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)

Simulating actual conditions of intravenous infusion, a number of routinely used additive drugs were tested for potential binding to an inline i.v. filter containing a cellulose ester membrane. Two infusion solutions, 5% dextrose and 0.9% sodium chloride, were used to deliver the drugs. Drug samples were assayed before and after passage through the filter by the following methods: bleomycin sulfate, cyanocobalamin, ergonovine maleate, mithramycin, vinblastine sulfate, and vincristine sulfate by direct spectrophotometry; oxytocin by biological assay; levarterenol by fluorescence; and folic acid, heparin, insulin, and digitoxin by radiotracer methods. Measurable reduction in potency occurred in both infusion solutions with digitoxin, insulin, mithramycin, and vincristine sulfate. No reduction in potency was observed in either infusion solution with bleomycin sulfate, cyanocobalamin, ergonovine maleate, folic acid, heparin, leverterenol bitartrate, oxytocin, and vinblastine sulfate. The study results indicate that the potency of drugs administered intravenously in small doses could be significantly reduced during inline filtration through a filter containing a cellulose ester membrane.
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PMID:Effect of inline filtration on the potency of low-dose drugs. 739 87

Rats drinking ad libitum tap water or hypertonic (i.e. 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.), for three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly decreased hypothalamic oxytocin content in both euhydrated (i.e. given tap water ad libitum) and salt-loaded rats. In rats drinking tap water, neurohypophysial oxytocin content decreased. Plasma oxytocin concentration was distinctly elevated under TRH treatment in rats euhydrated but, on the contrary, decreased in salt-loaded rats as compared with animals similarly drinking hypertonic saline but not TRH-treated. The present data suggest that TRH may be involved in some regulatory processes related to oxytocin biosynthesis and release from the rat hypothalamo-neurohypophysial system.
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PMID:Thyrotropin-releasing hormone (TRH) modifies oxytocin release from the hypothalamo-neurohypophysial system in salt-loaded rats. 767 Jan 25

Vasopressin (VP) and oxytocin (OT) are released within the hypothalamic nuclear region in response to direct microdialysis with hypertonic solutions. Experiments were performed to determine whether systemic osmotic stimulation causes changes in intranuclear peptide release within the supraoptic nucleus (SON). A hypertonic sodium chloride solution was injected intraperitoneally (i.p.) or intravenously (i.v.) and microdialysis techniques were used to simultaneously monitor central and peripheral peptide release in urethane anesthetized rats. Systemic osmotic stimuli elicited increases in intranuclear peptide release which were delayed and long-lasting, occurring over a 2.5 h period. In contrast, plasma peptide levels peaked at 30-min after the stimulus. The results demonstrate that increased plasma sodium elicits an increase in VP and OT release into the extracellular space of the hypothalamic SON. The different patterns of peptide release in plasma and brain point toward the possibility of independently regulated release into the different compartments.
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PMID:Systemic osmotic stimulation increases vasopressin and oxytocin release within the supraoptic nucleus. 798 66

Rats euhydrated and dehydrated during two or four days were given intracerebroventricularly (i.c.v.) thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. A single dose of TRH injected to euhydrated animals increased the hypothalamic vasopressin content but did not affect significantly the content of vasopressin in the neurohypophysis as well as that of oxytocin both in the hypothalamus and neurohypophysis. In rats deprived of water for two days TRH completely prevented the decrease of neurohypophysial oxytocin due to stimulation of osmoreceptor origin. Similarly, TRH restrained both the hypothalamic and the neurohypophysial vasopressin and oxytocin depletion in rats dehydrated for four days.
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PMID:Thyrotropin-releasing hormone (TRH) modulates vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in dehydrated rats. 824 30

We investigated the modulatory role of gonadal steroids on the expression of oxytocin (OT) and vasopressin (AVP) cytoplasmic mRNAs in the paraventricular nucleus and supraoptic nucleus of the osmotically stimulated rat. We chronically administered an oral salt load (2% sodium chloride solution for 5 days) to intact and gonadectomized female and male Sprague-Dawley rats and measured serum sodium, body weight, pituitary content of OT and AVP immunoreactivities, and size and abundance of hypothalamic cytoplasmic OT and AVP mRNA transcripts. Intact and gonadectomized rats that were administered an osmotic challenge developed comparable degrees of hypernatremia and loss of body weight as well as depletion of posterior pituitary stores of OT and AVP. Hyperosmolality induced elongation of the OT and AVP transcripts in intact and gonadectomized animals, but only intact rats had enhanced hypothalamic cytoplasmic OT and AVP mRNA concentrations to this stimulus. Replacement with gonadal steroids restored the up-regulation in OT and AVP gene expression in gonadectomized animals rendered hyperosmolar. The findings support a modulatory role for gonadal steroids in hypothalamic OT and AVP gene expression during osmotic stimulation.
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PMID:Gonadal steroid modulation of oxytocin and vasopressin gene expression in the hypothalamus of the osmotically stimulated rat. 824 94

Rats drinking and libitum tap water or hypertonic (i.e., 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.), during three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly increased hypothalamic oxytocin content in both euhydrated (i.e., given tap water ad libitum) and salt-loaded rats and vasopressin content only in euhydrated rats. Similarly, neurohypophysial vasopressin and oxytocin content significantly increased in animals drinking tap water or 2% sodium chloride during treatment with TRH. The present data suggest that TRH may be involved in some regulatory processes to vasopressin and oxytocin biosynthesis and release from the rat hypothalamo-neurohypophysial system.
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PMID:Influence of thyroliberin (TRH) on hypothalamo-neurohypophysial vasopressin and oxytocin content of rats drinking 2% NaCl. 830 34

In situ hybridization was used to measure the expression of members of the Fos/Jun family of immediate-early genes in hypothalamic neurons in vivo following defined stimuli that utilize different afferent pathways. Only c-jun messenger RNA was expressed in the hypothalamic supraoptic and paraventricular nuclei of control animals. Intravenous infusions of sodium chloride solutions of different tonicity produced a range of plasma osmolalities within physiological limits. While the induction of c-fos and jun B messenger RNAs followed the stimulus intensity, the expression of c-jun was repressed at low levels of stimulation. A higher level of osmotic stimulation was able to co-induce c-jun with the c-fos, jun B and fos B genes, suggesting that other signalling pathways may then be activated. Parturition or systemic administration of cholecystokinin, that activate supraoptic and paraventricular neurons via ascending afferent pathways from the brainstem, both induced c-fos, but not the other genes, in the magnocellular nuclei. Use of double in situ hybridization confirmed that, unlike with osmotic stimulation, induction of c-fos only occurred in oxytocin neurons. These two stimuli did not cause a concomitant repression of c-jun messenger RNA expression in magnocellular oxytocin neurons. These patterns of induction provide evidence for the differential regulation of members of this family of genes in a physiological context.
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PMID:Induction of members of the Fos/Jun family of immediate-early genes in identified hypothalamic neurons: in vivo evidence for differential regulation. 878 63

Osmotically stimulated vasopressin and oxytocin release were measured in pinealectomized and sham operated male rats infused with hypertonic sodium chloride. Neuronal activation in the hypothalamic regions associated with oxytocin and vasopressin release was investigated by quantitative assessment of Fos protein production. The osmotically stimulated release of both vasopressin and oxytocin was significantly lower in pinealectomized animals as compared to sham operated controls. The slope of regression lines between plasma osmolality and hormone concentrations in the sham animals showed a 1.0 +/- 0.1 pmol per mosm/kg rise in vasopressin and 2.0 +/- 0.4 pmol per mosm/kg rise in oxytocin whilst in the pinealectomized animals these values were significantly lower at 0.4 +/- 0.1 pmol vasopressin per mosm/kg and 0.8 +/- 0.2pmol oxytocin per mosm/kg. The osmotic thresholds for hormone release were unaffected by pinealectomy. Fos production was also significantly lower in the supraoptic nucleus and organ vasculosum of the lamina terminalis in the pinealectomized rat at 62 +/- 20 and 59 +/- 9 Fos immunoreactive cells/section as compared to corresponding values of 202 +/- 31 and 123 +/- 20 Fos immunoreactive cells/section in the shams. These observations suggest that reduced hormone release in the pinealectomized animal is due to lowered responsiveness of central osmoregulatory mechanisms and that melatonin may therefore influence the activation of the magnocellular system.
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PMID:The effect of pinealectomy on osmotically stimulated vasopressin and oxytocin release and Fos protein production within the hypothalamus of the rat. 891 Aug 3

Previous studies have shown that preweanling rats do not express an endogenous sodium appetite until postnatal day 12. The present studies tested the hypothesis that prior to 12 days of age sodium appetite, induced by either central administration of angiotensin II (AngII) or adrenalectomy, is inhibited by endogenous oxytocin (OT). After 9- or 10-day old animals were given a central injection of either an OT receptor antagonist or vehicle, they were infused intraorally with 4% sodium chloride which the animals could either swallow or reject. Intake was measured as the increase from initial body weight. There was very little sodium consumption by vehicle-injected animals that received sham surgery or adrenalectomy; however, the OT receptor antagonist significantly elevated sodium consumption in adrenalectomized animals. The OT antagonist also potentiated sodium intake after AngII pretreatment. These results suggest that the neurochemical circuits necessary for the expression of sodium appetite are present and functional as early as postnatal day 9; however, until 12 days of age this behavior is suppressed by endogenous OT.
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PMID:Brain oxytocin receptor antagonism disinhibits sodium appetite in preweanling rats. 911 Mar 83

In the initial experiments reviewed here, we show that atrial natriuretic peptide (ANP) plays an important inhibitory role in the control of sodium chloride and water intake since injections of ANP into the third ventricle (3V) caused a reduction in dehydration-induced drinking and also the drinking of salt in salt-depleted rats. Attention was then turned to the possible role of the brain ANP neurons in producing natriuresis which had earlier been shown to be caused by stimulations within the anterior ventral third ventricular region (AV3V). Stimulation in this region by carbachol produced natriuresis accompanied by a dramatic increase in plasma ANP concentrations and increased content of the peptide in medial basal hypothalamus (MBH), neurohypophysis (NH) and anterior pituitary gland (AP), without alterations in the content of ANP in lungs or atria. This suggested that the natriuresis resulting from the stimulation is brought about, at least in part, by the release of ANP from the brain. Conversely, there was a dramatic decline in plasma ANP at both 24 and 128 h after AV3V lesions had been placed. In view of the much larger quantities of the peptide stored in the atria, it is probable that the changes in the atrial release of the peptide were the main factors altering plasma ANP, but that there was concomitant alteration in the release of brain ANP as well. Blood volume expansion (BVE) by intraatrial injection of isotonic saline in the rat is a profound stimulus for ANP release. Lesions in the AV3V region, median eminence, or neurohypophysectomy blocked BVE-induced release of ANP indicating the crucial participation of the CNS in the response of ANP and natriuresis. Baroreceptor impulses from the carotid-aortic sinus regions and the kidney are important in the neuroendocrine control of ANP release since deafferentation of these regions lowered basal plasma ANP concentrations and prevented the increase after BVE. The evidence indicates that the ANP release, in response to BVE, is mediated by afferent baroreceptor impulses to the AV3V, which mediates the increased ANP release via activation of the hypothalamic ANP neuronal system. Our recent data support the hypothesis that BVE causes the release of ANP from ANPergic neurons in the hypothalamus that in turn stimulates release of oxytocin from the neurohypophysis. This oxytocin acts to release ANP from the right atrium that has negative chrono- and inotropic effects in the right atrium to reduce cardiac output, thereby reducing effective circulating blood volume. Then, the released ANP circulates to the kidneys and evokes natriuresis to return circulating blood volume to normal. This is further accomplished by reduction in intake of water and salt mediated also by brain ANP.
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PMID:The neuroendocrine control of atrial natriuretic peptide release. 932 24


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