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At least 1,099 records · Page 61Linked to original sources
PubMed1992

Escherichia coli enterotoxin (STa) binds to receptors, stimulates guanyl cyclase, and impairs absorption in rat colon.

To determine the contribution of the colon in Escherichia coli heat-stable enterotoxin-mediated diarrheal disease, toxin binding, guanyl cyclase activation, and toxin-induced water flux in the rat colon and ileum were compared. Scatchard analysis suggested a single class of heat-stable enterotoxin receptors with an affinity constant of binding of 10(9) L/mol in both colonocytes and ileocytes; however, the number of toxin receptors per cell was 3.5-fold greater in coloncytes than ileocytes (8.32 +/- 1.33 x 10(5) vs. 2.33 +/- 0.28 x 10(5) receptors per cell; P = 0.02). Heat-stable enterotoxin stimulated guanyl cyclase activation in an identical dose-dependent manner in proximal colonic and ileal membranes, with similar sensitivity and maximum response. Heat-stable enterotoxin also inhibited net water flux to a similar degree in both colon and ileum (-47.8 vs. -48.4 microL.cm-1.h-1, respectively) at a dose of 8 nmol/L. At this dose in the colon, because of a higher baseline of absorption, absorption continued, but at a diminished level. At this dose in the ileum, heat-stable enterotoxin induced net secretion. These data are consistent with the concept that heat-stable enterotoxin-induced diarrheal disease results from a decreased absorptive capacity in the colon in the face of increased small intestinal fluid secretion.

Analysis of Variance↗
PubMed1994

Acid-base interactions during exocrine pancreatic secretion. Primary role for ductal bicarbonate in acinar lumen function.

The role of acid-base interactions during coordinated acinar and duct cell secretion in the exocrine pancreas is described. The sequence of acid-base events may be summarized as follows: (1) Sorting of secretory proteins and membrane components into the regulated secretory pathway of pancreatic acinar cells is triggered by acid- and calcium-induced aggregation and association mechanisms located in the trans-Golgi network. (2) Cholecystokinin-stimulated exocytosis in acinar cells releases the acidic contents of secretory granules into the acinar lumen. (3) Secretin-stimulated bicarbonate secretion from duct and duct-like cells neutralizes the acidic pH of exocytic contents, which leads to dissociation of protein aggregates and solubilization of (pro)enzymes within the acinar lumen. (4) Stimulated fluid secretion transports solubilized enzymes through the ductal system. (5) Further alkalinization of acinar lumen pH accelerates the enzymatic cleavage of the glycosyl phosphatidyl-inositol anchor associated with GP2 and thus releases the GP2/proteoglycan matrix from lumenal membranes, a process that appears to be required for vesicular retrieval of granule membranes from the apical plasma membrane and their reuse in the secretory process. We conclude that the central function of bicarbonate secretion by centroacinar and duct cells in the pancreas is to neutralize and then alkalinize the pH of the acinar lumen, sequential process that are required for (a) solubilization of secreted proteins and (b) cellular retrieval of granule membranes, respectively.

Acid-Base Equilibrium↗
PubMed1984

Effect of secoverine and atropine on intestinal secretion and motor activity in the rat small intestine in-vivo.

The actions of secoverine and atropine on bethanechol-induced intestinal secretion, hypermotility and transintestinal potential difference were investigated in the rat jejunum in-vivo. Both secoverine (10(-7) mol kg-1) and atropine (1.2 X 10(-9) mol kg-1) inhibited motility at doses that did not affect secretion or transintestinal potential difference. However, secoverine was a less potent antagonist of all the bethanechol-induced changes than atropine. Increases in transintestinal potential difference were more closely related to production of fluid secretion than to increases in motility.

Animals↗
PubMed1998

Alkaline secretion by frog gastric glands measured with pH microelectrodes in the gland lumen.

1. In the present work we have measured the pH of the secreted fluid within the gland lumen of isolated but intact gastric mucosa of Rana esculenta. Tissues were mounted in a double chamber allowing continuous perfusion of the mucosal and serosal compartment, and the measurements were made with double-barrelled pH glass microelectrodes inserted into the glands from the serosal surface under microscopic inspection. 2. During inhibition of H+ secretion by cimetidine (100 microM) the luminal gland pH (pHgl) averaged 7.60 +/- 0.05 pH units (mean +/- s.e.m.; n = 35), a value significantly higher than bath solution pH (7.45 +/- 0.02; P < 0.001) and also higher than intracellular pH of oxyntopeptic cells (pHi), which averaged 7.53 +/- 0.06 (n = 18). 3. Stimulation of acid secretion with histamine (500 microM) reversibly decreased pHgl to values which could be as low as 2.5. Together with electrophysiological criteria this response was routinely used to verify the proper location of the microelectrode tip within the gland lumen. 4. Stimulation with carbachol (100 microM) or pentagastrin (50 microM) in the presence of cimetidine rapidly and reversibly increased pHgl by 0.10 +/- 0.01 pH units (n = 24; P < 0.001) and 0.09 +/- 0.02 pH units (n = 6; P < 0.05), respectively. 5. The observation that gastric gland fluid is more alkaline than the bath solutions and that carbachol or pentagastrin further alkalinize it strongly suggests that oxyntopeptic cells participate in gastric alkaline secretion at least under cholinergic stimulation.

Animals↗
PubMed1989

Hyperosmolarity but not histamine evokes secretion of nasal fluid in the rat.

Histamine (dihydrochloride or free base), mannitol or sodium chloride applied topically to the nasal mucosa of anaesthetized rats stimulated the secretion of fluid in a dose-dependent manner. Compound 48/80 applied in the same way and histamine given s.c. failed to evoke secretion. The secretion evoked by topically applied histamine was resistant to pretreatment with H1 and H2 receptor antagonists i.p. Furthermore, the secretion evoked by histamine and sodium chloride was resistant to pretreatment with atropine i.p. or lidocaine topically. The secretion evoked by mannitol or by sodium chloride was not reduced by H1 receptor antagonists and was not significantly different from that obtained after challenge with histamine of equivalent osmolality. We conclude that the response to topically applied histamine reflects the hyperosmolarity of the compounds applied and not the effect of histamine on histamine receptors.

Animals↗
PubMed2000

[Hyponatremia--with comments on hypernatremia].

Disorders of the serum sodium concentration (hypo- and hypernatremia) are amongst the most frequent electrolyte disorders in clinical medicine. They are attributable to disturbance of to water metabolism. Hyponatremia is almost always a condition of water excess while hypernatremia is due water deficiency. Physiological normonatremia (normal plasma osmolality) is maintained by an integrated system involving regulated water intake via thirst and control of water excretion via antidiuretic hormone secretion. Therefore hypo- and hypernatremia should be analyzed in terms of dysregulated ADH secretion, fluid intake and renal water excretion. Hyponatremia is usually a disorder of vasopressin excess, due to 'non-osmotic' vasopressin release. The latter may occur in two different settings: (I) SIADH, (II) baroreceptor mediated vasopressin secretion (cardiac failure, liver cirrhosis). This entities are easy to distinguish in clinical practice. SIADH is associated with striking lower plasma concentrations of urate, creatinine and urea. In SIADH the blood pressure is normal and there is no edema. In contrast in the hyponatremia of liver cirrhosis and heart failure the plasma measurements indicated are usually slightly elevated, the blood pressure is low and there is edema. The typical patient with hypernatremia is old and has no thirst sensation. Hypo- or hypernatremia may cause major neurologic symptoms. These symptoms are more related to the rate of change in the serum sodium concentration than to the absolute level of a hypo- or hypernatremia reached. The traditional treatment for hyponatremia used to be water restriction. However V2-Vasopressin-Antagonists may provide a better treatment modality in the future. Hypernatremia is treated by slow rehydratation.

Diagnosis, Differential↗
PubMed1990

Lacrimal gland inositol trisphosphate isomer and inositol tetrakisphosphate production.

In the lacrimal gland, cholinergic agonists stimulate protein and electrolyte/water secretion by producing inositol trisphosphate (IP3) from phosphatidylinositol bisphosphate. To determine which IP3 isomers were produced and whether inositol tetrakisphosphate (IP4) was produced during activation of secretion, rat exorbital gland acini were [3H]inositol-labeled and stimulated by the cholinergic agonist carbachol. Water-soluble inositol phosphates were separated by anion-exchange chromatography using Dowex columns or high-performance liquid chromatography. Intracellular Ca2+ concentration ([Ca2+]i) was measured by fluorescence using the Ca2+ dye fura-2. Carbachol (10(-3) M) produced a time-dependent increase in 1,4,5-IP3, 1,3,4-IP3, and 1,3,4,5-IP4 levels during 0-60 s of stimulation. The 1,4,5-IP3 level increased rapidly and was followed by a slower rise in 1,3,4-IP3 and 1,3,4,5-IP4 levels. A 3-s carbachol (10(-8) to 10(-2) M) stimulation caused a concentration-dependent rise in the 1,4,5-IP3 level. Carbachol (10(-9) to 10(-2) M) increased [Ca2+]i in a concentration-dependent manner. Carbachol (10(-3) M) increased [Ca2+]i to a maximum level by 10 s; by 60 s [Ca2+]i decreased by 38%. The maximum increase in 1,4,5-IP3 levels occurred at a higher carbachol concentration than the increase in [Ca2+]i or protein secretion. We concluded that cholinergic stimulation of the lacrimal gland rapidly increased 1,4,5-IP3 levels, which was responsible for the initial increase in [Ca2+]i and initial rapid phase of protein and fluid secretion. Cholinergic stimulation also increased 1,3,4-IP3 and 1,3,4,5-IP4, but more slowly; either acting alone or with 1,4,5-IP3, they could account for the slower phase of secretion.

Animals↗
PubMed1993

[Effect of arginine-vasopressin infusion on the secretion of tracheal fluid in sheep fetuses].

Timely evacuation of alveolar fluid, release of surfactant and the beginning of continuous breathing, are key processes for an adequate adaptation of the fetus to the extrauterine life. Fetal vasopressin increases during labor and inhibit the secretion of tracheal fluid through a mechanism still unknown. The aim of this study was to elucidate the mechanism whereby vasopressin inhibit the secretion of lung fluid. We used fetal sheep chronically catheterized and infused either with vasopressin, vasopressin agonist (V2; dDAVP) or vasopressin antagonist (V1). Tracheal flow was measured during basal and infusions periods of 2 hours, monitoring fetal blood pressure, heart rate and blood pH and gases. Vasopressin and the V1 vasopressin antagonist caused a significant reduction in tracheal fluid flow, effect that was potentiated when both peptides were infused together. The V2 vasopressin agonist had no effect on the secretion of lung fluid. We concluded that vasopressin causes a significant inhibition of lung liquid secretion through a mechanism different to the activation of V1 and V2 receptors, and we propose the existence of other (s) kind of receptors (or receptors) for vasopressin that is (are) active during fetal life.

Animals↗
PubMed1976

Organic anions induce colinic secretion.

Experiments were conducted by instilling test solutions into the cleaned colon of anesthetized rats. Isotonic test solutions at an acid (2.9% or neutral (7.0) pH and containing acetic acid or acetate ions were used. At the lower pH, acetic acid was absorbed well absorbed and the colon absorbed fluid. The secretory effect could not be reproduced by hydrochloric acid solutions at pH 2.9. Fluid secretion induced by acetic acid was associated with discharge of mucus from goblet cells. The interference of colonic absorption by acetic acid might be important in some diarrheal diseases.

Acetates↗
PubMed2002

Absent secretion to vasoactive intestinal peptide in cystic fibrosis airway glands.

We are testing the hypothesis that the malfunctioning of airway gland serous cells is a component of cystic fibrosis (CF) airway disease. CF is caused by mutations that disrupt CF transmembrane conductance regulator, an anion channel essential for proper fluid secretion in some epithelia. Submucosal glands supply most of the mucus in upper airways, and gland serous cells are the primary site of CF transmembrane conductance regulator expression in airways. We have discovered a major defect in CF glands by in situ optical monitoring of secretions from single human airway glands. CF glands did not secrete to agents that elevated [cAMP](i) (0 responses/450 glands, 8 subjects), whereas glands were responsive in all donor tracheas (605/827 glands, 15 subjects) and in bronchi from subjects who were transplanted because of other lung diseases (148/166 glands, n = 10). CF glands secreted to cholinergic stimulation, and serous cells were abundant in glands from all CF subjects. The complete absence of secretion to agents that elevate [cAMP](i) suggests that altered secretion of gland mucus could contribute to CF lung disease.

Adult↗
PubMed1984

Vasoactive intestinal polypeptide (VIP) in the pig pancreas: role of VIPergic nerves in control of fluid and bicarbonate secretion.

Vasoactive intestinal polypeptide (VIP) in the pig pancreas is localized to nerves, many of which travel along the pancreatic ducts. VIP stimulates pancreatic fluid and bicarbonate secretion like secretin. Electrical vagal stimulation in the pig causes an atropine-resistant profuse secretion of bicarbonate-rich pancreatic juice. In an isolated perfused preparation of the pig pancreas with intact vagal nerve supply, electrical vagal stimulation caused an atropine-resistant release of VIP, which accurately parallelled the exocrine secretion of juice and bicarbonate. Perfusion of the pancreas with a potent VIP-antiserum inhibited the effect of vagal stimulation on the exocrine secretion. It is concluded, that VIP is responsible for (at least part of) the neurally controlled fluid and bicarbonate secretion from the pig pancreas.

Animals↗
PubMed1976

The saccus dorsalis of the rainbow trout, Salmo gairdneri Richardson: histological, cytochemical, electron microscopical and autoradiographical observations.

The saccus dorsalis of the brain of the rainbow trout, Salmo gairdneri Richardson, has been investigated by means of histological, cytochemical, enzyme-cytochemical, electron microscopical autoradiographical techniques. The saccus dorsalis is a rostro-dorsal evagination of the diencephalic roof, and consists of a partly folded epithelial wall separating the cerebrospinal fluid from the meningeal matrix fluid. The well-developed vascular system around the epithelial wall, consisting of capillaries with different diameters, seems to be part of the pineal vascular system. No structures were found that may be involved in a possible mechanical or nervous blood flow control. The single-layered epithelium consists of highly specialized cells of one specific type. These cells are mainly characterized by infolded basal membranes, long microvilli of a peculiar shape, non-folded lateral membranes bordering intercellular spaces, apical concentrations of elongate and cup-shaped macromitochondria, a basally located rough endoplasmic reticulum, an apically situated smooth endoplasmic reticulum and apical concentrations of micropinocytotic vesicles. Morphological evidence is presented of a multiple function of these cells: (1) fluid secretion, (2) extrusion of low molecular weight organic substances into the ventricular system, (3) uptake of high molecular weight substances, and (4) uptake of low molecular weight organic substances (aminergic neurotransmitters [GABA]) from the cerebrospinal fluid. The significance of light and dark cells is discussed. Indications of a possible innervation of the saccus dorsalis epithelial cells were not observed. The functional significance of the saccus dorsalis (possible analogue of the choroid plexus?) is discussed.

Animals↗
PubMed1992

Study on the mechanism of Giardia lamblia induced diarrhoea in mice.

The transmucosal fluxes of Na+ and Cl- were studied in Giardia lamblia infected mice in the presence or absence of phorbol-12-myristate-13-acetate (PMA), the activator of protein kinase C (PKC) or 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine (H-7), the inhibitor of PKC or Ca(2+)-calmodulin. There was net secretion of Na+ and Cl- in infected animals, while in control animals there was net absorption of these ions. The addition of ionophore or PMA resulted in net secretion of Na+ and Cl- in the control group while in the infected group there was no change in the fluxes of these ions. The selective potent inhibitor of protein kinase C, H-7, reversed the secretion of Na+ and Cl- in infected group to absorption. The addition of PMA and Ca(2+)-ionophore together in the infected group had a partial additive effect. This study suggests that G. lamblia induced fluid secretion involves protein kinase C and further protein kinase C acts in synergism with calcium.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1988

Diarrhoea and constipation.

Drug-induced constipation is mostly caused by changes in gut motility, whilst diarrhoea is more frequently caused by an increase in intestinal fluid secretion. In both instances the drug has to reach the enteric nervous system or the enterocyte, either via the blood or from the lumen, in sufficient concentrations to affect the mediators that regulate motility and fluid transport. Diarrhoea and constipation are frequently mentioned as side-effects of drugs, and therapeutic agents for almost all organ systems have been implicated. However, both these side-effects are usually mild or moderate, and rarely necessitate interruption of drug treatment. An exception to this rule is the antibiotic-associated colitis seen in patients treated with antibiotics such as lincomycin or clindamycin; in principle almost all antibiotics may cause this severe and potentially life-threatening complication. Other rare forms of severe, drug-induced colitis and diarrhoea result from toxic or anaphylactic reactions against gold preparations, cytostatic agents and sulphonamides. Ischaemic colitis due to vascular complications has been described in some women taking oral contraceptives, and in patients treated with vasopressin or digitalis.

Constipation↗
PubMed2004

Expression of epithelial sodium channel alpha-subunit mRNAs with alternative 5'-untranslated regions in the developing human lung.

In preparation for birth, lung epithelia must switch from net fluid secretion, required for lung development, to net absorption, which prepares the lungs for postnatal gas exchange. The apical membrane amiloride-sensitive epithelial Na channel (ENaC) is the rate-limiting step for Na+ and fluid absorption. Expression of alpha-ENaC mRNA has been detected in human lung as early as the embryonic stage of development. However, humans express multiple transcripts for alpha-ENaC, containing differing 5'-untranslated regions (UTR) with unknown effects on protein translation, and different ontogenies for individual transcripts could provide a novel mechanism for developmental regulation of ENaC function. To assess the relative expression of the two most abundant alpha-ENaC transcripts (alpha-ENaC1 and alpha-ENaC2) during lung development, we performed nonradioactive in situ hybridization using probes specific to the alternative 5'-UTRs. Both transcripts were expressed throughout intrauterine lung development (8 to 40 wk gestation), and expression was localized to the surface epithelial cells of the conductive and respiratory airways in both ciliated cells and nonciliated Clara cells. alpha-ENaC mRNA expression was also identified in the serous cells of the submucosal glands surrounding the proximal airways. In the mature prenatal lung, subsets of alveolar type II (ATII) cells expressed one or both of the alpha-ENaC transcripts. Our observations demonstrate that a developmentally regulated switch between alpha-ENaC 5'-UTR variants is not the trigger by which the developing human lung becomes a fluid-absorbing organ at birth, that individual ATII cells express neither, one, or both of the alpha-ENaC transcripts, and that the overall expression is linked to epithelial cell differentiation and lung maturation.

5' Untranslated Regions↗
PubMedDate not supplied

Cystic fibrosis transmembrane conductance regulator in the kidney: clues to its role?

The cystic fibrosis transmembrane conductance regulator (CFTR) is a cyclic adenosine monophosphate dependent, low-conductance chloride channel found on the apical plasma membrane of secretory epithelia. Surprisingly, since cystic fibrosis patients have no kidney phenotype, CFTR is highly expressed in the kidney, present from 12 weeks of gestation in the human metanephric kidney. As well as the mature, full-length, 165-kD wild-type protein (WT-CFTR) associated with renal tubule plasma membranes, intracellular, partially glycosylated forms are also seen in normal kidneys. In addition, a kidney-specific splice variant of CFTR translates a cytoplasmic truncated protein (TNR-CFTR), apparently associated with a specific small endosomal population, and is predominantly expressed in the renal medulla. WT-CFTR and TNR-CFTR show different patterns of developmental regulation, WT-CFTR being the major form expressed early in metanephric development when it is localized at the apical plasma membrane of developing collecting tubules. By contrast, TNR-CFTR expression increases with gestational age, reaching adult levels at 23 weeks. Evidence suggests that WT-CFTR plays a role in chloride secretion into the apical lumen of normal distal tubules. In autosomal dominant polycystic kidney disease, normally targeted CFTR at the apical plasma membrane in association with mislocalized Na-K-ATPase may result in abnormal fluid secretion into cysts. Similar colocalization of WT-CFTR and Na-K-ATPase at the apical plasma membranes is found in collecting tubules during development when it is speculated to play a role in the initiation of opening of the tubule lumen.

Adult↗
PubMed1985

In vivo aspects of urogastrone-epidermal growth factor.

Recent evidence indicates that human urogastrone-epidermal growth factor originates in submandibular and Brunner's glands and that serum levels are low (less than 1 ng ml-1). It occurs in many secreted fluids to a much greater extent and many tissues are thus exposed to concentrations greater than 100 ng ml-1. Rapid actions in vivo of URO-EGF include the ability to inhibit gastric acid secretion at low doses (250 ng kg h-1 in humans) and to provide cytoprotective effects against ulcerogenic agents (250 ng kg h-1 in cats). More prolonged exposure of tissues shows increases in parameters related to wound healing, beneficial effects upon ulceration and also the ability to accelerate crypt cell production rate along the gastrointestinal tract. Synthetic material has been prepared with an identical structure to the natural URO-EGF thus enabling detailed studies of the biological effects to be pursued.

Animals↗
PubMed1998

Epithelial transport in polycystic kidney disease.

In autosomal dominant polycystic kidney disease (ADPKD), the genetic defect results in the slow growth of a multitude of epithelial cysts within the renal parenchyma. Cysts originate within the glomeruli and all tubular structures, and their growth is the result of proliferation of incompletely differentiated epithelial cells and the accumulation of fluid within the cysts. The majority of cysts disconnect from tubular structures as they grow but still accumulate fluid within the lumen. The fluid accumulation is the result of secretion of fluid driven by active transepithelial Cl- secretion. Proliferation of the cells and fluid secretion are activated by agonists of the cAMP signaling pathway. The transport mechanisms involved include the cystic fibrosis transmembrane conductance regulator (CFTR) present in the apical membrane of the cystic cells and a bumetanide-sensitive transporter located in the basolateral membrane. A lipid factor, called cyst activating factor, has been found in the cystic fluid. Cyst activating factor stimulates cAMP production, proliferation, and fluid secretion by cultured renal epithelial cells and also is a chemotactic agent. Cysts also appear in the intrahepatic biliary tree in ADPKD. Normal ductal cells secrete Cl- and HCO3-. The cystic ductal cell also secretes Cl-, but HCO3- secretion is diminished, probably as the result of a lower population of Cl-/HCO3- exchangers in the apical membrane as compared with the normal cells. Some segments of the normal renal tubule are also capable of utilizing CFTR to secrete Cl-, particularly the inner medullary collecting duct. The ability of Madin-Darby canine kidney cells and normal human kidney cortex cells to form cysts in culture and to secrete fluid and the functional similarities between these incompletely differentiated, proliferative cells and developing cells in the intestinal crypt and in the fetal lung have led us to suggest that Cl- and fluid secretion may be a common property of at least some renal epithelial cells in an intermediate stage of development. The genetic defect in ADPKD may not directly affect membrane transport mechanisms but rather may arrest the development of certain renal epithelial cells in an incompletely differentiated, proliferative stage.

Animals↗