Gastric gland, isolated

In the mouse, whereas no evidence of H3 receptors was found in isolated gastric glands (Muller et al., 1993), in the whole stomach, (R)a-methylhistamine actually increased, and thioperamide decreased acid secretion, thus indicating a definite stimulatory role for H3 receptors in this species (Table 2). Apparently, this excitatory effect, which contrasts with the observations obtained in other models, was due to an inhibitory effect on somatostatin release from fundic D cells (Schubert et al., 1993 Vuyyuru and Schubert 1993). Also, an inhibitory effect on somatostatin secretion mediated by H3 agonists was observed in other species (rat and dog). However, contrarily to what might have been expected, in these species, the inhibitory effect on somatostatin is not followed by an increase in acid secretion, but it is instead followed by a decrease, owing to the predominant H3-mediated inhibition on the release of excitatory mediators (histamine, acetylcholine) from other sites (ECL, cholinergic nerve terminals)... [Pg.63]

Bado, A, Moizo, L., Laigneau, J.P, Lewin, M.J.M., 1992a. Pharmacological characterization of histamine H3 receptors in isolated rabbit gastric glands. Am. J. Physiol. 262, G56-G61. [Pg.100]

Muller, M.J., Padol, I., Hunt, R.H., 1993. Acid secretion in isolated murine gastric glands classification of histaminergic and cholinergic receptors. Gastroenterology 104 (Suppl), A151. [Pg.108]

Omeprazole itself is not the active inhibitor of the H+, K+-ATPase, however. Rather, the transformation of omeprazole in acid is required to inhibit the H+, K+-ATPase in vitro and in vivo, whereas intact omeprazole is devoid of inhibitory action. Isolated H+, K+-ATPase is blocked by omeprazole only after the pretreatment of omeprazole with acid. Conversely, neutralization of the acid-secretory canaliculi of isolated gastric gland and parietal cell preparations by permeable buffers, which blocks the acid-catalyzed transformation of omeprazole, prevents inhibition of the enzyme. Furthermore, in-vivo blockade of acid secretion using an H2-receptor antagonist prior to omeprazole administration decreases the inhibitory potency of omeprazole, whereas the stimulation of acid secretion (e.g., by food intake) increases the potency. [Pg.93]

The last step in the omeprazole cycle (Scheme 1.2) finds support in the fact that the sulfide S is formed from omeprazole A in isolated gastric glands and in... [Pg.95]

Gastric acid formation in vitro has been studied very intensively in isolated parietal cells from dogs [32], guinea-pigs [33] and rabbits as well as in whole gastric glands from rabbits [32] and humans [34] by means of the accumulation of the weak base C-aminopyrine (pK 5.0) within the secretory compartment of the parietal cell [35]. Furthermore, oxygen... [Pg.239]

Bei lindh T, Helander HF, Obrink KJ. Effects of secretagogues on oxygen consumption, aminopyrine accumulation and morphology in isolated gastric glands. Acta Physiol Scand 1976 97 401. [Pg.38]

Gibert AJ, Mersey SJ. Morphometric analysis of parietal cell membrane transformations in isolated gastric glands. J Membr Biol 1982 67 113-124. [Pg.38]

Somatostatin inhibits acid secretion in vivo also by blocking gastrin release from antral G cells. Somatostatin inhibits histamine-stimulated acid secretion in vitro in isolated gastric glands and parietal cells where the release of gastrin is not involved. It has been suggested that somatostatin acts directly on the parietal cells, but part of the inhibitory action could result from somatostatin modulation of ECL cell activity. [Pg.90]

Chew CS, Hersey SJ, Sachs G, et al. Histamine responsiveness of isolated gastric glands. Am J Physiol 1980 238 G312. [Pg.126]

This compound had rather remarkable antlsecretory properties It Inhibited gastric acid secretion, whatever the stimulus It Inhibited secretion In Isolated gastric glands, whatever the stimulus, but was relatively acid unstable and showed Inhibition of Iodide uptake by the thyroid and was thymotoxic. [Pg.145]

Reaction of omeprazole with isolated gastric glands results in inhibition of add secretion. Treatment with thiol-redudng agents reversed the inhibition in the parietal cell. Omeprazole therefore depends on formation of disulfide bonds for its inhibitory action on gastric add secretion, as deduced from its chemistry. [Pg.150]

Im WB, Blakeman DP, Sachs G. Reversal of antisecretory activity of omeprazole by sulfhydryl compounds in isolated rabbit gastric glands. Biochim Biophys Acta 1985 845 54-59. [Pg.165]

The discovery and development of the proton pump inhibitor Isolated gastric glands from the rabbit... [Pg.12]

The relative potency of the various substituted benzimidazoles was identical in vivo (dog) and in vitro (isolated guinea pig gastric mucosa, gastric glands and isolated vesicles) [27]. Kinetic studies of the inhibition in isolated human glands confirmed the noncompetitive type of inhibition found in isolated guinea pig gastric mucosal preparation. [Pg.16]

Berglindh T (1977) Effects of common inhibitors of gastric acid secretion on secretagogue-induced respiration and aminopyrine accumulation in isolated gastric glands. Biochim Biophys Acta 464 217-233... [Pg.20]

Fellenius E, Elander B, Wallmark B, Helander HF, Berglindh T (1982) Inhibition of acid secretion in isolated gastric glands by substituted benzimidazoles. Am J Physiol 243 G505-510... [Pg.20]

Elander B, Fellenius E, Leth R, Olbe L, Wallmark B (1986) Inhibitory action of omeprazole on acid formation in gastric glands and on H, K -ATPase isolated from human gastric mucosa. Scand J Gastroenterol 21 268-272... [Pg.21]

Figure 3. Radiolabeling from 3H-omeprazole in isolated resting and stimulated gastric glands.

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