Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the role of alpha 2-adrenoceptors in transcriptional control in the rat brain, we localized the Fos-like immunoreactivity (Fos-LI) induced by alpha 2-adrenoceptor agonists and by an antagonist. Injections of yohimbine (5 mg/kg, i.p.) into rats led to the induction of Fos-LI in areas with a dense alpha 2-adrenoceptor binding such as the locus coeruleus, the bed nucleus of stria terminalis, the central nucleus of amygdaloid complex, the paraventricular nucleus, the nucleus tractus solitarius, and ventrolateral medulla oblongata. Clonidine (500 micrograms/kg, i.p.) suppressed the Fos expression by yohimbine in these nuclei, and clonidine (100 micrograms/kg, i.p.) or guanabenz (4 mg/kg, i.p.) induced Fos-LI in oxytocin neurons in the paraventricular and supraoptic nuclei in the hypothalamus. Thus, the alpha 2-adrenoceptor is involved in transcriptional control via Fos expression in neurons related to autonomic and other functions.
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PMID:Expression of Fos-like immunoreactivity by yohimbine and clonidine in the rat brain. 132 43

Oxytocin (OT) infusion in normal dogs increases plasma insulin and glucagon levels and increases rates of glucose production and uptake. The purpose of this study was to determine whether the effects of OT on glucose metabolism were direct or indirect. The studies were carried out in normal, unanesthetized dogs in which OT infusion was superimposed on infusion of either somatostatin, which suppresses insulin and glucagon secretion, or clonidine, which suppresses insulin secretion only. Infusion of 0.2 microgram/kg/min of somatostatin suppressed basal levels of plasma insulin and glucagon and inhibited the OT-induced rise of these hormones by about 60-80% of that seen with OT alone. The rates of glucose production and uptake by tissues, measured with [6-3H] glucose, were significantly lower than those seen with OT alone, and the rise in glucose clearance was completely inhibited. Clonidine (30 micrograms/kg, sc), given along with an insulin infusion to replace basal levels of insulin, completely prevented the OT-induced rise in plasma insulin and markedly reduced the glucose uptake seen with OT alone, but did not reduce the usual increase in plasma glucose and glucagon levels or glucose production. To determine whether the OT-induced rise in plasma insulin was in response to the concomitant increase in plasma glucose, similar plasma glucose levels were established in normal dogs by a continuous infusion of glucose and an OT infusion was superimposed. OT did not raise plasma glucose levels further, but plasma insulin levels were increased, indicating that OT can stimulate insulin secretion independently of the plasma glucose changes. Studies by others have shown that the addition of OT to pancreatic islets or intact pancreas can stimulate insulin and glucagon secretion, indicating a direct effect. Our studies agree with that and suggest that in vivo, OT raises plasma insulin levels, at least in part, through a direct action on the pancreas. These studies also show that OT increases glucose production by increasing glucagon secretion and, in addition, a direct effect of OT on glucose production is likely. The OT-induced increase in glucose uptake is mediated largely by increased insulin secretion.
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PMID:Role of insulin and glucagon in oxytocin effects on glucose metabolism. 134 36

The effect of selective alpha adrenergic agonists and antagonists on osmotic water permeability (Posm) across isolated skins of Bufo arenarum toads was investigated. Clonidine, an alpha-2 agonist, inhibited basal Posm and oxytocin, isoproterenol and theophylline stimulated Posm, but did not alter the hydrosmotic effect of exogenous cAMP. Blockade of the effect of clonidine on basal and stimulated Posm by the selective alpha-2 antagonist yohimbine supports the hypothesis that the inhibitory effect is mediated by the stimulation of alpha-2 adrenergic receptors.
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PMID:Alpha-2 adrenergic agonists inhibit basal and stimulated osmotic water permeability in toad skin. 287 50

The alpha2-adrenergic agonist clonidine and the neuropeptide oxytocin, inhibit sodium intake when injected intracerebroventricularly (i.c.v.). The present work investigates whether (1) vasopressin also inhibits sodium intake when injected i.c.v., and (2) the effect of oxytocin and of vasopressin on sodium intake is affected by i.c.v. injection of idazoxan, an alpha2-adrenergic antagonist. Clonidine (30 nmol), oxytocin (40, 80 nmol) and vasopressin (40, 80 nmol) were injected i.c.v. 20 min prior to a 1.5% NaCl appetite test, in rats depleted of sodium for 24 h by a combination of a single s.c. injection of furosemide (10 mg/rat) and removal of ambient sodium. Every dose of clonidine, oxytocin and vasopressin inhibited the 1.5% NaCl intake. Seizures were observed with the higher dose of vasopressin, but not with either dose of oxytocin. The effect of i.c.v. injection of clonidine (30 nmol), oxytocin (80 nmol) or vasopressin (40 nmol) was partially inhibited by prior i.c.v. injection of idazoxan (160, 320 nmol). The results suggest that the inhibition of 1.5% NaCl intake induced by i.c.v. injection of neuropeptides in sodium-depleted rats depends, in part, on the activation of central alpha2-adrenoceptors.
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PMID:Idazoxan and the effect of intracerebroventricular oxytocin or vasopressin on sodium intake of sodium-depleted rats. 922 97

The role of alpha-2 adrenoceptors in the milk-ejection reflex was investigated by making electrophysiological recordings from oxytocin neurones in the supraoptic nucleus of urethane-anaesthetised rats. Systemic administration of the alpha-2 adrenoceptor antagonist. Idazoxan (0.5 mg/kg, i.v.), temporarily suppressed OT cell bursting activity, while having no consistent action on basal neuronal activity. Clonidine (25 micrograms/kg, i.v.) caused an immediate increase in the frequency and amplitude of oxytocin cell bursting, coincident with a fall in basal activity. A higher dose of clonidine (50 micrograms/kg, i.v.), inhibited both bursting and basal activity. These results indicate that alpha-2 adrenoceptors are essential for the normal functioning of the milk-ejection reflex and may be involved in the facilitatory and inhibitory regulation of suckling-evoked bursting in oxytocin neurones.
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PMID:The role of alpha-2 adrenoceptors in the regulation of oxytocin neurones in the suckled rat. 929 10

Oxytocin treatment decreases blood pressure and changes the pattern of spontaneous motor activity. The aim of this study was to explore if alpha 2-adrenoreceptors that are involved in the regulation of blood pressure and spontaneous motor activity are influenced by oxytocin treatment. For this purpose, male rats were pretreated with oxytocin (1 mg/kg subcutaneously (s.c.)) or saline once a day during 5 days. Clonidine (alpha 2-adrenoreceptor agonist) decreased blood pressure (2.5 microg/kg intracerebroventricularly (i.c.v.) and 100 microg/kg s.c.) and changed spontaneous motor activity (100 microg/kg s.c.), observed in an open field arena, significantly more in oxytocin pretreated rats compared to saline pretreated controls (P < 0.05). In contrast, idazoxan (alpha 2-adrenoreceptor antagonist) (50 microg/kg i.c.v.) caused a significantly smaller elevation of blood pressure in the oxytocin pretreated rats (P < 0.05). In addition, the effect on blood pressure of an alpha 1-adrenoreceptor agonist, phenylephrine, was evaluated. It increased blood pressure equally in the oxytocin- and saline pretreated rats. The present study shows that subchronic oxytocin treatment increases the effects of clonidine on blood pressure and spontaneous motor activity in rats. These findings imply that alpha 2-adrenoreceptors are involved in the effects of oxytocin treatment on blood pressure and spontaneous motor activity.
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PMID:Oxytocin enhances the effects of clonidine on blood pressure and locomotor activity in rats. 1058 23

The aim of the present study was to clarify the cellular mechanisms underlying the alpha(2)-adrenoceptor-mediated contraction of porcine myometrium (nonvascular smooth muscle). Acetylcholine (3 nM-1 microM), clonidine (1 nM-10 microM) and 5-bromo-N-[2-imidazolin-2-yl]-6-quinoxalinamine (UK14304) (1 nM-10 microM) in Krebs solution caused a concentration-dependent contraction in the longitudinal muscles of the porcine uterus with similar EC(50) values and maximum responses. A lowered external Ca(2+) concentration and verapamil (10 nM-10 microM) decreased the contractile response to clonidine and UK14304 more markedly than the response to acetylcholine. However, in Kumagai solution, neither clonidine nor UK14304 caused contractile responses, but acetylcholine remained effective. The effects of alpha(2)-adrenoceptor agonists on intracellular Ca(2+) concentration ([Ca(2+)](i)) and smooth muscle force were measured simultaneously using fura-PE3-loaded muscle preparations. Clonidine and UK14304 caused increases in [Ca(2+)](i) and force of the longitudinal muscle. The increases in [Ca(2+)](i) and muscle force were markedly inhibited by verapamil and in Ca(2+)-free solution (EGTA, 1 mM). In the absence of external Ca(2+), clonidine caused only a small increase in [Ca(2+)](i) in Ca(2+)-loaded preparations compared with those increases caused by carbachol, histamine, and oxytocin. Ca(2+) (2.5 mM) caused increases in [Ca(2+)](i) and force of the longitudinal muscles in a Ca(2+)-free high K(+) solution. Clonidine concentration dependently potentiated the Ca(2+)-induced contraction without significantly changing the increase in [Ca(2+)](i), and this potentiation was inhibited by yohimbine. These results suggested that clonidine increases the Ca(2+) sensitivity of the contractile elements through activation of alpha(2)-adrenoceptors. During the development of the contractile response to clonidine (1 microM, 0-5 min), tissue cyclic AMP levels did not change significantly. In vitro treatment with pertussis toxin (1 microg/ml for 2 h) significantly decreased the contraction induced by clonidine without affecting the responses to carbachol and high K(+). The present results indicate that in porcine myometrium, alpha(2)-adrenoceptor stimulation caused contraction of the longitudinal muscles by mechanisms largely dependent on the influx of extracellular Ca(2+), probably through voltage-dependent Ca(2+) channels (VDCCs), and that the potentiation of the Ca(2+) sensitivity of the contractile elements is another mechanism of the contractile responses. These actions involve a pertussis-toxin-sensitive G protein (probably G(i) type) in the signal transduction pathway.
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PMID:The mechanisms of alpha(2)-adrenoceptor agonist-induced contraction in longitudinal muscle of the porcine uterus. 1070 23