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PubMed1981

Lacrimal gland electrolyte and water secretion in the rabbit: localization and role of (Na+ + K+)-activated ATPase.

1. The rate of acetylcholine (ACh)-induced fluid secretion was measured from the main secretory duct of rabbit lacrimal glands perfused in vivo with Krebs Henseleit bicarbonate solutions. 2. Perfusion with ouabain (10(-5) M) decreased the rate of lacrimal gland fluid secretion to 23% of the control value. 3. Perfusion with furosemide (10(-4) and 10(-3) M), which has been shown to inhibit the coupled transport of Na+ and Cl-, reversibly decreased the rate of secretion to 43 and 33% of the control value respectively. 4. (Na+ + K+)-activated ATPase was localized in slices of rabbit lacrimal gland using autoradiography with [3H]ouabain. 5. A high density of [3H]ouabain binding sites was present on ductal cells, whereas a very low density was found on acinar cells. For both types of cells the [3H]ouabain binding sites were located on the basolateral plasma membranes. 6. It is concluded that ACh-induced secretion of electrolytes and water is dependent upon (Na+ + K+)-activated ATPase. In addition, coupled transport of Na+ and Cl- appears to be involved in secretion. 7. Basolateral location of the (Na+ + K+)-activated ATPase implies that it plays an indirect role in electrolyte and water secretion. A possible role may be to energize a secondary active transport of Cl- that is mediated by a NaCl cotransport system.

Acetylcholine↗
PubMed1996

VIP-antiserum and indomethacin inhibit calcium and bicarbonate secretion by the inflamed feline gallbladder mucosa.

Ionized calcium (Ca2+) and bicarbonate (HCO(3)-) are important ions for gallstone formation. In the present study the effect of indomethacin and vasoactive intestinal peptide-antiserum (VIP-antiserum) on the Ca2+, HCO(3)- and fluid secretion in the inflamed gallbladder were tested in a validated experimental model in cats. The animals were studied in acute experiments 6 weeks after cystic duct ligation and gallstone implantation. During basal conditions there was a continuous secretion of Ca2+, HCO(3)- and fluid into the lumen of the inflamed gallbladder. Indomethacin and VIP-antiserum inhibited the Ca2+, HCO(3)- and fluid secretion across the inflamed gallbladder mucosa. Intraluminal amiloride inhibited the absorption of Ca2+, HCO(3)- and fluid after indomethacin infusion. An impaired absorption of Ca2+, HCO(3)- and fluid in the inflamed gallbladder is probably important for the solubility of calcium salts in the early stages of inflammation in the gallbladder mucosa.

Animals↗
PubMed2006

Interacting influences of pregnancy and corneal injury on rabbit lacrimal gland immunoarchitecture and function.

PURPOSE: Previous reports indicated that pregnancy and corneal injury (CI) trigger alterations of lacrimal gland (LG) growth factor expression and redistributions of lymphocytes from periductal foci to acini. The purpose of this study was to test our hypothesis that pregnancy would exacerbate the changes induced by CI. METHODS: Corneas were injured with scalpel blades, and, 2 weeks later, LGs were collected for immunocytochemistry and Western blot analysis. Lacrimal fluid was collected under basal- and pilocarpine-stimulated conditions for protein determination and Western blot analyses. RESULTS: There were significant increases of immunoreactivity for prolactin, TGF-beta1, and EGF in duct cells during pregnancy and after CI, most prominent in pregnant animals with CI. Pregnancy decreased baseline lacrimal fluid secretion, whereas CI did not have a noticeable effect; pregnancy and CI combined resulted in increased fluid production. Pregnancy and CI each increased pilocarpine-induced lacrimal fluid production, whereas protein concentrations were decreased. Prolactin, TGF-beta1, and EGF were detected in LG by Western blot analysis but were minimally detectable in lacrimal fluid. RTLA+ and CD18+ cells were redistributed from periductal to interacinar sites during pregnancy and after CI, most prominent in pregnant animals with CI. CONCLUSIONS: Like pregnancy, CI is associated with redistribution of immune cells from periductal to interacinar sites and enhanced immunoreactivity of prolactin, TGF-beta1, and EGF in ductal cells. Although baseline lacrimal fluid secretion varied, the glands of all three experimental groups produced significant amounts of fluid in response to pilocarpine, but protein concentrations were decreased.

Animals↗
PubMed1982

Evidence for cholera secretion emanating from the crypts. A study of villus tissue osmolality and fluid and electrolyte transport in the small intestine of the cat.

Villus tissue osmolality and fluid and electrolyte transport were measured in intestinal segments exposed to cholera toxin. The osmolality of the luminal fluid was kept at about 100, 300, or 600 mOsm X kg-1 by use of appropriate concentrations of mannitol. A net fluid secretion was seen in all experiments, the magnitude being dependent on the osmolality in the lumen. A secretion of sodium, potassium, and chloride was also seen in all experiments but the secretion rate of electrolytes was independent of the osmolality in the intestinal lumen. The hydraulic conductivity of the villus epithelium, calculated from the lumen and tissue osmolality, was the same as that estimated in the normal intestines. A villus tissue osmolality gradient was apparent in all experiments regardless of the mannitol concentration in the lumen, the tip osmolality being hypertonic while the tissue osmolality at the base was isotonic. This was the case also when the luminal fluid was hypotonic, a finding opposite to what we found in an earlier study on the normal feline intestine. A likely explanation for this observation is that the crypts of Lieberkühn secrete fluid containing sodium chloride, which is absorbed by the villus epithelial cells. Hence, a luminal "circulation" of electrolytes between crypts and villi was suggested in the present experimental circumstances.

Animals↗
PubMed1982

Pharmacological inhibition of chenodeoxycholate-induced fluid and mucus secretion and mucosal injury in the rabbit colon.

The effects of various pharmacological agents on bile acid-induced fluid secretion, mucus secretion, and mucosal injury were investigated using a perfusion technique in rabbit colon. Atropine markedly reduced and carbachol potentiated the fluid secretion, mucus output, and mucosal damage observed during bile acid perfusion. In contrast, pretreatment of the colonic mucosa with lignocaine and parenteral administration of methysergide and somatostatin produced a modest reduction in the fluid secretory response without apparent effects on mucus output or mucosal damage. These results suggested that cholinergic agonists and antagonists influence the mucosal resistance to bile acid-induced injury possibly through their effects on mucus secretion. Increasing or decreasing mucosal resistance to the detergent effects of bile acids appeared to have marked effects on the magnitude of induced fluid secretion. A minor reduction in overall secretory response to bile acids was also apparent with agents not influencing mucus secretion or mucosal injury.

Animals↗
PubMed1983

Effect of charcoal-treated bovine follicular fluid on secretion of LH and FSH in ovariectomized heifers.

The objective of the experiment was to determine whether pools of charcoal-treated bovine follicular fluid (bFF) removed from large (greater than 10 mm) follicles during the preovulatory (d 18 to 1), postovulatory (d 2 to 6) or mid-cycle (d 7 to 17) stages of the bovine estrous cycle altered secretion of luteinizing hormone (LH) or follicle-stimulating hormone (FSH) in ovariectomized heifers. After a 20-ml injection of bFF given at three consecutive 6-h intervals, secretion of FSH was depressed from approximately 116 to 53 ng/ml by each pool of bFF. In contrast, bFF did not affect secretion of LH. Serum from an ovariectomized cow (control) had no effect on secretion of LH or FSH. We concluded that bFF contained a nonsteroidal component (perhaps inhibin) that suppressed FSH secretion in heifers.

Animals↗
PubMed1980

Inhibition of Escherichia coli heat-stable enterotoxin by indomethacin and chlorpromazine.

Purified heat-stable enterotoxin (ST) from a procine strain of enterotoxigenic Escherichia coli activates quanylate cyclase in particulate fractions of rat intestinal tissue and induces fluid accumulation in suckling mice. These effects of ST were examined in the presence of either indomethacin or chlorpromazine. We also examined the effects of these two drugs on fluid accumulation in suckling mice induced by the 8-bromo analog of cyclic guanosine monophosphate. Either indomethacin or chlorpromazine reduced ST activation of guanylate cyclase. Both drugs also reduced intestinal fluid accumulation in suckling mice that resulted from submaximal doses of ST (both P < 0.001). However, there was no reduction in fluid secretion by either drug when a maximally effective dose of ST was used, suggesting that inhibition of fluid secretion by both drugs can be overcome by increasing the ST dose and that a threshold level of guanylate cyclase activity results in maximal secretory response. Both drugs also reduced basal guanylate cylase activity in rat intestinal tissue and fluid secreton in suckling mice. Chlorpromazine also reduced intestinal secretion mediated by 8-bromo cyclic guanosine monophosphate (P < 0.001). These findings indicate that chlorpromazine interferes with the effects of ST both before and after its activation of guanylate cyclase, whereas indomethacin interfers with ST only before its activation of guanylate cyclase.

Animals↗
PubMed1985

Stimulus-secretion coupling in exocrine glands: the role of inositol-1,4,5-trisphosphate, calcium and cAMP.

Enzyme, electrolyte and fluid secretion from exocrine glands is stimulated by neurotransmitters and peptide hormones. Whereas for some of these secretagogues calcium is an important intracellular messenger, for others it is cyclic AMP. Regulation of steady state free Ca2+ concentration at rest and at stimulation have been studied in isolated permeabilized acinar cells from pancreas, parotid and lacrimal glands by measuring the free Ca2+ concentration of the surrounding incubation medium with a Ca2+-specific macroelectrode. Ca2+ transport mechanisms have been further characterized in subcellular membrane fractions by measuring 45Ca2+ uptake into membrane vesicles from rough endoplasmic reticulum (RER) and plasma membranes (PM). The data show that the intracellular messenger for secretagogue-induced Ca2+ release from RER is inositol-1,4,5-trisphosphate (IP3) which is produced during stimulation by phospholipase C mediated hydrolysis of phosphatidylinositol-bisphosphate. At rest both Ca2+ uptake into RER and Ca2+ extrusion from the cell is promoted by (Ca2+ + Mg2+)-ATPases with different characteristics in both types of membranes and by a coupled Na+/Ca2+ countertransport in the PM which keep cytosolic free Ca2+ concentration at a low level of approximately 2 - 4 X 10(-7) mol/l. During stimulation the Ca2+ permeability of endoplasmic reticulum membrane increases via IP3 and that of the PM by a yet unknown "receptor-operated" mechanism. These events lead to increase in cytosolic free Ca2+ concentration that is a trigger for enzyme, electrolyte and fluid secretion.

Animals↗
PubMed2001

An investigation into the effects of inhibitors of fluid production by Locusta Malpighian tubule Type I cells on their secretion and elemental composition.

The intracellular elemental concentrations of K, Na, Cl, P, Mg and Ca within Type I cells of the Malpighian tubules of Locusta migratoria have been measured using electron probe X-ray microanalysis. The distribution of Na, K and Cl was not homogeneous within the cells and concentration gradients exist from basal to apical surfaces. The rate of secretion and the cationic composition of the secreted tubule fluid have also been determined. Furosemide (1 mM) inhibited fluid secretion by about 60%, raised the [Na(+)] but did not significantly alter the [K(+)] of the secreted tubule fluid. When Rb(+) replaced K(+) in the saline fluid secretion was also inhibited by about 60%, but no additional inhibition occurred by the simultaneous inclusion of furosemide. Thus, Rb(+) and furosemide probably act at the same transport site, and Rb(+) cannot substitute for K(+) at the basal membrane cotransporter. Bafilomycin (1 µM) dramatically inhibited fluid production by 85%, the [K(+)] of the secreted fluid was reduced by about 30% but the [Na(+)] was almost doubled. Furosemide, in common with other inhibitors of fluid secretion acting at the basal surface (ouabain and Rb(+)), caused a fall in intracellular [K] and a rise in [Na]. Bafilomycin, in common with N-ethyl maleimide, which acts at the apical surface, increased the intracellular [K] but did not affect the [Na].

Journal Article↗
PubMed2003

Lillian Jean Kaplan International Prize for advancement in the understanding of polycystic kidney disease. Understanding polycystic kidney disease: a systems biology approach.

Understanding polycystic kidney disease: A systems biology approach. Fluid secretion was discovered in the mammalian nephron in the early 1970s upon a chance observation. This finding aroused interest in the possibility that a similar process might be involved in the filling of renal epithelial cysts. A research strategy was formulated to understand the life cycle of human renal cysts using a systems biology approach. A not-for-profit foundation was begun to increase the number of researchers in the United States and abroad working on the polycystic kidney disease (PKD) problem. Primary outcomes related to PKD include (1). explication of the transport mechanisms underlying the transepithelial secretion of chloride, sodium and fluid, and the regulation of that secretion by cyclic adenosine monophosphate (AMP); (2). the discovery that cyclic AMP stimulates the proliferation of cyst epithelial cells through activation of of B-Raf and the mitogen-activated protein (MAP) kinase pathway; and (3). the discovery that normal medullary collecting ducts secrete solutes and fluid under the control of cyclic AMP. The Polycystic Kidney Disease Foundation has become an international leader in promoting the research of these disorders and is a strong advocate for increased translation of fundamental laboratory discoveries to the care of the millions of patients with PKD.

Animals↗
PubMed1978

On the receptors involved in the nervous control of salivary secretion by Nauphoeta cinerea Olivier.

1. It has been shown that the isolated salivary glands of Nauphoeta cinerea Olivier produce fluid secretion in response to nerve stimulation or bath applications of dopamine, noradrenaline, adrenaline and 5-HT. These catecholamines, of which dopamine is the most potent, evoked maximal responses matching that to nerve stimulation whereas 5-HT was less effective. 2. The receptors combining with 5-HT could be distinguished from those for the catecholamines and the transmitter at this salivary neuroglandular junction. 3. The results of experiments where glands were stimulated by dopamine in the presence of noradrenaline or adrenaline suggested that there are receptors with specific binding sites for dopamine. 4. The effects of several antagonists (Ginsborg, House & Silinsky, 1976) of the hyperpolarizing responses from acinar cells to nerve stimulation and the above agonists have been examined. Phentolamine reversibly suppressed the secretory responses to these stimuli whereas methysergide had no effect and ergometrine elicited fluid secretion in a dose-dependent manner.

Animals↗
PubMed2001

Role of CFTR in autosomal recessive polycystic kidney disease.

An extensive body of in vitro data implicates epithelial chloride secretion, mediated through cystic fibrosis transmembrane conductance regulator (CFTR) protein, in generating or maintaining fluid filled cysts in MDCK cells and in human autosomal dominant polycystic kidney disease (ADPKD). In contrast, few studies have addressed the pathophysiology of fluid secretion in cyst formation and enlargement in autosomal recessive polycystic kidney disease (ARPKD). Murine models of targeted disruptions or deletions of specific genes have created opportunities to examine the role of individual gene products in normal development and/or disease pathophysiology. The creation of a murine model of CF, which lacks functional CFTR protein, provides the opportunity to determine whether CFTR activity is required for renal cyst formation in vivo. Therefore, this study sought to determine whether renal cyst formation could be prevented by genetic complementation of the BPK murine model of ARPKD with the CFTR knockout mouse. The results of this study reveal that in animals that are homozygous for the cystic gene (bpk), the lack of functional CFTR protein on the apical surface of cystic epithelium does not provide protection against cyst growth and subsequent decline in renal function. Double mutant mice (bpk -/-; cftr -/-) developed massively enlarged kidneys and died, on average, 7 d earlier than cystic, non-CF mice (bpk -/-; cftr +/+/-). This suggests fundamental differences in the mechanisms of transtubular fluid secretion in animal models of ARPKD compared with ADPKD.

Animals↗
PubMed2000

Tear secretion by lacrimal glands in transgenic mice lacking water channels AQP1, AQP3, AQP4 and AQP5.

The expression of three aquaporin (AQP)-type water channels has been reported in the lacrimal gland: AQP5 in the apical membranes of acinar and duct cells, AQP4 in the basolateral membranes of acinar cells, and AQP1 in microvascular endothelia. Recent experiments indicate that water movement through AQP5 in the salivary gland is important in saliva secretion. To investigate the role of aquaporins in lacrimal gland function, basal and pilocarpine-stimulated tear secretion was compared in wildtype mice and knockout mice lacking AQP1, AQP4 and AQP5, as well as AQP3, which was found here to be expressed in the basolateral membrane of acinar cells. Tear fluid was collected in anesthetized mice using microcapillary tubes before and at 4 min intervals after pilocarpine administration. Tear fluid volumes were (in microliter per 4 min, S.E.): 0.69 +/- 0.06 (wildtype mice), 0.70 +/- 0.07 (AQP1 -/-), 0.81 +/- 0.13 (AQP3 -/-), 0.62 +/- 0.14 (AQP4 -/-), and 0.78 +/- 0.09 (AQP5 -/-) (differences not significant). Chloride concentrations (average 155 +/- 13 mM) measured by a fluorescence assay were also not different in tear fluid collected from wildtype vs aquaporin null mice. These findings provide direct evidence against an essential role for aquaporins in lacrimal gland fluid secretion. The requirement for aquaporins in salivary but not lacrimal gland secretion, may involve the substantially slower fluid secretion rate across lacrimal gland acinar cells.

Animals↗
PubMed1979

Ca2+ control of electrolyte permeability in plasma membrane vesicles from cat pancreas.

The influence of Ca2+ and other cations on electrolyte permeability has been studied in isolated membrane vesicles from cat pancreas. Ca2+ in the micromolar to millimolar concentration range, as well as Mg2+, Sr2+, Mn2+ and La3+ at a tested concentration 10(-4) M, increased Na+ permeability when applied at the vesicle inside. When added to the vesicle outside, however, they decreased Na+ permeability. Ba2+ was effective from the outside but not from the vesicle inside. When Ca2+ was present at both sides of the membrane, Na+ efflux was not affected as compared to that in the absence of Ca2+. Monovalent cations such as Rb+, Cs+, K+, Tris+ and choline+ decreased Na+ permeability when present at the vesicle outside at a concentration range of 10 to 100 mM. Increasing Na+ concentrations from 10 to 100 mM at the vesicle inside increased Na+ permeability. The temperature dependence of Na+ efflux revealed that the activation energy increased in the lower temperature range (0 to 10 degrees C) when Ca2+ was present at the outside or at both sides, but not when present at the vesicle inside only or in the absence of Ca2+. The results suggest that the Ca2+ outside effect is due to binding of calcium to negatively charged phospholipids with a consequent reduction of both fluidity and Na+ permeability of the membrane. The Ca2+-inside effect most likely involves interaction with proteins with consequent increase in Na+ permeability. The data are consistent with current hypotheses on secretagogue-induced fluid secretion in acinar cells of the pancreas according to which secretagogues elicit NaCl and fluid secretion by liberating Ca2+ from cellular membranes and by stimulating Ca2+ influx into the cell. The increased intracellular Ca2+ concentration in turn increases the contraluminal Na+ permeability which leads to NaCl influx. The luminal sodium pump finally transports Na+ ions into the lumen.

Animals↗
PubMed2005

Saccharomyces boulardii inhibits water and electrolytes changes induced by castor oil in the rat colon.

The biotherapeutic agent Saccharomyces boulardii has been shown to inhibit castor oil-induced diarrhoea in rats. The present study investigated the mechanism(s) of this antidiarrhoeal effect in terms of water and electrolyte (sodium, potassium and chloride) changes using two rat models. A single oral dose of S. boulardii of up to 12 x 10(10) CFU/kg of viable cells did not inhibit castor oil-induced fluid secretion in the enteropooling model. However, the yeast dose dependently reduced castor oil induced fluid secretion into the colon, with a significant protection at 12 x 10(10) CFU/kg. In this model, castor oil reversed net sodium and chloride absorption into net secretion, and increased net potassium secretion into the lumen. Single pre-treatment with S. boulardii at 4 and 12 x 10(10) CFU/kg dose dependently decreased these electrolyte changes. In conclusion, S. boulardii possesses potent anti-secretory properties versus water and electrolyte secretion induced by castor oil in the rat colon.

Animals↗
PubMed1989

Properties of rabbit pepsinogen granules.

Pepsinogen granules were isolated from the rabbit stomach using isoosmotic Percoll density gradients, low free calcium (10(-7) M), and conditions that minimize physical damage. These granules were enriched approximately eightfold with respect to pepsinogen and were free from contamination by mitochondria and endoplasmic reticulum. Electrophoretic examination shows pepsinogen to account for approximately 80% of the Coomassie Blue-stainable intragranular protein and the granule membrane to yield a simple spectrum of proteins similar to other granule systems. In addition to purity, the isolated granules displayed a high degree of osmotic stability at physiologic conditions of pH, temperature, and ionic strength. This stability suggests strict regulation of the granule electrolyte transport pathways, which are shown to include a Cl- conductance, Cl-/anion exchange, and a K+ conductance. These transport systems in the granule membrane are consistent with the promotion of primary fluid secretion. Furthermore, granule-mediated ion transport would allow the chief cell to couple fluid secretion directly to exocytotic pepsinogen secretion and flush the enzyme from the base of oxyntic glands.

Animals↗
PubMed1999

Ion transport and signalling in human labial glands.

Recent reports characterizing the physiological properties of normal human labial acini are reviewed with particular emphasis on mechanisms related to fluid secretion. In contrast to the salivary glands of several experimental animals, human labial acinar cells do not appear to have a1-adrenergic receptors, substance P peptidergic receptors, or significant levels of Cl-/HCO3- exchange. Nor do they appear to secrete HCO3- in response to Ca2+ mobilizing stimuli. The data presently available indicates that fluid secretion by these glands is mainly under muscarinic control and is due to acinar Cl- secretion driven by a basolateral Na+ -K+ -2Cl- cotansporter.

Animals↗