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PubMedDate not supplied

Calcium modulation of the effects of serotonin, carbachol, and histamine on rabbit ileal ion transport.

In mammalian intestine, a number of secretagogues have been shown to work through either cyclic nucleotide or calcium mediated pathways to elicit ion secretion. Because excessive intestinal electrolyte and fluid secretion is central to the pathogenesis of a variety of diarrheal disorders, understanding of these processes is essential to the development of future clinical treatments. In the current study, the effects of serotonin (5HT), histamine, and carbachol on intestinal ion transport were examined in in vitro preparations of rabbit ileum. All three agonists induced a rapid and transient increase short-circuit current (delta Isc) across ileal mucosa. Inhibition of the delta Isc response of all three agents in chloride-free solution or in the presence of bumetanide confirmed that chloride is the main electrolyte involved in electrogenic ion secretion. Pretreatment of tissue with tetrodotoxin or atropine did not effect secretagogue-mediated electrolyte secretion. While tachyphylaxis of delta Isc response was shown to develop after repeated exposure of a secretagogue to tissue, delta Isc responses after sequential addition of different agonists indicate that cross-tachyphylaxis between agents did not occur. Serotonin, histamine, and carbachol have previously been reported to mediate electrolyte secretion through calcium-dependent pathways. To access the role of extracellular calcium in regulating ion secretion, the effect of verapamil on each agent was tested; verapamil decreased 5HT-induced delta Isc by 65.2% and histamine response by 33.5%, but had no effect on carbachol-elicited chloride secretion. An additive secretory effect was found upon simultaneous exposure of 5HT and carbachol to the system; no other combination of agents produced a significant additive effect. Findings from this study support previous work which has suggested that multiple calcium pathways may be involved in mediating chloride secretion in mammalian intestine.

Animals↗
PubMed1979

Inhibition of rat pancreatic secretion by neurotensin: mechanism of action.

The effect of neurotensin on rat pancreatic secretion was studied in the conscious animal as well as on pancreatic lobules. In vivo neurotensin induced a dose-related inhibition of both water and protein basal secretion. Protein secretion was much more depressed than fluid secretion. Neurotensin did not modify the pancreatic response to exogenous secretin or cholecystokinin-pancreozymin, or to intraduodenal infusion of HCl. On the other hand neurotensin totally inhibited the increase in volume as well as in protein output to an intraduodenal infusion of oleic acid, but did not change the delayed inhibitory effect on protein output. In vitro, neurotensin did not affect basal and cholecystokinin stimulated pancreatic secretion. These results indicate that: 1) neurotensin could interfere with the release of hormones from the gut (cholecystokinin, and possibly VIP), 2) neurotensin did not mimic the delayed protein inhibitory effect observed after administration of oleic acid.

Amylases↗
PubMed1994

Developmental aspects of fluid and electrolyte secretion in salivary glands.

The salivary glands of rodents undergo considerable cytodifferentiation after birth and are useful models for the study of functional development, including the mechanisms of fluid and electrolyte secretion. In the rat submandibular gland, secretion of salivary fluid cannot be elicited until approximately 2 weeks of age. The currently accepted model of salivary fluid secretion indicates that this process depends on the activation, on stimulation of cholinergic receptors, of several ion transport systems, resulting in a net transport of osmotically active ions (primarily Cl- and Na+) across the acinar epithelium. This creates the necessary osmotic gradient for the transacinar movement of water. The process is associated with a signal transduction pathway involving the formation of phosphoinositide products (primarily inositol triphosphate or IP3) and the mobilization of Ca2+. The latter regulates monovalent ion conductances (K+, Cl-), which are critical for the secretory process. Immature submandibular glands and cells of early postnatal rats have a lower density of cholinergic receptors and release less K+ and Cl- than mature cells and gradually develop other ion transport systems (such as a Na, K, 2Cl cotransport system) involved in the secretory process. Surprisingly, they form more IP3 and show a larger increase in cytosolic Ca2+ when stimulated with maximal or supramaximal concentrations of agonist. Therefore, they show some interesting dissociations in the signal transduction mechanism that suggest differences in the coupling between receptors and membrane phosphoinositides, between IP3 and IP3-dependent Ca2+ stores, and between the Ca2+ signal and the monovalent ion transport systems which are critical for secretion.

Acetylcholine↗
PubMed1997

Lithium secretion in kidneys of amphibians and reptiles under hydrated conditions.

Renal lithium transport was studied at different hydration levels in five species of anuran amphibians (Bufo bufo, B. danatensis, B. viridis, Rana ridibunda, and R. temporaria), two species of urodeles (Triturus vulgaris and T. cristatus) and four species of reptiles (lizards Eremias multiocellata, Lacerta vivipara, Trapelus sanguinolentus, and Teratoscincus scincus). Under dehydration conditions, Li+ was reabsorbed in the kidneys of amphibians ans reptiles, but to a lesser degree than in mammalian kidneys: the ratio of lithium clearance (CLi) to glomerular filtration rate (GFR)--fractional lithium excretion--in dehydrated animals was in the range 0.5-0.8. The transition to the hydrated state resulted in a cessation of net renal lithium reabsorption. Under condition of high hydration, all the animals studied, except for urodeles, showed net renal secretion of Li+, i.e., CLi exceeded GFR. The ratio CLi/GFR was 1.2-1.3 in hydrated anurans and 1.7-2.3 in hydrated lizards. In urodeles, this ratio was approximately unity. It is suggested that renal lithium secretion in hydrated amphibians and reptiles reflects fluid secretion in the proximal tubule, which is additional to the glomerular filtration mechanism of fluid delivery to nephron under water loading.

Amphibians↗
PubMed1984

The involvement of the enteric nervous system in the intestinal secretion evoked by cyclic adenosine 3'5'-monophosphate.

Intestinal fluid secretion was evoked in vivo in rats and cats by introducing dibutyrylcyclic adenosine 3,5-monophosphate (db-cAMP) or theophylline, a phosphodiesterase inhibitor, in the intestinal lumen. The intestines were denervated periarterially. It was demonstrated that three compounds of varying chemical structure and with different modes of action on nerves (tetrodotoxin, lidocaine, hexamethonium) decreased the secretory response 60-70%. It is concluded that the secretion induced by increasing the intracellular cAMP concentrations is in part evoked via the enteric nervous system.

Animals↗
PubMed1976

[Morphology of salivary gland diseases].

The human salivary glands represent a functional system with manifold responsibilities and interactions to the organism. The major and minor salivary glands show a common construction schedule consisting of an acinar functional system for the production of an enzyme- and mucin-containing primary saliva and a ductal functional system with manifold secretory, resorptive and regulatory responsibilities for the transport and the definitive composition of the saliva. The cyclic AMP and calcium iones localized in the glandular acini have an exceptional importance for the course of the secretory process. The neurohormonal control of the salivary secretion results by adrenergic and cholinergic transmitter substances. Moreover the secretory process shows a daily cycle combined with morphological alterations of the glandular cells (so called circadian structures). The fluid secretion of the salivary duct system (the output of sodium-, potassium- and chlorine-iones) represents an active energy-consumed transport process which will be regulated by several factors (autonomic nervous system, quantity of perfusion, hydrostatic pressure in the blood capillaries, transepithelial active transport by ATP-consumed pump systems). The striated ducts are the functional most important sector of the duct system for a rapid fluid- and electrolyte excretion. The terminal axons of the postganglionic sympathic and parasympathic neurits are characterized by spindle-shaped enlargements (varicosities) which contain neurosecretory granules. In the region of the acinar and intercalated duct cells a direct synaptic contact exists for the stimulation transmission, in the course of which the terminal axon contacts immediately with the effector cell by penetration of the basement membrane. The salivary glands form a part of the stabil tissues with reversible postmitotic cells in regard of the tissue regeneration. Under pathological conditions (inflammations, impediment of secretion fluid, radiation effects etc.) metaplasias and proliferations of the duct system arise with development of indifferent duct formations analogous to the type of an embryonal salivary gland. The terminal zone between intercalated and striated ducts represents an indifferent zone with large regeneratory potency. A special behaviour shows the myoepithelial cells which are developed as well to the outside of primitive embryonic duct buds as differentiated intercalated and striated ducts. Morphologically three types of diseases can be classified in the salivary glands: sialadenosis, sialadenitis and tumours.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2001

New models of the tracheal airway define the glandular contribution to airway surface fluid and electrolyte composition.

Antibacterial defenses in the airway are dependent on multifactorial influences that determine the composition of both fluid and/or electrolytes at the surface of the airway and the secretory products that aid in bacterial killing and clearance. In cystic fibrosis (CF), these mechanisms of airway protection may be defective, leading to increased colonization with Pseudomonas aeruginosa. Submucosal glands, a predominant site of cystic fibrosis transmembrane conductance regulator (CFTR) protein expression in the airway, have been hypothesized to play an important role in protection of the airway. Furthermore, recent studies have suggested that the salt concentration at the airway surface may be a key factor in regulating the activity of antibacterial substances in the airway. To explore these issues, we have used a new model of the ferret tracheal airway to evaluate the contribution of submucosal glands in regulating airway surface fluid and electrolyte composition. Using tracheal xenograft models with and without submucosal glands, we have characterized several aspects of airway physiology that may be important in defining antibacterial properties. These endpoints included the contribution of submucosal glands in defining bioelectric properties of the surface airway epithelium, airway surface fluid (ASF) chloride composition, ASF volumes, and secretion of the antibacterial factor lysozyme. Findings from these studies demonstrate a significantly elevated secreted fluid volume (Vs) and chloride concentration ([Cl](s)) in ASF from airways with submucosal glands (Vs = 47 +/- 4 microl; [Cl](s) = 128 +/- 5 mM), as compared with xenograft airways without glands (Vs = 36 +/- 2 microl; [Cl](s) = 103 +/- 6 mM). Furthermore, a temperature labile factor secreted by submucosal glands appears to alter the baseline activation of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and/or diphenylamine-2-carboxylic acid-sensitive chloride channels in the surface airway epithelium. Lastly, the lysozyme content of tracheal airways with submucosal glands was 8.5-fold higher than were airways without glands. These studies demonstrate that submucosal glands affect both the ionic composition and bioelectric properties of the airway and suggest that models evaluating antibacterial properties of the airway in CF should take into account the contribution of glands in airway physiology.

Animals↗
PubMed2002

Physiological importance of aquaporin water channels.

Aquaporins (AQP) are a family of at least ten homologous water transporting proteins in mammals that are expressed in many epithelial, endothelial and other tissues. Abnormalities in humans and mice lacking AQPs provide direct evidence for their physiological importance. Humans lacking AQP1 or AQP2 manifest polyuria with defective urinary concentrating ability and humans with mutations in MIP (AQP0) develop cataracts. Transgenic knockout mice lacking AQP1 or AQP3 are also remarkably polyuric, and knock-in mice expressing a mutant AQP2 have severe nephrogenic diabetes insipidus resulting in impaired neonatal survival. Other interesting phenotypes in AQP knockout mice include reduced pain sensation, reduced intraocular pressure, defective corneal fluid transport and impaired dietary fat processing (AQP1), dry skin (AQP3), protection from brain swelling and impaired hearing/vision (AQP4), and reduced fluid secretion by salivary and airway submucosal glands (AQP5). However, many phenotype studies were negative, such as normal airway/lung and skeletal muscle function despite AQP expression, indicating that tissue-specific aquaporin expression does not indicate physiological significance. The general paradigm from studies on transgenic mouse models of AQP deletion is that AQPs facilitate rapid near-isosmolar transepithelial fluid absorption / secretion, as well as rapid vectorial water movement driven by osmotic gradients. The transgenic mouse studies suggest that aquaporin inhibitors may have clinical indications as diuretics and in the treatment of cerebral edema, elevated intraocular pressure, and other conditions of abnormal fluid homeostasis.

Animals↗
PubMed1991

Secretagogue response of azaserine-induced rat pancreatic acinar tumors in vivo.

This study investigates digestive and lysosomal enzyme secretion of azaserine-induced pancreatic acinar carcinomas in response to cholecystokinin in rats. After 15-20 months of treatment, 95% of the animals developed pancreatic acinar carcinomas encompassing more than 90% of the tissue. In anesthetized rats basal trypsin output was significantly elevated in the tumor group despite diminished fluid secretion. There was a linear correlation between tumor size and basal amylase and trypsin secretion. Intravenous infusion of cholecystokinin (25 IDU.kg-1.h-1) induced a significantly lower secretion of fluid per gram pancreas, as well as decreased amylase and trypsin output, in the tumor group compared with the control group. Plasma amylase and lipase levels were significantly elevated in the tumor group under both basal and stimulated conditions. The output of the lysosomal enzymes beta-D-glucuronidase and alpha-D-glucosidase was significantly increased in the tumor group under background secretin infusion. Additional cholecystokinin infusion caused a sharp increase in glucuronidase output in this group with only minimal increase in controls. Glucosidase output increased similarly in both groups. Amylase, lipase, and trypsin tumor tissue concentrations were markedly reduced by 85%, 90%, and 87%, respectively. It was concluded that the decreased secretory response of digestive enzymes may result from decreased synthesis, lowered storage capabilities, and/or a decreased/increased responsiveness to cholecystokinin. Increased glucuronidase secretion may reflect an augmented cell turnover of malignant tissue.

Adenoma↗
PubMed1989

Production, purification and characterization of Clostridium difficile toxic proteins different from toxin A and from toxin B.

The purification and characterization of three new proteins called C1, C2, and C3 from Clostridium difficile are described. Their estimated molecular mass were about 350 (C1), 270 (C2) and 140 (C3) kDa, consisting of subunits of 39 (C1), 43 (C2) and 41 (C3) kDa, respectively. Immunodiffusion revealed that the three proteins contained similar but not identical antigenic determinants to toxin A. Each protein induced a cytotonic effect on hamster ovaric cells; the combined proteins, had a specific activity on cells 5-times higher than that of toxin A. In rat intestinal loops, they induced a clear fluid secretion, while toxin A elicited a haemorrhagic fluid response. The cytotonic activities of all three proteins were abolished by antiserum against toxin A, while antiserum against toxin B inhibited only the activity of the 270 kDa protein. In contrast to toxin A, the cytotoxicity of the three proteins was inactivated by trypsin. Thus, the chemical, antigenic and biological properties of these proteins differed from those of toxin A and toxin B.

Bacterial Toxins↗
PubMed2006

Pharmacological profile of inhibition of the chloride channels activated by extracellular acid in cultured rat Sertoli cells.

Sertoli cells from mammalian testis are key cells involved in the development and maintenance of stem cell spermatogonia as well as in the secretion of a Cl(-) and K(+)-rich fluid into the lumen of seminiferous tubules. The pharmacology and contribution of Cl(-) channels to the physiology of Sertoli cells were investigated using whole-cell patch clamp and iodide efflux experiments applied to cultured rat Sertoli cells. We characterized an outwardly rectifying Cl(-) current stimulated by various acid species including the physiologically relevant lactic acid. Using the iodide efflux technique, the pharmacological properties of this Cl(-) current, noted ICl(acid), revealed Ca(2+)-independent inhibition by DIDS (IC(50) = 27 microM), glibenclamide (IC(50) = 31 microM) and DPC (IC(50) = 86 microM). ICl(acid) was neither affected by calix[4]arene nor by 9-AC. The order of potency for inhibition of ICl(acid) is DIDS approximately glibenclamide > DPC >> calix[4]arene, 9-AC. For comparison, the inhibitory profile of the swelling- and ATP-activated Cl(-) currents in Sertoli cells is DPC = DIDS >> glibenclamide = 9-AC for ICl(swell) and DPC = 9-AC = DIDS >> glibenclamide for ICl(ATP). This description provides new insights into the physiology and pharmacology of the endogenous Cl(-) channels expressed and potentially involved in fluid secretion in Sertoli cells.

Adenosine Triphosphate↗
PubMed1997

Physiology of amniotic fluid volume regulation.

Although there are fairly wide variations AFV normally undergoes characteristic changes across gestation in which it increases from 10-20 ml at 10 weeks gestation to average 800 ml at 24 weeks. Little change occurs from then until near term when AFV begins to decrease, and large decreases can occur in postterm pregnancies. Across gestation, 95% of AFVs are within the range of 1/2.57-2.57 times the gestational mean volume and 99% are within the range of 1/3.40-3.40 times the gestational mean. Although there are six pathways in which fluid and solutes can enter and/or leave the amniotic sac, there are only four primary pathways that contribute to AFV during late gestation. These include fetal urine and lung fluid secretion as the two primary sources of fluid, with fetal swallowing and intramembranous absorption as the two primary routes of amniotic water clearance. The intramembranous pathway also appears to be a primary source of amniotic solutes (e.g., sodium and chloride). Although fetal hypoxia has been widely believed to cause oligohydramnios, fetal hypoxic hypoxia and anemic hypoxia both appear to be associated with an increased AFV and polyhydramnios rather than oligohydramnios. It is speculated that the oligohydramnios associated with fetal hypoxia is caused by placental dysfunction in addition to the hypoxia.

Amniotic Fluid↗
PubMed1970

Investigations into the mechanism of the antifertility action of minimal doses of megestrol acetate in the rabbit.

1. Experiments have been performed to investigate the mechanism by which low doses of megestrol acetate have an antifertility action.2. It was found that the dose of megestrol acetate required to prevent pregnancy in nine of ten New Zealand White rabbits when given on 3 consecutive days, the last of which was the day of insemination, was 50 mug/kg daily.3. This treatment reduced the numbers of sperm recoverable from the uterus at various times after insemination, but egg transfer experiments showed that neither egg viability nor fertilization was affected on day 1 of pregnancy.4. Treatment with megestrol acetate for 3 days caused the fertilized eggs to enter the uterus approximately 48 h prematurely. Treatment with megestrol acetate for longer periods caused a similar but more marked increase in the rate of transport of eggs in the oviduct.5. Megestrol acetate did not modify oviduct opening pressure, but the volume of oviduct fluid secretion was reduced earlier and transport of fluid through the oviduct was accelerated compared with controls.6. Transfer of eggs on various days from the uteri of untreated rabbits to the uteri of treated rabbits indicated that the development of the endometrium which occurs in pregnancy may be advanced by megestrol administration. Histological examination of the endometrial proliferation induced by megestrol acetate confirmed that this was so.7. It is concluded that the antifertility action of megestrol acetate in doses that do not necessarily inhibit ovulation is due to a combination of accelerated egg transport and advanced endometrial development.

Animals↗
PubMed1997

Epithelial cell polarity and disease.

The establishment and maintenance of epithelial polarity is essential for the integrity and function of epithelial organs and is particularly critical in the kidney, where vectorial reabsorption and secretion are effected in different segments of the nephron by the differential polarized insertion of channels, transporters, and related proteins into apical membranes lining the tubule lumen or basolateral membranes adjacent to the interstitium and blood space. Faulty intracellular delivery and polarization of membrane proteins can lead to serious diseases such as cystic fibrosis, I cell disease, and renal cystic diseases. The best understood disease of epithelial polarity is autosomal dominant polycystic kidney disease (ADPKD) caused by mutations in a >462-kDa, developmentally regulated membrane protein, "polycystin." ADPKD cysts are characteristically lined by a single layer of structurally polarized epithelial cells with normal functional intercellular tight junctions but with aberrant polarization of some important membrane proteins. Abnormal apical membrane polarity of biochemically active, ouabain-sensitive Na-K-adenosinetriphosphatase (Na-K-ATPase) in ADPKD cyst epithelia leads to abnormal sodium ion secretion and provides a mechanism for aberrant fluid secretion. In addition, apically mislocated, functional epidermal growth factor (EGF) receptors on cyst epithelia, together with EGF synthesis and secretion into cyst lumens, provide a mechanism for autocrine regulation of increased epithelial cell proliferation in ADPKD. Underlying mechanisms for these abnormalities in polarized distribution of membrane proteins include the aberrant expression of fetal gene products, such as the beta2-subunit of Na-K-ATPase, in ADPKD kidneys. Overexpression of polycystin protein in ADPKD cyst epithelia, low levels restricted to medullary collecting tubules in normal adult kidneys, and high levels in ureteric bud-derived structures in human fetal kidneys further suggest a failure of downregulation of fetal genes as a mechanism for the polarity abnormalities that characterize ADPKD.

Adult↗
PubMed2006

Involvement of cAMP response element-binding protein activation in salivary secretion.

OBJECTIVE: Saliva secretion is mediated by cAMP and the calcium signaling pathway in salivary acinar cells. The PKA signaling pathway plays an important role in protein secretion through the activation of cAMP, in fluid secretion through the elevation of intracellular calcium and in the activation of cAMP response element-binding protein (CREB), which is involved in these signaling cascades. In this study, we investigated whether the activation of CREB plays a part in the salivary secretion in mice. METHODS: We examined CREB activation by assessing phosphorylation at the serine-133 position using Western blotting. RESULTS: Carbachol (a muscarinic acetylcholine agonist) and isoproterenol (a beta-adrenergic agonist) markedly activated CREB in parotid acinar cells. Carbachol and isoproterenol-induced CREB phosphorylation was blocked by atropine (a muscarinic acetylcholine antagonist) and propranolol (a beta-adrenergic antagonist), respectively. The PKA inhibitor H89 inhibited CREB activation, but the PLC inhibitor U73122 did not. Moreover, carbachol- and isoproterenol-stimulated amylase secretion from parotid acinar cells was inhibited by H89 and adenoviral dominant-negative CREB. CONCLUSION: These results indicate that the muscarinic and beta-adrenergic activation of CREB was mediated through the PKA pathway and that CREB is involved in protein secretion from parotid acinar cells.

Adrenergic beta-Agonists↗
PubMed1978

Functional profile of the isolated uremic nephron. Role of compensatory hypertrophy in the control of fluid reabsorption by the proximal straight tubule.

An in vitro approach to the study of single nephron function in uremia has been employed in evaluating the control of fluid reabsorption by the renal superficial proximal straight tubule (PST). Isolated segments of PSTs from the remnant kidneys of uremic rabbits (stage III) were perfused in vitro and their rate of fluid reabsorption compared with normal PSTs and with PSTs derived from the remnant kidneys of nonuremic rabbits (stage II). All segments were exposed to a peritubular bathing medium of both normal and uremic rabbit serum thereby permitting a differentiation to be made between adaptations in function which are intrinsic to the tubular epithelium and those which are dependent upon a uremic milieu.Compared with normal and stage II PSTs, there was significant hypertrophy of the stage III tubules as evidenced by an increase in length and internal diameter, and a twofold increase in the dry weight per unit length. Fluid reabsorption per unit length of tubule was 70% greater in stage III than in normal and stage II PSTs, and was closely correlated with the increase in dry weight. Substitutions between normal and uremic rabbit serum in the peritubular bathing medium did not affect fluid reabsorption significantly in any of the three groups of PSTs. Perfusion of the tubules with an ultrafiltrate of normal vs. uremic serum likewise failed to influence the rate of net fluid reabsorption. It has previously been observed that net fluid secretion may occur in nonperfused or stop-flow perfused normal rabbit PSTs exposed to human uremic serum. Additional studies were thus performed on normal and stage III PSTs to evaluate whether net secretion occurs in the presence of rabbit uremic serum. No evidence for net secretion was found. These studies demonstrate that fluid reabsorption is greatly increased in the superficial PST of the uremic remnant kidney and that this functional adaptation is closely correlated with compensatory hypertrophy of the segment. Humoral factors in the peritubular environment do not appear to be important mediators of the enhanced fluid reabsorption.

Absorption↗
PubMed1993

Comparative effects of nicotinic acid and nicotinamide on cholera toxin-induced secretion in rabbit ileum.

Nicotinic acid reduces the cholera-toxin induced fluid secretion in experimental animals but its toxicity at high doses prevent its therapeutic use in patients suffering from cholera. This study aimed to determine whether nicotinamide, the non toxic amide derivative of nicotinic acid, is as effective as nicotinic acid in inhibiting cholera toxin induced intestinal secretion in vivo. Four intestinal loops, with their blood supply intact, were isolated in 30 rabbits and injected with either (i) 30 mM mannitol, (ii) 30 mM mannitol + 10 micrograms cholera toxin, (iii) 30 mM glucose, or (iv) 30 mM glucose + 10 micrograms cholera toxin. These rabbits were then randomly assigned to three groups receiving intraluminally either 100 mg/kg of nicotinic acid, 100 mg/kg of nicotinamide, or 10 ml/kg of Ringer solution. Measurement of intestinal fluid accumulation showed that nicotinic acid, but not nicotinamide, significantly reduced cholera toxin induced intestinal secretion.

Animals↗