scholarly journals Ion Transport and the Development of Hydrogen Ion Secretion in the Stomach of the Metamorphosing Bullfrog Tadpole

1969 ◽  
Vol 54 (1) ◽  
pp. 76-95 ◽  
Author(s):  
John G. Forte ◽  
Liangchai Limlomwongse ◽  
Dinkar K. Kasbekar
Keyword(s):  
Ion Transport ◽  
Active Transport ◽  
Hydrogen Ion ◽  
Equilibrium Potential ◽  
Flux Analysis ◽  
Cell Interior ◽  
Ion Secretion ◽  
Hcl Secretion ◽  
Bullfrog Tadpole ◽  
Induced Changes

Isolated bullfrog tadpole stomachs secrete H+ by stage XXIV of metamorphosis, when tail reabsorption is nearly complete. At this stage the PD shows characteristic responses identical to those of the adult. The appearance of HCl secretion correlates well with other studies showing the morphogenesis of oxyntic cells. Prior to the development of H+ secretion tadpole stomachs maintain a PD similar in polarity and magnitude to that of the adult; i.e., secretory (S) side negative with respect to the nutrient (N) side. The interdependence with aerobic metabolism appeared to increase progressively through metamorphosis; however, glycolytic inhibitors always abolished the PD. Isotopic flux analysis showed that the transepithelial movement of Na+ was consistent with passive diffusion, whereas an active transport of Cl- from N to S was clearly indicated. Variations in [Na+], [K+], and [Cl-] in the bathing solutions induced changes consistent with the following functional description of the pre-H+-secreting tadpole stomach. (a) The S side is relatively permeable to Cl-, but not to Na+ or K+. (b) An equilibrium potential for K+ and Cl- exists at the N interface. (c) Ouabain abolishes the selective K+ permeablity at the N interface and reduces the total PD. (d) Effects of Na+ replacement by choline in the N solution become manifest only below 10–20 mM. It is concluded that prior to development of H+ secretion, the tadpole gastric PD is generated by a Cl- pump from N to S and a Na+ pump operating from the cell interior toward the N side.

Hydrogen ion secretion by the rat distal nephron: adaptation to chronic alkali and acid ingestion

1983 ◽  
Vol 245 (3) ◽  
pp. F349-F358
Author(s):  
C. Kornandakieti ◽  
R. Grekin ◽  
R. L. Tannen
Keyword(s):  
Ion Transport ◽  
Rat Kidney ◽  
Hydrogen Ion ◽  
Distal Nephron ◽  
Urine Ph ◽  
Ion Secretion ◽  
Titratable Acid ◽  
Chronic Ingestion ◽  
Hydrogen Ion Transport ◽  
Secretory Capacity

Isolated rat kidneys perfused at a low bicarbonate concentration were subjected to increased rates of buffer excretion, provided as creatinine, in order to examine the maximal hydrogen ion secretory capacity of the distal nephron. Preliminary experiments with kidneys from normal rats indicated that the quantity of hydrogen ion that titrated creatinine from urine pH to a pH of 6.0, designated TA-pH 6.0, provided an index of net hydrogen ion secretion by a functional segment of the distal nephron. With this technique the response of distal nephron hydrogen ion transport to ingestion of both acid and alkali loads was examined. Perfused kidneys from rats with chronic metabolic acidosis, produced by drinking 1.5% NH4Cl for 3-5 days, excreted urine with a lower pH and higher total titratable acid and TA-pH 6.0 than appropriate controls. Perfused kidneys from rats that ingested NaHCO3 for 7 days exhibited a higher urine pH and lower rates of total titratable acid and TA-pH 6.0 than controls. By contrast, kidneys from rats acutely tube-fed NaHCO3 3 h prior to study showed no change in urinary acidification parameters. Thus, chronic ingestion of an acid load stimulates, and chronic ingestion of an alkali load inhibits, the intrinsic hydrogen ion secretory capacity of the rat kidney at a distal nephron site. This intrinsic adaptation of the hydrogen ion transport mechanism is not secondary to changes in aldosterone because rats that ingested NaHCO3 chronically had higher plasma aldosterone levels than controls.

Ionic fluxes of Rana pipiens stomach bathed by sulfate solutions

1964 ◽  
Vol 207 (6) ◽  
pp. 1173-1176 ◽  
Author(s):  
Sachiko Kaneko-Mohammed ◽  
C. Adrian M. Hogben
Keyword(s):  
Gastric Mucosa ◽  
Active Transport ◽  
Rana Pipiens ◽  
Sucrose Solution ◽  
Chloride Ion ◽  
Hydrogen Ion ◽  
Ion Pump ◽  
Ion Secretion ◽  
Sulfate Solutions ◽  
Ionic Fluxes

Efforts to understand the interdependence of the active transport of hydrogen and chloride ion by bathing gastric mucosae with sulfate-substituted salines have not led to agreement. For Rana pipiens, an independent hydrogen ion pump has been proposed, and an anion transporting system has been implicated in H+ transport by Rana catesbiana. This discrepancy prompted further study of the former gastric mucosa. The results show that the R. pipiens stomach does not actively transport SO4– and is able to secrete H+ without concomitant transport of anion. This is in agreement with the initial observation of Heinz and Durbin. Reversal of the spontaneous transepithelial potential upon exposure of the stomach to sulfate salines, however, is highly variable and in these experiments is attributed to a net transfer of Na+ from serosa to mucosa as well as to secretion of H+, not to the transport of the latter ion alone. For the gastric mucosa whose serosal aspect is bathed by sulfate saline, substitution of the mucosal fluid by an isoosmotic sucrose solution resulted in a reversible cessation of hydrogen ion secretion.

Cholinergic nerves mediate stress-induced intestinal transport abnormalities in Wistar-Kyoto rats

1997 ◽  
Vol 273 (2) ◽  
pp. G486-G490 ◽  
Author(s):  
P. R. Saunders ◽  
N. P. Hanssen ◽  
M. H. Perdue
Keyword(s):  
Acute Stress ◽  
Intestinal Transport ◽  
Wistar Rat ◽  
Ussing Chambers ◽  
Ion Secretion ◽  
Wistar Kyoto Rats ◽  
Release Of Acetylcholine ◽  
Rat Strain ◽  
Wistar Kyoto ◽  
Induced Changes

We have previously reported that acute stress alters intestinal transport physiology in Wistar-Kyoto rats, a stress-susceptible strain. In this study, we tested the hypothesis that the abnormalities in these rats are due to cholinergic mechanisms. Atropine- or saline-treated rats were exposed to acute restraint stress, and, subsequently, electrophysiological parameters of excised jejunal segments were assessed in Ussing chambers. Compared with the parent Wistar rat strain, Wistar-Kyoto rats demonstrated significantly greater stress-induced changes in ion secretion and permeability. The activity of cholinesterase in intestinal mucosal homogenates was significantly less in Wistar-Kyoto than in Wistar rats. Atropine pretreatment of rats before stress corrected the epithelial pathophysiology. Our results suggest that stress stimulated the release of acetylcholine, resulting in altered epithelial function in these genetically predisposed rats.

The Development of Intracellular Membranes Concomitant with the Appearance of HCL Secretion in Oxyntic Cells of the Metamorphosing Bullfrog Tadpole

1969 ◽  
Vol 4 (3) ◽  
pp. 709-727
Author(s):  
GERTRUDE M. FORTE ◽  
L. LIMLOMWONGSE ◽  
J. G. FORTE
Keyword(s):  
Endoplasmic Reticulum ◽  
Apical Cell ◽  
Morphological Development ◽  
Structural Development ◽  
Gastric Glands ◽  
Cytoplasmic Matrix ◽  
Stage Of Development ◽  
Hcl Secretion ◽  
Bullfrog Tadpole

Bullfrog tadpole stomachs of various metamorphic stages were examined to determine the fine-structural development of oxyntic cells and to correlate observed morphological development with the capacity to secrete HCl. It was found that in vitro tadpole stomachs can consistently be stimulated to secrete acid by stage XXIV of metamorphosis, when tail reabsorption is nearly complete. Concomitant with the appearance of HCl secretion, identifiable oxyntic cells were found in the gastric glands. Prior to stage XXIV (stages XXI and XXII) the majority of cells present in the developing gastric glands exhibit features of cytological organization characteristic of undifferentiated cells: large nuclei, relatively scantry cytoplasm, and numerous ribosomal particles within the cytoplasmic matrix. The newly differentiated oxyntic cells of stage XXIV tadpole stomachs are recognizable by the accumulation of tubular members of the smooth-surfaced endoplasmic reticulum in the apical portion of the cells. These membranous structures appear to be formed by the Golgi complex which is extremely elaborate at this stage of development. As the animals complete metamorphosis (stage XXV) further development of the oxyntic cells occurs, especially the elaboration of the tubular components of the smooth-surfaced endoplasmic reticulum. The abundance of these membranous tubules within the apical cell regions and the pattern of their packing is similar to that observed in oxyntic cells of adult frogs. Also consistent with studies on adult frogs, structural alterations associated with HCl secretion were seen in the later stages of metamorphosis. In stages XXIV and XXV tadpole stomachs, which had been stimulated to secrete acid by addition of histamine, the apical surfaces of oxyntic cells were invested with long filamentous microvilli which projected into the glandular lumen. These observations support the hypothesis that membrane transformations play an integral role in the mechanism of HCl secretion and they implicate the morphogenesis of the smooth-surfaced endoplasmic reticulum as a basic prerequisite in the development of gastric secretory function.

GH elevates serum IGF-I levels but does not alter mucosal atrophy in parenterally fed rats

1997 ◽  
Vol 272 (5) ◽  
pp. G1100-G1108 ◽  
Author(s):  
C. A. Peterson ◽  
H. V. Carey ◽  
P. L. Hinton ◽  
H. C. Lo ◽  
D. M. Ney
Keyword(s):  
Specific Activity ◽  
Growth Parameters ◽  
Villus Height ◽  
Intestinal Growth ◽  
Factor I ◽  
Ion Secretion ◽  
Igf I ◽  
Mucosal Mass ◽  
And Function ◽  
Induced Changes

Growth hormone (GH) action is primarily mediated by insulin-like growth factor I (IGF-I), although both growth factors show tissue-selective effects. We investigated the effects of GH, IGF-I, and GH plus IGF-I on jejunal growth and function in rats maintained with total parenteral nutrition (TPN) and given recombinant human GH (rhGH) (400 micrograms/day sc, twice daily) and/or rhIGF-I (800 micrograms/day in TPN solution) for 5 days. Administration of GH or IGF-I alone produced similar increases in serum IGF-I levels and body weight; GH plus IGF-I further increased these parameters. TPN reduced mucosal mass, protein and DNA content, villus height, crypt depth, and enterocyte migration rate. IGF-I or GH plus IGF-I produced equivalent increases in all intestinal growth parameters; GH alone had no effect. GH, IGF-I, or GH plus IGF-I reduced TPN-induced increases in sucrase-specific activity. IGF-I, but not GH, attenuated TPN-induced increases in tissue conductance and carbachol-stimulated ion secretion. In contrast to IGF-I, GH does not stimulate intestinal growth during TPN and has less effect on normalizing TPN-induced changes in epithelial function.

Relationship between potassium, acid secretion and bioelectric potentials of frog gastric mucosa in the presence of histamine and thiocyanate

1959 ◽  
Vol 196 (6) ◽  
pp. 1266-1269 ◽  
Author(s):  
John B. Harris ◽  
Isidore S. Edelman
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Potassium Concentration ◽  
Hydrogen Ion ◽  
Ion Secretion ◽  
Transient Rise ◽  
Net Flux ◽  
Bioelectric Potentials ◽  
Sustained Increase

The transmucosal potential difference (PD), the rate of H+ secretion and the net flux of potassium from nutrient to secretory phases (JnsK) of the frog gastric mucosa were studied in vitro by the chamber method. Histamine produced a fall in PD, a sustained increase in H+ production and an equivocal rise in JnsK. Increasing the nutrient potassium concentration (Kn) to 8.5 mEq/l. in the presence of histamine induced a depression in PD, although the rate of acid secretion was unchanged. Hydrogen ion secretion decreased when the nutrient potassium concentration was decreased to 1 mEq/l. despite the continued presence of histamine. The response of JnsK to alterations in nutrient potassium concentration was unaffected by the presence of either histamine or thiocyanate. Thiocyanate produced almost complete inhibition of H+ secretion and a rise in PD. Raising the nutrient potassium concentration in the presence of thiocyanate produced a prompt and sustained fall in PD, followed by a transient rise when Kn was lowered. Alterations of the nutrient potassium concentration in the presence of thiocyanate had no effect on the rate of acidification. The data indicate that under certain circumstances PD and H+ secretion can be uncoupled and that the inverse relationship between Kn and PD is substantially independent of the rate of H+ secretion.

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