Sodium transport in the diseased human gallbladder and the effects of indomethacin

1988 ◽  
Vol 75 (2) ◽  
pp. 147-149 ◽  
Author(s):  
M. R. Jacyna ◽  
P. E. Ross ◽  
D. Hopwood ◽  
I. A. D. Bouchier
Keyword(s):  
Sodium Transport ◽  
Sodium Ion ◽  
Slight Reduction ◽  
Gallbladder Epithelium ◽  
Principal Function ◽  
Na Transport ◽  
Flux Chamber ◽  
Human Gallbladder ◽  
Gallbladder Mucosa

1. Sodium ion (Na+) transport, a principal function of the gallbladder epithelium, was studied by measuring the flux of 22Na across isolated, inflamed human gallbladder mucosa maintained in a modified ‘Ussing’ flux chamber. Tissue was obtained from cholecystectomy specimens in symptomatic patients with cholelithiasis. 2. In 30 gallbladders studied, 57% had a net Na+ flux from mucosa to serosa (Na+ absorption), while 23% had a net Na+ flux from serosa to mucosa (Na+ secretion). The remaining 20% showed no overall net Na+ flux. 3. Indomethacin added to the serosal fluid reversed the direction of net Na+ flux in secreting gallbladders and caused an absorption of Na+. In Na+-absorbing gallbladders, indomethacin caused a slight reduction in Na+ absorption. No change in Na+ flux was induced in gallbladders with no initial net Na+ flux. 4. These results demonstrate that instead of absorbing Na+, some inflamed human gallbladders may secrete Na+. As this secretion can be reversed to the more usual absorption by indomethacin, it is likely that this secretion is mediated by prostaglandins.

scholarly journals Effects of Dinitrophenol and Oligomycin on the Coupling between Anaerobic Metabolism and Anaerobic Sodium Transport by the Isolated Turtle Bladder

1966 ◽  
Vol 49 (3) ◽  
pp. 483-499 ◽  
Author(s):  
Neal S. Bricker ◽  
Saulo Klahr
Keyword(s):  
Sodium Transport ◽  
Anaerobic Metabolism ◽  
Sodium Pump ◽  
High Energy ◽  
Mitochondrial Atpase ◽  
Anaerobic Glycolysis ◽  
Anaerobic Conditions ◽  
Na Transport ◽  
Anaerobic System ◽  
Mitochondrial Atpase Activity

Dinitrophenol (1 x 10-5 M) has been found to inhibit anaerobic sodium transport by the isolated urinary bladder of the fresh water turtle. Concurrently, anaerobic glycolysis was stimulated markedly. However, tissue ATP levels diminished only modestly, remaining at approximately 75% of values observed under anaerobic conditions without DNP. The utilization of glucose (from endogenous glycogen) corresponded closely to that predicted from the molar quantities of lactate formed. Thus the glycolytic pathway was completed in the presence of DNP and if ATP were synthesized normally during glycolysis, synthesis should have been increased. On the other hand, the decrease in Na transport should have decreased ATP utilization. Oligomycin did not block sodium transport either aerobically or anaerobically, but ATP concentrations did decrease. When anaerobic glycolysis was blocked by iodoacetate, pyruvate did not sustain sodium transport thus suggesting that no electron acceptors were available in the system. Two explanations are entertained for the anaerobic effect of DNP: (a) Stimulation by DNP of plasma membrane as well as mitochondrial ATPase activity; (b) inhibition of a high energy intermediate derived from glycolytic ATP or from glycolysis per se. The arguments relevant to each possibility are presented in the text. Although definitive resolution is not possible, we believe that the data favor the hypothesis that there was a high energy intermediate in the anaerobic system and that this intermediate, rather than ATP, served as the immediate source of energy for the sodium pump.

scholarly journals Histopathological changes in gallbladder mucosa associated with cholelithiasis

1970 ◽  
Vol 2 (3) ◽  
pp. 224-225 ◽  
Author(s):  
R Baidya ◽  
B Sigdel ◽  
NL Baidya
Keyword(s):  
Retrospective Study ◽  
Intestinal Metaplasia ◽  
Gastrointestinal Disorder ◽  
Gallstone Formation ◽  
Epithelial Hyperplasia ◽  
Pathological Changes ◽  
Histopathological Changes ◽  
Gallbladder Epithelium ◽  
Gallbladder Mucosa ◽  
Gross Examination

Background: Gallstone is a very common gastrointestinal disorder. It is known to produce histopathological changes in the gallbladder. It is also one of the predisposing factors for the development of cancer of gallbladder. Materials and Methods: This was a retrospective study carried out in the Department of Histopathology, B and B Hospital during a period of 1 year from April 2010 to May 2011. The study included 396 cases of cholecystectomy specimens. Results: On gross examination, outer gallbladder surface was congested in 116 patients (28%), wall thickness was increased in 181 (45.7%) and mucosal abnormalities were present in 126 (31.6%) patients. At microscopy, epithelial hyperplasia was observed in 183 (46.2%), intestinal metaplasia in 112 (28.2%), dysplasia in 5 (1.3%) and cholesterolosis in 56 (14%) patients. Conclusion: The pathological changes of the gallbladder epithelium may play an important role in the process of gallstone formation. DOI: http://dx.doi.org/10.3126/jpn.v2i3.6027 JPN 2012; 2(3): 224-225

Anterior pituitary control of active sodium transport across frog skin

1961 ◽  
Vol 200 (3) ◽  
pp. 444-450 ◽  
Author(s):  
R. M. Myers ◽  
W. R. Bishop ◽  
B. T. Scheer
Keyword(s):  
Sodium Transport ◽  
Rana Pipiens ◽  
Sodium Current ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Anterior Lobe ◽  
Sodium Ion ◽  
Resting Potential ◽  
Active Sodium ◽  
Active Sodium Transport

Removal of the anterior lobe of the pituitary from the frog Rana pipiens is followed by an increase in the outflux of Na22 across the skin, which persists at least 4 months, and by a decrease in resting potential and sodium (‘short-circuit’) current, which persists no more than 3 weeks. The increased outflux is interpreted as resulting from increased permeability of the skin to sodium ion, and the decreased sodium current is interpreted as a decreased rate of active sodium transport. Either change is opposed by treatment with mammalian ACTH or with aldosterone. Effects of other hormones could not be established with certainty. The increased permeability of the skin to sodium appears to be associated with a decrease in the amount of a mucopolysaccharide in the dermis. The evidence suggests that the pituitary effects involve the interrenal bodies.

Transcellular sodium transport and intracellular sodium activities in rabbit gallbladder

1986 ◽  
Vol 251 (1) ◽  
pp. G155-G159
Author(s):  
W. M. Moran ◽  
R. L. Hudson ◽  
S. G. Schultz
Keyword(s):  
Small Intestine ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Gallbladder Epithelium ◽  
Na Transport ◽  
Twofold Increase ◽  
Average Value ◽  
Intracellular Na Activity ◽  
Rabbit Gallbladder ◽  
Sustained Increase

This study was designed to explore the relation between the rate of transcellular active Na+ transport by rabbit gallbladder epithelium, JNa, and the intracellular Na+ activity, (Na)c; the latter was determined by use of highly selective Na+ microelectrodes. The underlying strategy was based on the well-established observation that JNa is stimulated by the presence of bicarbonate in the bathing solutions. Our results confirm previous observations that the addition of bicarbonate to the bathing solutions results in a twofold increase in JNa. In the absence of bicarbonate, (Na)c averaged 16 mM. Within 2–4 min after the addition of bicarbonate to both bathing solutions, (Na)c increased to an average value of 22 mM and then gradually declined and by 15 min did not differ significantly from the value observed in the absence of bicarbonate. Thus, a twofold increase in JNa is not associated with an increase in (Na)c. These results are in accord with earlier observations on Necturus urinary bladder and small intestine and contradict the notion that an increase in the rate of active Na+ extrusion from the cell across the basolateral membrane in response to an increase in the rate of Na+ entry across the apical membrane is necessarily the result of a sustained increase in (Na)c.

Increase of lung sodium-potassium-ATPase activity during recovery from high-permeability pulmonary edema

1996 ◽  
Vol 271 (6) ◽  
pp. L896-L909 ◽  
Author(s):  
D. Zuege ◽  
S. Suzuki ◽  
Y. Berthiaume
Keyword(s):  
Atpase Activity ◽  
Pulmonary Edema ◽  
Sodium Transport ◽  
Sodium Ion ◽  
Type Ii ◽  
Active Sodium ◽  
Sodium Potassium ◽  
Sodium Ion Transport ◽  
Active Sodium Transport

Previous studies have suggested that recovery from pulmonary edema may be dependent on active sodium ion transport. Most of the data supporting this concept came from work done in isolated type II cells, isolated lung preparations, or in models of alveolar flooding. There is a limited amount of information regarding the role of active sodium ion transport in vivo. Furthermore, most of this information was obtained in one model of pulmonary edema, the hyperoxic lung injury model. The purpose of these experiments was then to measure the activity of the sodium-potassium-adenosinetriphosphatase (Na(+)-K(+)-ATPase), the active component of the sodium transport process and an indirect marker of active sodium transport, during recovery from thiourea-induced pulmonary edema in rats. Na(+)-K(+)-ATPase activity was significantly increased during recovery from lung edema. This increase could not be accounted for by the Na(+)-K(+)-ATPase activity present in inflammatory cells recruited in the lung by the injury process or by a direct impact of thiourea on the enzyme. Alveolar flooding, induced by instillation of a protein-containing solution into the airways of ventilated rats also increased the activity of Na(+)-K(+)-ATPase, suggesting that activation of the enzyme is probably secondary to either the presence of edema or the physiological consequences associated with edema. The quantity of lung Na(+)-K(+)-ATPase protein was also elevated during edema resolution, indicating that augmented synthesis of this enzyme underlies the increased enzyme activity observed. The quantity of Na(+)-K(+)-ATPase protein in alveolar type II cells was also significantly enhanced during recovery from edema, suggesting that these cells contribute to active sodium transport in vivo. The results of this study suggest that active sodium transport could participate in the resolution of pulmonary edema.

Aldosterone and corticosterone binding and effects on Na+ transport in cultured kidney cells

1982 ◽  
Vol 242 (6) ◽  
pp. F610-F619 ◽  
Author(s):  
C. O. Watlington ◽  
F. M. Perkins ◽  
P. J. Munson ◽  
J. S. Handler
Keyword(s):  
Sodium Transport ◽  
Binding Sites ◽  
Glucocorticoid Receptors ◽  
Qualitative Difference ◽  
Na Transport ◽  
Binding Studies ◽  
Lower Affinity ◽  
High Affinity ◽  
Competition Binding ◽  
Transport Response

A continuous line of cells (A6) derived from toad kidney has been shown to form epithelia in culture that manifest aldosterone-stimulatable transepithelial sodium transport. In this study an efficient filtration assay for nuclear binding of [3H]aldosterone was validated. Specific high-affinity aldosterone and corticosterone binding sites in the particulate (nuclear-enriched) fraction were characterized in intact epithelia. Despite metabolism of both steroids, two high-affinity binding sites for each were demonstrable: aldosterone, K'd1 = 0.85 (+/- 0.19) X 10(-10) and K'd2 = 1.6 (+/- 0.42) X 10(-8) M; corticosterone, K'd1 = 0.5 (+/- 0.31) X 10(-10) and K'd2 = 0.32 (+/- 0.19) X 10(-8) M. Analogue competition-binding studies indicated a qualitative difference in the two sites and co-occupancy of both sites by the two steroids. The sodium transport response to aldosterone and corticosterone approximated a linear function of occupancy of the lower affinity sites. Although the lower affinity sites resemble mammalian glucocorticoid receptors in terms of relative binding affinities for analogues, we conclude that they are the receptors which mediate the aldosterone and corticosterone stimulation of Na+ transport in these epithelia.

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