Effect of ambient temperature on gastric secretion and food intake in the rat

Witty, RT; Jiang, Long

doi:10.1152/ajplegacy.1970.219.5.1359

Cited by 25 publications

(3 citation statements)

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“…More recent investigations have confirmed a reduction in gastric acid output following exposure to stress induced by a large variety of stimuli including restraint (4), rotation (5), high ambient temperature (6), unpredictable electrical shocks (7), endotoxin (8), or ionizing radiation (9). It has not, however, been apparent whether such an inhibitory response to stress is the consequence of a local mechanism or, as suggested more recently, has centrally mediated components involving the release of various neuropeptides (10)(11)(12).…”

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confidence: 97%

Inhibition of gastric acid secretion by stress: A protective reflex mediated by cerebral nitric oxide

Esplugues

Barrachina

Beltrán

et al. 1996

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

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Moderate somatic stress inhibits gastric acid secretion. We have investigated the role of endogenously released NO in this phenomenon. Elevation of body temperature by 3؇C or a reduction of 35 mmHg (1 mmHg ‫؍‬ 133 Pa) in blood pressure for 10 min produced a rapid and long-lasting reduction of distension-stimulated acid secretion in the rat perfused stomach in vivo. A similar inhibitory effect on acid secretion was produced by the intracisternal (i.c.) administration of oxytocin, a peptide known to be released during stress. Intracisternal administration of the NO-synthase inhibitor, N G -nitro-L-arginine methyl ester (L-NAME) reversed the antisecretory effect induced by all these stimuli, an action prevented by intracisternal coadministration of the NO precursor, L-arginine. Furthermore, microinjection of L-NAME into the dorsal motor nucleus of the vagus nerve reversed the acid inhibitory effects of mild hyperthermia, i.v. endotoxin, or i.c. oxytocin, an action prevented by prior microinjection of L-arginine. By contrast, microinjection of L-NA ME into the nucleus tractus solitarius failed to affect the inhibitory effects of hyperthermia, i.v. endotoxin, or i.c. oxytocin. Immunohistochemical techniques demonstrated that following hyperthermia there was a significant increase in immunoreactivity to neuronal NO synthase in different areas of the brain, including the dorsal motor nucleus of the vagus. Thus, our results suggest that the inhibition of gastric acid secretion, a defense mechanism during stress, is mediated by a nervous ref lex involving a neuronal pathway that includes NO synthesis in the brain, specifically in the dorsal motor nucleus of the vagus.

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confidence: 97%

Inhibition of gastric acid secretion by stress: A protective reflex mediated by cerebral nitric oxide

Esplugues

Barrachina

Beltrán

et al. 1996

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

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“…A synergism occurs between restraint and exposure to cold (42). Cold restraint usually increases gastric acid secretion (45,46), which is mediated by the release of histamine in the stomach, and by histamine-2 (H 2 ) receptors under vagal influence (47). Cold restraint usually increases gastric acid secretion (45,46), which is mediated by the release of histamine in the stomach, and by histamine-2 (H 2 ) receptors under vagal influence (47).…”

Section: Gastric Hydrochloric Acid Secretionmentioning

confidence: 99%

From simplicity to complexity (1950–1990): the case of peptic ulceration—II. Animal studies.

Weiner

1991

Psychosomatic Medicine

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Considerable progress has been made in the understanding of the formation of gastric erosions in rats. The role of gastric acid secretion in their pathogenesis has been clarified. Gastric erosions are also associated with slow gastric contractions. With several experimental procedures, the body temperature falls; preventing this decrease averts erosions. A fall in body temperature or exposure to cold is associated with the secretion of thyrotropin-releasing hormone (TRH), and both an increase and decrease in corticotropin-releasing factor (CRF) in discrete regions of rat brains. TRH produces gastric erosions, increases in acid secretion, and slow contractions, while CRF has the opposite effects. One of the major sites of interaction of the two peptides is in the dorsal motor complex of the vagus nerve. TRH increases serotonin (5-HT) secretion into the stomach. 5-HT counter-regulates acid secretion and slow contractions. Many other peptides stimulate or inhibit gastric acid secretion.

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“…The immunoreactivity is localized in nerve fibers and terminals, whereas TRH cell bodies are contained in the raphe nuclei (43, 74). The endogenous release of brain TRH in response to cold exposure (1) mimics the stimulatory effect induced by central injection of TRH (72,82,126). Recent studies demonstrated that intracerebroventricular injection of TRH antiserum significantly inhibited gastric acid secretion stimulated by pylorus ligation in rats (32).…”

Section: Physiological Rolementioning

confidence: 99%

CNS Peptides and Regulation of Gastric Acid Secretion

Taché¹

1988

Annu. Rev. Physiol.

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INTRODUCTIONThe influence of the central nervous system (eNS) on gastric secretory and motor function has been recognized for one and a half centuries, ever since William Beaumont's studies of his fistulous subject. In 1833 he reported that "fear, anger, whatever depresses or disturbs the nervous system" was accom panied by suppression of gastric secretion and by a marked delay in gastric digestion and emptying (4). A landmark in the establishment of a physiolog ical role for the brain in the regulation of gastric secretion was Pavlov's work at the beginning of this century. He discovered that sham feeding, anticipation of eating, and the sight or smell of food were powerful stimulants of hoth gastric acid and pepsin secretion in the dog (78). These studies were extended to humans in 1907 (40) and since then have been amply confinued (17). Brain pathways influencing gastric secretion were subsequently investigated via electrical stimulation or lesions of specific nuclei in various experimental animals (5, 25). More recently, advances in neurophysiological techniques, the development of sensitive anterograde and retrograde transport techniques and the discovery of a large number of peptides and their receptors in brain structures influencing gastric function have provided new tools and impetus to the investigation of the anatomical and chemical substrates mediating brain gut interactions. Further ANNUAL REVIEWS 20 TACHE This review emphasizes recent advances in the elucidation of brain sites, mechanisms of action, and possible physiological roles of neuropeptides in the regulation of gastric secretion. NEUROANATOMIC BASIS OF CNS PEPTIDERGIC CONTROL OF GASTRIC ACID SECRETION Several brain sites have been identified as involved in the control of gastric acid secretion on the basis of experiments using electrical stimulation or lesion of these areas, namely the hypothalamus (lateral, ventromedial, and paraventricular nucleus), the locus coeruleus, the amygdala (centromedial), and the dorsal vagal complex (medial dorsal motor nucleus of the vagus) (5, 45, 103). Subsequently, the introduction of sensitive anterograde and retro grade transport techniques and electrophysiological approaches has allowed the delineation of the central organization of gastric afferent and efferent pathways, particularly in the medulla, and their connections with forebrain nuclei (84, 94, 103). The bulk of sensory and motor innervation of the stomach is carried within the vagus nerve (94). Gastric vagal afferent fibers terminate predominantly within the nucleus of the solitary tract and to a lesser extent in the ventral part of the area postrema and the dorsal motor nucleus (94). Gastric efferent fibers arise mostly from cells located in the medial subnucleus of the dorsal motor nucleus of the vagus and the nucleus ambiguus (45, 94). Gastric neurons in the dorsal motor nucleus of the va � us possess an extensive plexus of dendrites that penetrates the nucleus tractus solitarius. This interconnection provides an anatomical basis for monosynap...

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Effect of ambient temperature on gastric secretion and food intake in the rat

Cited by 25 publications

References 0 publications

Inhibition of gastric acid secretion by stress: A protective reflex mediated by cerebral nitric oxide

Inhibition of gastric acid secretion by stress: A protective reflex mediated by cerebral nitric oxide

From simplicity to complexity (1950–1990): the case of peptic ulceration—II. Animal studies.

CNS Peptides and Regulation of Gastric Acid Secretion

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