Potassium movement across serosal and mucosal surfaces of frog gastric mucosa

1965 ◽  
Vol 208 (3) ◽  
pp. 528-530 ◽  
Author(s):  
Horace W. Davenport ◽  
Peter H. Abbrecht

Frog gastric mucosa was formed into a sac, filled with 1 ml salt solution and incubated in a large volume of identical salt solution containing 3 mm potassium and K42. Total potassium and specific activities of tissue and fluid were measured at 5, 10, 20, 40, 80, and 160 min after start of incubation. The measurements were repeated on mucosas formed into sacs with the mucosal side out. Both types of sacs were also incubated in solutions containing 0.1 mm histamine. Results confirm observations of others that there is net movement of potassium from fluid bathing the serosal surface into the tissue and mucosal fluid and that histamine stimulates potassium movement from tissue into mucosal fluid. The data were used to calculate the ratio of the rate of movement of potassium across the serosal and mucosal surfaces, Rs/Rm. The numerical value of 4.72 was obtained without histamine and 7.16 with histamine.

1980 ◽  
Vol 239 (6) ◽  
pp. G485-G492
Author(s):  
P. C. Sen ◽  
L. L. Tague ◽  
T. K. Ray

The transport of K+ and H+ (both expressed as mueq/h) by in vitro chambered bullfrog (Rana catesbeiana) gastric mucosa have been studied under a variety of conditions such as anoxia, addition of p-chloromercuribenzene sulfonic acid (PCMBS) into the secretory solution, inclusion of ouabain in the nutrient solution, addition of thiocyanate (SCN-) into the mucosal solution, and replacement of nutrient chloride (Cl-) with sulfate (SO4(2-)), or gluconate (Gl). Anoxia reversibly reduced the H+ transport close to zero within 15 min and gradually reduces the K+ transport throughout the 2-h period of anoxia. The presence of 2.5 X 10(-4) M mucosal PCMBS in the histamine-stimulated mucosa increases the K+ transport, which is promptly reduced by changing the gas phase to 95% N2-5% CO2. Addition of ouabain to the nutrient solution of the histamine-stimulated mucosa with PCMBS on the mucosal side significantly (P < 0.05) reduces the K+ transport within 60 min. Addition of SCN- to the mucosal solution of a histamine-stimulated mucosa with regular nutrient or O, K+ nutrient and 10, K+ mucosal solution reduces the H+ transport to near zero within 60 min. This SCN- inhibition can be reversed by elevating secretory K+. Substitution of nutrient Cl- with SO4(2-) or Gl in the histamine-stimulated mucosa reversibly inhibits H+ transport and reduces K+ transport to a low level (0.7 +/- 0.05). Our data suggest that the K+ transport across the apical membranes of gastric cells is to a large extent a passive carrier-mediated process, and the transport of both K+ and Cl- are coupled at the apical membrane.


1986 ◽  
Vol 251 (4) ◽  
pp. C643-C648 ◽  
Author(s):  
J. R. Demarest ◽  
C. Scheffey ◽  
T. E. Machen

The short-circuit current (Isc) of resting Necturus gastric mucosa (approximately 20 microA/cm2) can be attributed to the algebraic sum of the net Cl- secretion and amiloride-inhibitable net Na+ absorption. We have attempted to identify the cell types [surface epithelial cells (SCs) or oxyntic cells (OCs)] responsible for the transport of these ions in Necturus gastric mucosa using microelectrodes (ME) and a vibrating probe (VP). Mucosae were mounted horizontally in an open-topped Plexiglas chamber either serosal side up for basolateral ME impalements of OCs or mucosal side up for apical impalements of SCs and VP measurements. Cell impalements were made under open-circuit conditions, and VP measurements were performed under short-circuit conditions. Impalements of OCs indicate that neither the ratio of their apical to basolateral cell membrane resistances (Ra/Rb = 1.3 +/- 0.2) nor their cell membrane potentials were affected by 10(-6) M mucosal amiloride. In contrast, impalements of SCs indicate that amiloride increased their Ra/Rb from 3.5 +/- 0.2 to 15.6 +/- 1.8 and hyperpolarized both cell membrane potentials by greater than 20 mV. VP measurements showed that the amiloride-induced change in the current from SCs (5.6 microA/cm2) accounted for the amiloride-induced change in the Isc (5.5 microA/cm2). A non-zero current (4.4 +/- 1.0 microA/cm2) measured over SCs in the presence of amiloride was due to contamination from current arising from the gastric crypts that contain the OCs.(ABSTRACT TRUNCATED AT 250 WORDS)


1977 ◽  
Vol 232 (3) ◽  
pp. E294
Author(s):  
N Takeguchi ◽  
I Horikoshi ◽  
M Hattori

The K+ content in frog gastric mucosa (K+) was measured as a function of the submucosal K+ concentration ([K+sm]) in the absence of K+ on the mucosal side. The (K+) in HCO3- buffer with 95% O2-5% CO2 gas showed that the removal of external K+ induced a 27% K+ loss from the control value of 5 mM K+sm, that there was no linear relation between (K+) and [K+sm, and that the change in the (K+) versus the [K+sm] was hyperbolic, indicating that there are two different types of K+ in the mucosa: bound and free K+.


1989 ◽  
Vol 257 (5) ◽  
pp. G836-G844
Author(s):  
E. B. Ekblad ◽  
D. G. Warnock ◽  
V. Licko

Uptake and release of acridine orange (AO), a fluorescent weak base that accumulates in acidic spaces, were studied in perfused frog gastric mucosa. Tissue was mounted between two flow-through chambers and loaded with AO on the mucosal side. AO washout and acid secretion rate were monitored simultaneously by a flow-through fluorescence detector and a pH-stat, respectively. Data were displayed on a computer screen, stored, and analyzed. AO, in concentrations as high as 0.02 mM, does not affect the acid secretion rate. Nonlinear least-squares analysis of AO washout curves resolved two exponential components: a faster component associated mainly with AO washout from the chamber and a slower component reflecting primarily AO washout from the tissue. The slower exponential declines more slowly at higher concentrations and/or longer duration of AO loading, whereas the faster exponential is unaffected. AO washout is unaffected by the level of the steady-state acid secretion rate. Nitrite inhibits the acid secretion rate but does not affect the AO washout. When nitrite is removed, acid secretion rate and fluorescence (AO concentration in the mucosal medium) increase simultaneously and transiently. The net amount of AO released from the tissue is proportional to the net amount of acid released. Stimulation by secretagogue in basally secreting tissue causes synchronous transient increases in acid secretion rate and fluorescence. We conclude that accumulation of AO provides evidence for the existence of an intracellular storage pool of free protons within the transporting epithelium.


1966 ◽  
Vol 49 (6) ◽  
pp. 1111-1124 ◽  
Author(s):  
H. BURR STEINBACH

Intact living frogs (Rana pipiens) were partially immersed in dilute salt solution labeled with K42 or Na24 or, alternatively, injected with Ringer’s fluid containing the appropriate isotope and then partially immersed in unlabeled dilute salt. Before isotopic equilibrium, the animals were sacrificed and specific activities of K42 and Na24 were determined for medium, skin, plasma, and other tissues. With Na24, entering from the medium or escaping to the medium, specific activities of the skin approach that of the plasma. For K42, entering from the medium, the specific activity exceeds that of the plasma. The results are interpreted as indicating that the exchange rate for Na is greater plasma to skin than medium to skin, with the reverse situation for K. Values are given for average Na, K, and Cl contents of the various organ systems.


1967 ◽  
Vol 50 (10) ◽  
pp. 2377-2389 ◽  
Author(s):  
H. Burr Steinbach

Fresh, empty, isolated sacs of leg skin from R. pipiens manufacture a salt solution reasonably balanced with respect to ions and approximating a somewhat dilute Ringer's fluid. Concentrations of ions bear little relationship to concentrations in the external medium even down to 12 mM. An effective regulatory mechanism is indicated whereby the amount of salt transported is adjusted to the amount of water or vice versa, the rate of movement of either salt or water being largely independent of osmotic or ionic gradients (outer fluid to manufactured inner fluid). Concentrations of the inner fluids appear to be regulated to conform to a fairly constant concentration within the skin. Some evidence is presented that a major factor in regulating concentration of the inner fluid is triggered by an initial dilution of the inner fluid, followed by stimulation of salt uptake.


1997 ◽  
Vol 41 (6) ◽  
pp. 1246-1249 ◽  
Author(s):  
A F Goddard ◽  
R C Spiller

A novel animal model for studying antibiotic transfer across gastric mucosa was developed by using adult rats. Gastric corpus mucosa was mounted in an Ussing chamber system and bathed in oxygenated Krebs solution. Metronidazole flux from serosa to mucosa (J(S-->M)) was measured over 60 min under basal conditions and compared with mucosa-to-serosa flux (J(M-->S)). The effects of varying the chamber cross-sectional diameter and of stimulation by histamine and carbachol were assessed. Metronidazole J(M-->S) was measured with the mucosal pH at 2.2, 2.7, 3.2, and 7.4. Amoxicillin J(S-->M) under basal conditions was also measured and compared with metronidazole J(S-->M). Metronidazole J(S-->M) was proportional to serosal concentration (P < 0.001) under basal conditions, being 3.98 nmol x h(-1) x cm(-2) with a serosal concentration of 0.2 mmol/liter. Amoxicillin J(S-->M) was significantly lower under similar conditions at 0.50 nmol x h(-1) x cm(-2) (P < 0.01). Metronidazole J(S-->M) was not significantly different from J(M-->S), between chambers of different sizes, or following stimulation. When the mucosal pH was changed, J(M-->S) was proportional to the un-ionized concentration on the mucosal side (P < 0.001). Therefore, this model shows properties analogous to those of human gastric mucosa in vivo, with partitioning of metronidazole on the mucosal side according to pH, diffusion of metronidazole across the mucosa in both directions, and selectivity for different antibiotics, and it will be useful for the study of other therapeutic agents in the treatment of Helicobacter pylori.


2006 ◽  
Vol 231 (3) ◽  
pp. 277-281 ◽  
Author(s):  
Malin Josefsson ◽  
Lena Evilevitch ◽  
Björn Weström ◽  
Torsten Grunditz ◽  
Eva Ekblad

In vivo studies on rats have demonstrated that considerable amounts of iodide are transported from the bloodstream into the gastric lumen. The mechanisms for and functional significance of this transport are poorly understood. Active (driven by Na+/K+-ATPase) iodide transport into thyroid follicular cells is mediated by the sodium-iodide symporter (NIS), which is also abundantly expressed in gastric mucosa. We aimed to further investigate the iodide transport in gastric mucosa and the Possible role of NIS in this transport process. Iodide transport in rat gastric mucosa was studied in vitro in an Ussing chamber system using 125I as a marker. The system allows measurements in both directions over a mucosal specimen. A considerable transport of iodide (from the serosal to the mucosal side) was established across the gastric mucosa, whereas in the opposite direction (mucosa to serosa), iodide transport was negligible. Sodium Perchlorate (NaClO4), a competitive inhibitor of NIS, and ouabain, an inhibitor of the Na+/K+-ATPase, both attenuated gastric iodide transport from the serosal to the mucosal side. To investigate a possible neuroendocrine regulation of the iodide transport identified to occur from the serosal to the mucosal side of the stomach, thyroid-stimulating hormone (TSH), thyrotropin-releasing hormone (TRH), vasoactive intestinal peptide (VIP), histamine, or nitric oxide donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) was added. None of these substances influenced the iodide transport. We conclude that iodide is actively transported into the gastric lumen and that this transport is at least partly mediated by NIS. Additional investigations are needed to understand the regulation and significance of this transport.


1980 ◽  
Vol 238 (4) ◽  
pp. G298-G302
Author(s):  
L. Villegas

The effects of hyperosmolality of the serosal and mucosal bathing solutions on the transmucosal net water and ion fluxes were studied in frog gastric mucosa. Addition of 100 mosM glucose to the solution at the serosal surface produces a reversed mucosal-to-serosal net water flux of 7.1 +/- 1.4 microliter . cm-2 . h-1. When added to the abolished spontaneous net water flux, this results in an increment in the net water flux of -17.8 +/- 1.4 microliter . cm-2 . h-1. Addition of the same amount of glucose to the solution at the mucosal surface produces an increment in the serosal-to-mucosal net water flux of 3.7 +/- 1.1 microliter . cm-2 . h-1 when the solution at the opposite surface was kept in 220 mosmol/kg H2O. Simultaneous increments of both solutions of 320 to 420 and 420 to 520 mosM changes the osmotic serosal-to-mucosal induced fluxes to 1.9 +/- 0.9 and 3.4 +/- 1.6 microliter . cm-2 . h-1, respectively. The initial spontaneous net water fluxes measured in 220, 320, and 420 mosM solutions were 11.3 +/- 0.9, 6.9 +/- 1.6, and -1.5 +/- 1.5 microliter . cm-2 . h-1. It is proposed that the osmotic water flux is asymmetric, independent of the solutions tonicities, and not significantly affected by the sweep of solutes at the mucosal surface.


1986 ◽  
Vol 251 (3) ◽  
pp. G287-G292
Author(s):  
D. Serfilippi ◽  
R. M. Donaldson

During 24 h of organ culture, rabbit gastric fundic mucosal explants maintain constant tissue levels of intrinsic factor (IF) while steadily secreting this glycoprotein into culture medium. Mucosal explants thus generate in one day an average of 1.8 pmol of new IF per milligram mucosal protein, an amount corresponding to 70% of IF present in explant tissue. Cultured explants also incorporate [35S]methionine into tissue IF and secreted IF at a constant rate. Histamine combined with isobutylmethylxanthine stimulates explants to release IF into the culture medium, but tissue levels of IF are diminished and specific activities of tissue and secreted IF remain the same. Fluorograms of 35S-labeled proteins generated by cultured explants fail to show cobalamin-binding precursors or breakdown products of IF. These findings complement previous morphological documentation of IF synthesis by gastric mucosa. Histamine appears to stimulate IF secretion without altering IF synthesis.


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