Central noradrenergic inhibition of gastric mucosal blood flow and acid secretion in rats

Osumi, Yoshitsugu; Aibara, Shigeo; Sakae, Koichiro; Fujiwara, Motohatsu

doi:10.1016/0024-3205(77)90369-1

Cited by 80 publications

(8 citation statements)

References 23 publications

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“…The relationships between neurotransmitters and gastric acid secretion were widely studied with regard to aspects such as inhibitory effects of norepi nephrine (2), dopamine (3), calcitonin-gene related peptide (CGRP) (4), nicotine (5), bombesin (6), neurotensin (7) and somato statin (8) and secretagogue effects of nicotine (9) and thyrotropin-releasing hormone (TRH) (10). Gamma -amino-n-butyric acid (GABA) is well-established as an inhibitory transmitter in the CNS.…”

mentioning

confidence: 99%

Acid secretagogue action of structurally gamma-aminobutyric acid(GABA)-related compounds in rats.

Yamasaki

Gotō

1990

Jpn.J.Pharmacol

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confidence: 99%

Acid secretagogue action of structurally gamma-aminobutyric acid(GABA)-related compounds in rats.

Yamasaki

Gotō

1990

Jpn.J.Pharmacol

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“…The level of aminopyrine in the plasma and gastric samples was assayed by the method of Brodie and Axelrod (17). The plasma level of amino pyrine at each 15 min interval during the experimental period was estimated by inter polating between two measured points, just before and after each experiment, and then paired with each aminopyrine level in the gastric juice (18,19). After these measure ments, the gastric MBF was calculated to be gastric output of aminopyrine (,ug/15 min)/ arterial plasma aminopyrine (fig/ml).…”

Section: Inhibitorymentioning

confidence: 99%

Inhibitory effect of somatostatin on gastric acid secretion in rats.

Nishikawa

Yokotani²,

Fujiwara

1987

Jpn.J.Pharmacol

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Abstract-Effects of somatostatin on parasympathetically induced increases in gastric acid secretion and mucosal blood tlow (MBF) were studied in anesthetized rats with a gastric fistula. Intravenous infusion of small doses of somatostatin (0.1-0.5 ug/kg/min) dose-dependently inhibited the increases in the vagally stimulated gastric acid secretion. Larger doses of somatostatin (0.5-2.5 ,ug/kg/ min) also dose-dependently inhibited the bethanechol-induced gastric acid secre tion. The dose of somatostatin required to inhibit the gastric acid secretion by about 50% of the preinfused control values was 0.25 ,ug/kg/min for vagally stimu lated acid secretion and 2.5 ,cg/kg/min for bethanechol-induced acid secretion. Thus, the inhibitory potency of somatostatin on the vagally stimulated gastric acid secretion was about 10-fold higher than that on bethanechol-induced acid secretion. Somatostatin had no effect on the increase in gastric MBF during vagus nerve stimulation or bethanechol infusion. Pretreatment with indomethacin or phentol amine had no effect on the inhibitory effect of somatostatin on the increase in gastric acid secretion during vagus nerve stimulation or bethanechol infusion. These results suggest that somatostatin exerts an inhibitory effect on gastric acid secretion by acting on the parasympathetic neurons in the gastric wall more than on the structures peripheral to the parasympathetic nerve terminals, and it reduces para sympathetically stimulated gastric acid secretion in rats. This inhibitoty effect of somatostatin on the gastric acid secretion is independent of the changes in the gastric MBF and probably not related to prostaglandin-involved or alpha adreno ceptor-mediated mechanisms.

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“…In rats, several studies have demonstrated that the hypothalamus influences gastric secretion. Stimulation of the lateral hypothalamus, but not of the surrounding area, caused a vagally mediated increase in acid output (3,4). On the other hand, stimulation of the ventromedial hypothalamus decreased acid secretion (3), whereas lesion experiments had opposite effects (5).…”

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confidence: 99%

“…On the other hand, stimulation of the ventromedial hypothalamus decreased acid secretion (3), whereas lesion experiments had opposite effects (5). Previous studies of chemical signals participating in the brain modulation of gastric secretion seem to indicate that cholinergic-stimulatory (6) and noradrenergicinhibitory mechanisms play a role (4,7).…”

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confidence: 99%

Brain regulation of gastric secretion: influence of neuropeptides.

Taché¹,

Vale²,

Rivier³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

121

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Several neuropeptides injected intracisternally were assessed for their effects on gastric secretion in rats.Bombesin (1 #g) completely suppressed gastric acid secretion, reduced the volume of gastric secretion, and partially blocked insulin-or 2-deoxy-D-glucose-induced stimulation of gastric acid output. The inhibitory effect of this peptide is dose-dependent, long-acting, reversible, and specific. Bombesin response appears to be central nervous system-mediated; its expression is not dependent on the vagus nerve or the adrenal glands, and does not rely on a decrease in gastrin secretion. Among seven other peptides tested, only 19-endorphin and a potent gonadotropin releasing-factor (gonadoliberin) agonist significantly reduced gastric acid secretion, with an activity ca. 100 times less than that of bombesin. The presence of bombesin-like material in rat brain and the high potency of bombesin to inhibit gastric secretion suggest that this peptide may be of physiologic significance as a chemical messenger involved in brain modulation of gastric secretion. The original observation that discrete brain lesions induced pathological changes in the gastric mucosa (1, 2) focused attention on the role of the central nervous system in the pathophysiological regulation of gastric function. Subsequently, numerous investigators attempted to elucidate brain structures and neurogenic/humoral pathways involved in the control of gastric secretion. In rats, several studies have demonstrated that the hypothalamus influences gastric secretion. Stimulation of the lateral hypothalamus, but not of the surrounding area, caused a vagally mediated increase in acid output (3, 4). On the other hand, stimulation of the ventromedial hypothalamus decreased acid secretion (3), whereas lesion experiments had opposite effects (5). Previous studies of chemical signals participating in the brain modulation of gastric secretion seem to indicate that cholinergic-stimulatory (6) and noradrenergicinhibitory mechanisms play a role (4, 7).The presence in mammalian brain of oligopeptides acting in the central nervous system to influence glucoregulation (8, 9), thermoregulation (10, 11), blood pressure (12, 13), sympa-

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Central noradrenergic inhibition of gastric mucosal blood flow and acid secretion in rats

Cited by 80 publications

References 23 publications

Acid secretagogue action of structurally gamma-aminobutyric acid(GABA)-related compounds in rats.

Acid secretagogue action of structurally gamma-aminobutyric acid(GABA)-related compounds in rats.

Inhibitory effect of somatostatin on gastric acid secretion in rats.

Brain regulation of gastric secretion: influence of neuropeptides.

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