Involvement of cholecystokinin receptor in the inhibition of gastric emptying by oxytocin in male rats

Wu, Chiu-Lung; Hung, Chen‐Road; Chang, Full‐Young; Pau, Francis K.-Y.; Wang, Jui-Ling; Wang, Paulus S.

doi:10.1007/s00424-002-0925-7

Cited by 38 publications

(55 citation statements)

References 53 publications

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“…The dose of devazepide chosen in the present study blocked the inhibitory actions of exogenously administered CCK-8 on splanchnic sympathetic nerve activity and CCK-sensitive RVLM neurons (39; present study). Furthermore, many investigators have demonstrated that similar doses of devazepide are capable of reversing the effects of endogenously released CCK on pancreatic enzyme secretion (23,33,34), vagal afferent nerve discharge (7,11,18), gastric emptying (51), and food intake (37), suggesting that the dose chosen in our study is likely to have been adequate.…”

Section: Discussionmentioning

confidence: 78%

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Sartor¹,

Shulkes²,

Verberne³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Sartor, Daniela M., Arthur Shulkes, and Anthony J. M. Verberne. An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats. Am J Physiol Regul Integr Comp Physiol 290: R625-R633, 2006. First published October 20, 2005 doi:10.1152/ajpregu.00639.2005.-Ingestion of a meal results in gastrointestinal (GI) hyperemia and is associated with systemic and paracrine release of a number of peptide hormones, including cholecystokinin (CCK) and 5-hydroxytryptamine (5-HT). Systemic administration of CCK octapeptide inhibits a subset of presympathetic neurons of the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor tone to the GI viscera. The aim of this study was to determine whether endogenous release of CCK and/or 5-HT also inhibits CCK-sensitive RVLM neurons. The effects of intraduodenal administration of the secretagogues sodium oleate (SO) and soybean trypsin inhibitor (SBTI) on circulating levels of CCK and 5-HT were examined. In separate experiments, the discharge rates of barosensitive, medullospinal, CCK-sensitive RVLM presympathetic vasomotor neurons were recorded after rapid intraduodenal infusion of SO-SBTI or water. Alternatively, animals were pretreated with the CCK 1 receptor antagonists devazepide and lorglumide or the 5-HT 3 antagonist MDL-72222 before SO-SBTI administration. Secretagogue infusion significantly increased the level of circulating CCK, but not 5-HT. SO-SBTI significantly decreased (58%) the neuronal firing rate of CCKsensitive RVLM neurons compared with water (5%). CCK 1 receptor antagonists did not reverse SO-SBTI-induced neuronal inhibition (58%), whereas the 5-HT 3 antagonist significantly attenuated the effect (22%). This study demonstrates a functional relation between a subset of RVLM presympathetic vasomotor neurons and meal-related signals arising from the GI tract. It is likely that endogenously released 5-HT acts in a paracrine fashion on GI 5-HT 3 receptors to initiate reflex inhibition of these neurons, resulting in GI vasodilatation by withdrawal of sympathetic tone. rostroventrolateral medulla; cholecystokinin; devazepide; MDL-72222; 5-hydroxytryptamine GASTROINTESTINAL HYPEREMIA is a physiological consequence of food consumption. Gastrointestinal hormones such as cholecystokinin (CCK) have been implicated in gastrointestinal vasodilatation associated with postprandial increase in splanchnic blood flow. The involvement of the sympathetic vasomotor system in this response is poorly understood. We recently suggested that food-related signals may produce gastrointestinal vasodilatation via a reflex withdrawal of sympathetic vasomotor outflow (39,45). In healthy individuals, the sympathetic nervous system compensates for postprandial splanchnic blood pooling by activating sympathetic vasoconstrictor drive to skeletal muscle resistance vessels in response to baroreceptor unloading. In patients with cardiovascular disease associated with diabetic neuropathy or autonomic dysfunction, poor baroreflex comp...

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Section: Discussionmentioning

confidence: 78%

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Sartor¹,

Shulkes²,

Verberne³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In adipose tissue, for instance, OT stimulates in vitro synthesis of protein and glycogen and facilitates lipogenesis but suppresses lipolysis (Mirsky and Perisutti, 1961;Krahl, 1964;Muchmore et al, 1981). Furthermore, peripheral OT may favor satiety by stimulating CCK release (Wu et al, 2002) and by potentiating glucose-induced insulin secretion in vitro and in vivo (Altszuler and Hampshire, 1981;Knudtzon, 1983;Gao et al, 1991;VanderWeele, 1994). It is likely, therefore, that the combination of high GC levels with concomitant low levels of leptin during fasting favors the release of endocannabinoids in the PVN, reducing the excitation of both parvocellular and magnocellular OT neurons in response to inputs triggered by satiety factors, such as CCK.…”

Section: Discussionmentioning

confidence: 99%

Opposing Crosstalk between Leptin and Glucocorticoids Rapidly Modulates Synaptic Excitation via Endocannabinoid Release

Malcher‐Lopes

Shi

Marcheselli

et al. 2006

Journal of Neuroscience

250

179

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The hypothalamic paraventricular nucleus (PVN) integrates preautonomic and neuroendocrine control of energy homeostasis, fluid balance, and the stress response. We recently demonstrated that glucocorticoids act via a membrane receptor to rapidly cause endocannabinoid-mediated suppression of synaptic excitation in PVN neurosecretory neurons. Leptin, a major signal of nutritional state, suppresses CB 1 cannabinoid receptor-dependent hyperphagia (increased appetite) in fasting animals by reducing hypothalamic levels of endocannabinoids. Here we show that glucocorticoids stimulate endocannabinoid biosynthesis and release via a G␣ s -cAMPprotein kinase A-dependent mechanism and that leptin blocks glucocorticoid-induced endocannabinoid biosynthesis and suppression of excitation in the PVN via a phosphodiesterase-3B-mediated reduction in intracellular cAMP levels. We demonstrate this rapid hormonal interaction in both PVN magnocellular and parvocellular neurosecretory cells. Leptin blockade of the glucocorticoid-induced, endocannabinoid-mediated suppression of excitation was absent in leptin receptor-deficient obese Zucker rats. Our findings reveal a novel hormonal crosstalk that rapidly modulates synaptic excitation via endocannabinoid release in the hypothalamus and that provides a nutritional state-sensitive mechanism to integrate the neuroendocrine regulation of energy homeostasis, fluid balance, and the stress response.

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“…In recent years, more evidence has indicated that OT may play a role in regulation of the gastrointestinal (GI) functions such as motility, sensation (13,18), and immune response to inflammation (4,10). Exogenous OT influences the GI motility, although the reports are diverse because of the differences of species, methods, and area of the gut (18,24). It has been suggested that the effect of OT on GI motility might be physiological.…”

mentioning

confidence: 99%

Estradiol upregulates the expression of oxytocin receptor in colon in rats

Feng

Qin²,

Wang³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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The study was designed to investigate the effect of estradiol on the excitatory effect of oxytocin (OT) on colon motility. Female Wistar rats were used, and some of them were ovariectomized (OVX) and treated with vehicle or estradiol (E2). A plastic balloon made of condom was inserted into colon to monitor the change of colonic pressure in vivo. Longitudinal muscle strips of distal colon were prepared to monitor the spontaneous contraction of colon in vitro. Expression of OT receptor (OTR) was investigated by Western blot analysis. Expression of OTR mRNA was detected by RT-PCR. Immunohistochemistry was used to locate OTR. In OVX rats, pretreatment of E2 (4 -100 g/kg sc) dose-dependently increased the excitatory effect of OT on colon motility both in vivo and in vitro and increased the expression of OTR and OTR mRNA in colon. Systemic administration of OT excited the colon motility in vivo in rats at perioda of proestrus and estrus but did not influence it at diestrus period, when the concentration of plasma E2 was lowest in the estrous cycle. Pretreatment of atosiban, the specific OTR antagonist, and TTX, the blocker of voltage-dependent sodium channel on nerve fiber, attenuated the excitatory effect of OT on colon motility. OTR was located in myenteric plexus of colon. These results suggested that E2 increased the excitatory effect of OT on colon motility by upregulating the expression of OTR in myenteric plexus.colon; motility OXYTOCIN (OT) has been traditionally regarded as a hormone that is involved in parturition and milk ejection. In recent years, more evidence has indicated that OT may play a role in regulation of the gastrointestinal (GI) functions such as motility, sensation (13, 18), and immune response to inflammation (4, 10). Exogenous OT influences the GI motility, although the reports are diverse because of the differences of species, methods, and area of the gut (18, 24). It has been suggested that the effect of OT on GI motility might be physiological. OT is released in response to a fatty meal in women (16). Systemic administration of atosiban, the antagonist of OT receptor (OTR), inhibited the spontaneous contraction of gallbladder in rabbits (12) and gastric emptying in humans (16). It has been well established that mRNA for OT and its receptor can be found throughout the human GI tract (15), but the cell types that express OTR were undetectable in human gut by indirect immunofluorescence (19).In women, colonic dysmotility is very common, and bowel function changes during the reproductive cycle. Although the fluctuation of steroid hormones, especially estradiol (E 2 ) and progesterone, were believed to be the major reason, the mechanism has not been clearly illustrated. Steroid hormones regulate the activity of OTR via both genomic and nongenomic pathways (26). E 2 induced the mRNA expression of the OTR and increased the OTR density on the membranes of the uterine smooth muscle and central nervous system (8, 21). The recent study of our group also indicated that the pretreatment of E 2 increas...

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Involvement of cholecystokinin receptor in the inhibition of gastric emptying by oxytocin in male rats

Cited by 38 publications

References 53 publications

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Opposing Crosstalk between Leptin and Glucocorticoids Rapidly Modulates Synaptic Excitation via Endocannabinoid Release

Estradiol upregulates the expression of oxytocin receptor in colon in rats

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