The role of aquaporins in pancreatic ductal fluid secretion

Pancreatology ◽  
2017 ◽  
Vol 17 (3) ◽  
pp. S25-S26
Author(s):  
Viktória Venglovecz ◽  
Petra Pallagi ◽  
Eszter Becskeházi ◽  
Anita Balázs ◽  
Matthias Sendler ◽  
...  
Keyword(s):  
Fluid Secretion ◽  
Ductal Fluid

scholarly journals Estrogen Modulates Glycerol Permeability in Sertoli Cells through Downregulation of Aquaporin-9

Cells ◽  
2018 ◽  
Vol 7 (10) ◽  
pp. 153 ◽  
Author(s):  
Raquel Bernardino ◽  
David Carrageta ◽  
Ana Silva ◽  
Giuseppe Calamita ◽  
Marco Alves ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Reproductive Tract ◽  
Fluid Secretion ◽  
Male Reproductive Tract ◽  
Aquaporin 9 ◽  
Important Regulator ◽  
17Β Estradiol ◽  
And Function ◽  
Glycerol Permeability

High 17β-Estradiol (E2) levels are known to cause alterations of spermatogenesis and environments throughout the male reproductive tract. Sertoli cells (SCs) ensure an adequate environment inside the seminiferous tubule. Glycerol stands as essential for the maintenance of blood–testis barrier created by SCs, however, the role of E2 in this process is not known. Herein, we hypothesized that the effect of E2 on glycerol permeability in mouse SCs (mSCs) could be mediated by aquaglyceroporins. The expression of aquaglyceroporins was assessed by RT-PCR and qRT-PCR. Glycerol permeability was evaluated by stopped-flow light scattering. We were able to identify the expression of AQP3 and AQP9 in mSCs where AQP9 is more abundant than AQP3. Our results show that high E2 levels decrease AQP9 mRNA abundance with no influence on AQP3 in mSCs. Interestingly, high E2 levels decreased mSCs’ permeability to glycerol, while downregulating AQP9 expression, thus suggesting a novel mechanism by which E2 modulates fluid secretion in the testis. In conclusion, E2 is an important regulator of mSCs physiology and secretion through changes in AQP9 expression and function. Thus, alterations in glycerol permeability induced by E2 may be the cause for male infertility in cases associated with the presence of high E2 levels.

Preliminary isolation of mosquito natriuretic factor

1985 ◽  
Vol 249 (4) ◽  
pp. R379-R386 ◽  
Author(s):  
D. H. Petzel ◽  
H. H. Hagedorn ◽  
K. W. Beyenbach
Keyword(s):  
Fluid Secretion ◽  
Malpighian Tubules ◽  
Reverse Phase Hplc ◽  
Saline Extract ◽  
Natriuretic Factor ◽  
K Secretion ◽  
Transepithelial Voltage ◽  
Nacl Secretion ◽  
Fraction I

A natriuretic factor that triggers diuresis in isolated Malpighian tubules of the mosquito was isolated from the head of the yellow-fever mosquito Aedes aegypti by passing a saline extract of mosquito heads through low-pressure and then high-pressure liquid chromatography (HPLC) columns. Three fractions with biologic activity eluted during a reverse-phase HPLC linear acetonitrile gradient run. Fraction I depolarized the transepithelial voltage (Vt) of isolated perfused Malpighian tubules but did not not stimulate fluid secretion in the Ramsay assay (J. A. Ramsay, J. Exp. Biol. 31: 104–113, 1954). Fraction II depolarized and fraction III hyperpolarized Vt, and both stimulated fluid secretion three- to fourfold. Even though the effects of fractions II and III on Vt differed, both stimulated fluid secretion by increasing the rate of NaCl secretion without affecting K secretion. The selective stimulation of active secretory Na transport by fraction III is mimicked by cyclic AMP (cAMP), suggesting the second messenger role of cAMP in the effects of fraction III. Because fraction III stimulates a NaCl-rich, as opposed to KCl-rich, fluid, the term mosquito natriuretic factor is proposed for this active fraction.

Serotonin triggers cAMP and PKA-mediated intracellular calcium waves in Malpighian tubules of Rhodnius prolixus

2014 ◽  
Vol 307 (7) ◽  
pp. R828-R836 ◽  
Author(s):  
Paula Gioino ◽  
Brendan G. Murray ◽  
Juan P. Ianowski
Keyword(s):  
Second Messenger ◽  
Fluid Secretion ◽  
Rhodnius Prolixus ◽  
Malpighian Tubules ◽  
Insect Vector ◽  
Excess Water ◽  
Intracellular Ca ◽  
Single Meal ◽  
Hematophagous Insect

Rhodnius prolixus is a hematophagous insect vector of Chagas disease capable of ingesting up to 10 times its unfed body weight in blood in a single meal. The excess water and ions ingested with the meal are expelled through a rapid postprandial diuresis driven by the Malpighian tubules. Diuresis is triggered by at least two diuretic hormones, a CRF-related peptide and serotonin, which were traditionally believed to trigger cAMP as an intracellular second messenger. Recently, calcium has been suggested to act as a second messenger in serotonin-stimulated Malpighian tubules. Thus, we tested the role of calcium in serotonin-stimulated Malpighian tubules from R. prolixus. Our results show that serotonin triggers cAMP-mediated intracellular Ca2+ waves that were blocked by incubation in Ca2+-free saline containing the cell membrane-permeant Ca2+ chelator BAPTA-AM, or the PKA blocker H-89. Treatment with 8-Br-cAMP triggered Ca2+ waves that were blocked by H-89 and BAPTA-AM. Analysis of the secreted fluid in BAPTA-AM-treated tubules showed a 75% reduction in fluid secretion rate with increased K+ concentration, reduced Na+ concentration. Taken together, the results indicate that serotonin triggers cAMP and PKA-mediated Ca2+ waves that are required for maximal ion transport rate.

Sa1484 The Crucial Role of Aquaporins in the Diminished Fluid Secretion During Acute Pancreatitis

2012 ◽  
Vol 142 (5) ◽  
pp. S-317-S-318
Author(s):  
Peter Hegyi ◽  
Lajos V Kemeny ◽  
Rakonczay Zoltan ◽  
Zvara Agnes ◽  
Laszlo Puskas ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Crucial Role ◽  
Fluid Secretion

Evaluating the role of testosterone in cerebrospinal fluid secretion

2017 ◽  
Author(s):  
Connar Westgate ◽  
Hannah Botfield ◽  
Michael O'Reilly ◽  
David Hodson ◽  
Alexandra Sinclair
Keyword(s):  
Cerebrospinal Fluid ◽  
Fluid Secretion ◽  
Cerebrospinal Fluid Secretion

scholarly journals THE NATURE & ROLE OF MUCOSAL DAMAGE IN RELATION TO SALMONELLA TYPHIMURIUM-INDUCED FLUID SECRETION IN THE RABBIT ILEUM

1986 ◽  
Vol 20 (7) ◽  
pp. 691-691 ◽  
Author(s):  
T S Wallis ◽  
W G Starkey ◽  
J Stephen ◽  
S J Haddon ◽  
M P Osborne ◽  
...  
Keyword(s):  
Salmonella Typhimurium ◽  
Fluid Secretion ◽  
Mucosal Damage ◽  
Rabbit Ileum

scholarly journals Mice lacking NKCC1 are protected from development of bacteremia and hypothermic sepsis secondary to bacterial pneumonia

2007 ◽  
Vol 204 (6) ◽  
pp. 1383-1393 ◽  
Author(s):  
MyTrang Nguyen ◽  
Amy J. Pace ◽  
Beverly H. Koller
Keyword(s):  
Klebsiella Pneumoniae ◽  
Physiological Response ◽  
Bacterial Pneumonia ◽  
Acute Inflammation ◽  
Inflammatory Responses ◽  
Fluid Secretion ◽  
Specific Inhibition ◽  
Pulmonary System ◽  
Number Of Cells

The contribution of the Na+-K+-Cl− transporter (NKCC1) to fluid in ion transport and fluid secretion in the lung and in other secretory epithelia has been well established. Far less is known concerning the role of this cotransporter in the physiological response of the pulmonary system during acute inflammation. Here we show that mice lacking this transporter are protected against hypothermic sepsis and bacteremia developing as a result of Klebsiella pneumoniae infection in the lung. In contrast, this protection was not observed in NKCC1−/− mice with K. pneumoniae—induced peritonitis. Although overall recruitment of cells to the lungs was not altered, the number of cells present in the airways was increased in the NKCC1−/− animals. Despite this robust inflammatory response, the increase in vascular permeability observed in this acute inflammatory model was attenuated in the NKCC1−/− animals. Our studies suggest that NKCC1 plays a unique and untoward unrecognized role in acute inflammatory responses in the lung and that specific inhibition of this NKCC isoform could be beneficial in treatment of sepsis.

scholarly journals Role of Various Enterotoxins in Aeromonas hydrophila-Induced Gastroenteritis: Generation of Enterotoxin Gene-Deficient Mutants and Evaluation of Their Enterotoxic Activity

2002 ◽  
Vol 70 (4) ◽  
pp. 1924-1935 ◽  
Author(s):  
Jian Sha ◽  
E. V. Kozlova ◽  
A. K. Chopra
Keyword(s):  
Biological Activity ◽  
Mouse Model ◽  
Aeromonas Hydrophila ◽  
Fluid Secretion ◽  
The Other ◽  
Enterotoxin Gene ◽  
Knockout Mutant ◽  
Heat Stable ◽  
Isogenic Mutants

ABSTRACT Three enterotoxins from the Aeromonas hydrophila diarrheal isolate SSU have been molecularly characterized in our laboratory. One of these enterotoxins is cytotoxic in nature, whereas the other two are cytotonic enterotoxins, one of them heat labile and the other heat stable. Earlier, by developing an isogenic mutant, we demonstrated the role of a cytotoxic enterotoxin in causing systemic infection in mice. In the present study, we evaluated the role of these three enterotoxins in evoking diarrhea in a murine model by developing various combinations of enterotoxin gene-deficient mutants by marker-exchange mutagenesis. A total of six isogenic mutants were prepared in a cytotoxic enterotoxin gene (act)-positive or -negative background strain of A. hydrophila. We developed two single knockouts with truncation in either the heat-labile (alt) or the heat-stable (ast) cytotonic enterotoxin gene; three double knockouts with truncations of genes encoding (i) alt and ast, (ii) act and alt, and (iii) act and ast genes; and a triple-knockout mutant with truncation in all three genes, act, alt, and ast. The identity of these isogenic mutants developed by double-crossover homologous recombination was confirmed by Southern blot analysis. Northern and Western blot analyses revealed that the expression of different enterotoxin genes in the mutants was correspondingly abrogated. We tested the biological activity of these mutants in a diet-restricted and antibiotic-treated mouse model with a ligated ileal loop assay. Our data indicated that all of these mutants had significantly reduced capacity to evoke fluid secretion compared to that of wild-type A. hydrophila; the triple-knockout mutant failed to induce any detectable level of fluid secretion. The biological activity of selected A. hydrophila mutants was restored after complementation. Taken together, we have established a role for three enterotoxins in A. hydrophila-induced gastroenteritis in a mouse model with the greatest contribution from the cytotoxic enterotoxin Act, followed by the Alt and Ast cytotonic enterotoxins.

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