Expression of NKCC1 and NKCC2 in gastric mucosa and their possible role in acid secretion

2010 ◽  
Vol 34 (8) ◽  
pp. S2-S2
Author(s):  
Tuo Ji ◽  
Hong Xue ◽  
Zhangfeng Dou ◽  
Yue Zhang ◽  
Jinxia Zhu
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion

Nitric oxide inhibits gastric acid secretion by increasing intraparietal cell levels of cGMP in isolated human gastric glands

2005 ◽  
Vol 289 (6) ◽  
pp. G1061-G1066 ◽  
Author(s):  
Anna Berg ◽  
Stefan Redéen ◽  
Magnus Grenegård ◽  
Ann-Charlott Ericson ◽  
Sven Erik Sjöstrand
Keyword(s):  
Nitric Oxide ◽  
Gastric Mucosa ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Enzymatic Digestion ◽  
Human Gastric Mucosa ◽  
Gastric Glands ◽  
Oxyntic Mucosa ◽  
No Donor

We have previously identified cells containing the enzyme nitric oxide (NO) synthase (NOS) in the human gastric mucosa. Moreover, we have demonstrated that endogenous and exogenous NO has been shown to decrease histamine-stimulated acid secretion in isolated human gastric glands. The present investigation aimed to further determine whether this action of NO was mediated by the activation of guanylyl cyclase (GC) and subsequent production of cGMP. Isolated gastric glands were obtained after enzymatic digestion of biopsies taken from the oxyntic mucosa of healthy volunteers. Acid secretion was assessed by measuring [14C]aminopyrine accumulation, and the concentration of cGMP was determined by radioimmunoassay. In addition, immunohistochemistry was used to examine the localization of cGMP in mucosal preparations after stimulation with the NO donor S-nitroso- N-acetylpenicillamine (SNAP). SNAP (0.1 mM) was shown to decrease acid secretion stimulated by histamine (50 μM); this effect was accompanied by an increase in cGMP production, which was histologically localized to parietal cells. The membrane-permeable cGMP analog dibuturyl-cGMP (db-cGMP; 0.1–1 mM) dose dependently inhibited acid secretion. Additionally, the effect of SNAP was prevented by preincubating the glands with the GC inhibitor 4 H-8-bromo-1,2,4-oxadiazolo[3,4-d]benz[b][1,4]oxazin-1-one (10 μM). We therefore suggest that NO in the human gastric mucosa is of physiological importance in regulating acid secretion. Furthermore, the results show that NO-induced inhibition of gastric acid secretion is a cGMP-dependent mechanism in the parietal cell involving the activation of GC.

Effect of dimethyl sulfoxide applications on gastric secretory function

1982 ◽  
Vol 63 (3) ◽  
pp. 24-25
Author(s):  
S. G. Vaynshteyn ◽  
Yu. V. Afanasyeva ◽  
D. H. Maksudova ◽  
M. I. Pivikova
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Dimethyl Sulfoxide ◽  
Chronic Gastritis ◽  
Secretory Function ◽  
Normal Acid

The use of applications of dimethyl sulfoxide in patients with ulcerative disease and chronic gastritis leads to suppression of increased acid secretion, ambivalence with normal acid secretion and has no effect in patients with atrophy of the gastric mucosa. The normalizing effect of dimethyl sulfoxide (DMSO) applications in persons with acidic, decompensated ^ and subcompensated states of the stomach by stimulating the neutralizing function of the antral glands was established. The use of dimethyl sulfoxide as a transporter of various drugs in physiotherapy can be indicated in patients with HC1 hypersecretion in the interdigestive phase of ventricular secretion.

Intracellular pH measurements in gastric mucosa.

1979 ◽  
Vol 237 (1) ◽  
pp. E82
Author(s):  
S J Hersey
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Intracellular Ph ◽  
Ph Indicator ◽  
Active Secretion ◽  
Ph Measurements ◽  
Tubular Cells ◽  
A Value ◽  
Indicator Dye ◽  
Secretion Rates

Intracellular pH was measured in bullfrog gastric mucosa using a pH-indicator dye, bromthymol blue (BTB), with a spectrophotometric technique. Studies showed that BTB is taken up by the gastric mucosa and bound to intracellular components. The binding of BTB was shown to cause a shift in the pKa of the dye from the solution value of 6.95 to a value of 8.0. During the nonsecreting state, intracellular pH was estimated to be 7.4 (metiamide inhibition) or 7.1 (SCN inhibition). During active secretion of acid, intracellular pH increased with increasing secretion rates, reaching values in excess of pH 8. Using preparations from which the surface epithelial cells had been removed, it was shown that at least a portion of the alkaline response to stimulation occurs in the oxyntic or tubular cells. The results are interpreted in view of existing models for the chemical reaction involved in gastric acid secretion.

scholarly journals Effects of Cyclic Adenosine 3':5'-Monophosphate and Related Agents on Acid Secretion by Isolated Rabbit Gastric Mucosa

1975 ◽  
Vol 69 (2) ◽  
pp. 453-462 ◽  
Author(s):  
David Fromm ◽  
John H. Schwartz ◽  
Reynaldo Quijano
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion

Gastric acid secretion and parietal cell mass: effects of thyroidectomy and thyroxine

1989 ◽  
Vol 256 (6) ◽  
pp. G975-G978 ◽  
Author(s):  
K. O. Adeniyi ◽  
M. O. Olowookorun
Keyword(s):  
Gastric Mucosa ◽  
Thyroid Hormones ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Parietal Cell ◽  
Cell Function ◽  
Cell Mass ◽  
Chronic Administration ◽  
Basal Acid

The role of thyroid hormones on parietal cell function and number was studied in the rat. Chronic administration of thyroxine (6-8 micrograms/100 g body wt/day) for 35 days significantly increased parietal cell mass (from 21.18 +/- 0.13 x 10(6) to 26.71 +/- 0.14 x 10(6] as well as basal acid secretion (from 3.69 +/- 0.08 to 4.99 +/- 0.16 mueq/10 min) and histamine-stimulated acid secretion (from 2.45 +/- 0.12 to 3.69 +/- 0.21 mueq/10 min). Thyroidectomy decreased the number of parietal cells in the gastric mucosa (to 10.48 +/- 0.09 x 10(6] and basal acid secretion (to 3.09 +/- 0.08 mueq/10 min). Histamine (0.2 mg) injection into the thyroidectomized rats increased acid secretion by only 1.41 +/- 0.06 mueq/10 min as against 2.45 +/- 0.12 mueq/10 min obtained for control rats. The results suggest that thyroid hormones regulate basal and secretagogue-stimulated acid secretion via their effects on parietal cell mass.

Effect of thyroid on gastric secretion and metabolism

1961 ◽  
Vol 201 (3) ◽  
pp. 567-570 ◽  
Author(s):  
E. S. Nasset ◽  
Dale P. J. Goldsmith
Keyword(s):  
Oxygen Consumption ◽  
Gastric Mucosa ◽  
Gastric Secretion ◽  
Thyroid Hormones ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Early Summer ◽  
Tissue Concentrations ◽  
Oxygen Ratio

The effect of administration of thyroid products on gastric acid secretion and metabolism was studied in dogs with gastric pouches and in gastric mucosa from rats and frogs. Whole thyroid, thyroxin, triiodothyronine, and iodinated casein generally reduced secretion in thyroidectomized dogs and in dogs with intact thyroids. The thyroid substances elevated BMR above euthyroid levels in normal dogs but not always in thyroidectomized dogs. In dogs with intact thyroids 2,4-dinitrophenol raised oxygen consumption but did not affect secretion. Whole thyroid elevated BMR in rats and frogs but did not change resting mucosal oxygen consumption. During spring and early summer thyroid feeding reduced histamine-stimulated acid secretion and mucosal oxygen consumption during secretion in frogs, but the acid-to-oxygen ratio was unaffected. These findings suggest that elevated tissue concentrations of thyroid hormones reduce the ability of the gastric mucosa to mobilize secretory energy in response to a stimulus. This effect of the thyroid hormones is apparently not directly correlated with their calorigenic properties.

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