secretory effect of 0.1 mM EA does not appear to result from inhibition of adenylate cyclase since secretion stimulated by addition of 5 mM cAMP was abolished. Furthermore, 0.1 mM EA did not significantly reduce theophylline-augmented and cholera toxin-augmented cAMP levels in ileal mucosa. We conclude that EA interacts specifically with the active Cl (or NaCl) secretory mechanism of the small intestine at a step beyond generation of cAMP.

Animals↗

Potassium transport at the blood-brain and blood-CSF barriers.

Figure 5 gives a summary of K transporters at the BBB based on the available evidence. It appears that the cerebral endothelial cells have an array of potassium channels, although the degree to which each is open under physiological conditions is uncertain. Different channels are present on the luminal and abluminal membranes, and the opening and closing of these channels may allow modulation of the brain K influx and efflux rates and play a role in brain K homeostasis. These channels may also play a role in hyperosmotic brain volume regulation by increasing the entry rate of potassium into brain and may be involved in volume regulation of the endothelial cell itself. The nature of fluid transport at the BBB remains to be fully elucidated, with the presence of a Na/K/2Cl co-transporter being uncertain. The abluminal inwardly-rectifying channel may act as a leak pathway to allow modulation of fluid secretion by the Na/K ATPase without altering the K concentration of that fluid. Finally, there is some evidence that K transport at the BBB is under hormonal and neuronal control. The cerebral capillaries possess receptors for many of the hormones present in blood and brain.

Animals↗

Effect of prostaglandins on Cl and K transport in rat submandibular salivary acini.

Dispersed acini were used to investigate the effects of prostaglandins (PG) on transmembrane Cl and K transport with the aid of radioactive tracers. Neither PGE1, PG2, PGF2 alpha, arachidonic acid or phosphatidic acid (all in 1 microM final concentrations) modified the time-dependent uptake of 36Cl. Steady-state isotope content reached 6-7 nmol/mg protein with or without these substances. PG did not alter the inhibitory effect of 1 mM furosemide on 36Cl uptake, and failed to induce a net efflux of 36Cl from tracer-preloaded cells or to modify the efflux of tracer induced by 1 microM acetylcholine. PG had no significant effect on K uptake, as measured with 86Rb, and did not modify the effect of 1 mM ouabain, which inhibited K uptake or accumulation by 60 per cent. PG did not induce K (86Rb) efflux from acini preloaded with tracer, and did not prevent or enhance the K efflux induced by acetylcholine. Thus PG do not influence the major ion-transport systems that may be involved in saliva secretion by acinar cells. Any inhibitory effects of PGE1 on salivary-fluid secretion in vivo are therefore likely to be the result of extra-acinar PG actions, and not of a direct effect on ion-transport mechanisms.

Acetylcholine↗

The importance of the enteric nervous system for the bile-salt-induced secretion in the small intestine of the rat.

We have investigated the possible involvement of the enteric nervous system in the intestinal secretion induced by sodium deoxycholate. Hexamethonium, lidocaine, and tetrodotoxin significantly inhibited the fluid secretion in extrinsically innervated and denervated rat jejunal segments. Atropine had no effect. We conclude that the sodium-deoxycholate-induced intestinal secretion is partly caused by the activation of local nervous reflexes.

Animals↗

Octreotide (SMS 201-995) as an antisecretory agent in cholera toxin & bile acid induced intestinal secretion in an in vivo animal study.

The effect of Octreotide (SMS 201-995), synthetic somatostatin analogue on small intestinal and colonic fluid secretion induced respectively by cholera toxin (CT) and deoxycholic acid (DCA) was investigated in rabbits using in vivo isolated loops. After exposure to CT and DCA, marked fluid accumulation was observed in the small intestinal and colonic loops, along with elevation of jejunal and colonic mucosal cyclic AMP concentrations. Octreotide inhibited CT and DCA induced small intestinal and colonic secretion, dose-dependently. This anti-secretory effect was observed after both intramuscular and oral administration of octreotide. In contrast, octreotide did not affect the elevated mucosal cyclic AMP concentrations. These results suggest that octreotide inhibits CT and DCA induced intestinal secretion, and this anti-secretory effect is produced by affecting processes beyond cyclic AMP formation.

Animals↗