Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In several models of salt appetite in the rat, stimulated NaCl intake can be severely blunted by treatments associated with pituitary release of oxytocin (OT). Central administration of the potent dipsogen angiotensin II (ANG II) is known to elicit a limited salt appetite as well as thirst, but it has also been reported to stimulate pituitary OT secretion. These results suggest the possibility that the expression of ANG II-induced salt appetite in rats may be inhibited by a simultaneous central release of OT in response to this stimulus. To investigate this possibility, rats were given intracerebroventricular injections of OT-receptor antagonists before administration of 5 ng ANG II intracerebroventricularly in a 1-h two-bottle (water and 0.3 M NaCl) drinking test. This pretreatment resulted in a three- to fourfold potentiation of ANG II-induced saline ingestion, which was most prominent during the first 15 min of the test. OT-receptor antagonism did not, however, interfere with the dipsogenic properties of ANG II, nor did it stimulate saline ingestion alone in the absence of ANG II. Immunocytochemical studies demonstrated that central administration of ANG II at this dose caused pronounced c-fos expression in hypothalamic magnocellular OT and vasopressin neurons and also in OT neurons in parvocellular subdivisions of the paraventricular nucleus. These results therefore demonstrate that central administration of small doses of ANG II activates both magnocellular and parvocellular OT neurons in rats and indicate that some of the activated central OT pathway(s) may mediate an inhibitory effect that limits the salt ingestion induced by this treatment.
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PMID:Central oxytocin inhibition of angiotensin-induced salt appetite in rats. 133 19

The magnocellular vasopressin system of the rat has been studied intensively in recent years. This review outlines the electrophysiological characteristics of vasopressin neurons, the characteristics of stimulus-secretion coupling in the neural lobe, and describes some of the major features of the neural regulation of this system which underlie physiological regulation of vasopressin release by osmoregulatory stimuli. The major afferent pathways to the magnocellular system are now well characterised. Those involved in osmoregulation have been mapped using expression of the primary response gene c-fos as a marker for neuronal activation.
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PMID:Mechanisms of vasopressin secretion. 139 74

Immunoreactivity to Fos protein (Fos-IR) was detected in rat hypothalamic neurons within 1 h of onset of hemorrhage by withdrawing 4-5 ml of blood, which lowered the arterial blood pressure to 50-70 mm Hg. About 70% of vasopressin (AVP)-containing neurons in the supraoptic nucleus (SON) and 20% in the paraventricular nucleus (PVN) expressed Fos-IR. In contrast, 5% of oxytocin (OXY)-containing neurons in the SON and < 1% in PVN were Fos-IR. Intravenous infusion of the vasodilating agent, nitroprusside, which lowered the blood pressure to levels comparable to that attained by hemorrhage, induced Fos-IR in greater than 65% of AVP-containing neurons in the SON, while relatively few AVP neurons in the PVN were Fos positive. These results suggest that hemorrhage or hypotension preferentially induces c-fos expression in supraoptic AVP-containing neurons.
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PMID:Hypotension preferentially induces c-fos immunoreactivity in supraoptic vasopressin neurons. 145 16

The expression of c-fos protein was examined in the basal forebrains of male rats 60 min following intracerebroventricular infusions of 250 pmol angiotensin II. Levels of corticosterone and vasopressin were also measured at the same time point. In animals not allowed access to water after infusion, angiotensin II induced intense c-fos expression in a band of neurons extending throughout the anterior region of the third ventricle region, including the organum vasculosum of the lamina terminalis, the median preoptic nucleus (nucleus medianus) and the subfornical organ. There were also high levels of expression in the hypothalamic supraoptic nucleus and the paraventricular nucleus, particularly its lateral (magnocellular) region, though other, parvicellular areas were also affected. No other area of the hypothalamus was altered. There was increased c-fos expression in the central nucleus of the amygdala and the bed nucleus of the stria terminalis. Allowing rats to drink during the 60-min survival period modified this pattern of response. c-fos was markedly reduced in the supraoptic nucleus and the paraventricular nucleus but not in the other areas examined, including the anterior region of the third ventricle and the amygdala. When water was withheld for 15 min, but then allowed, rats drank the same total volume but c-fos expression was no longer inhibited in either the supraoptic nucleus or paraventricular nucleus. When rats were given 0.9% saline to drink, they ingested about three times as much as water, but angiotensin II-induced c-fos expression was similar to that in rats denied access to water. The pattern was similar following access to 1.8% saline, though levels in the organum vasculosum of the lamina terminalis were reduced. There was a marked correlation between the number of c-fos-positive neurons in the supraoptic nucleus or paraventricular nucleus and plasma levels of corticosterone 60 min after infusion, but not with arginine-vasopressin levels. These experiments show that angiotensin II induces highly localized expression of c-fos in areas known to be concerned with the dipsogenic and endocrine actions of this peptide, and that this pattern is selectively altered by allowing the animal to drink solutions of different tonicity. Immediate-early gene expression is a novel and valuable method of determining the neural response to peptides at the cellular level.
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PMID:Regional expression of c-fos antigen in the basal forebrain following intraventricular infusions of angiotensin and its modulation by drinking either water or saline. 148 27

Water deprivation induces the production of the transcription factor Fos in neurons of the neurohypophysial system. These neurons, which are located primarily in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON), produce the antidiuretic hormone vasopressin. The present immunocytochemical study has analyzed the distribution of Fos in brain regions involved in osmoregulation and compared the extent of Fos immunoreactivity (Fos-IR) in vasopressin-deficient Brattleboro and normal Long-Evans rats under stimulated and non-stimulated conditions. Rats were osmotically challenged by means of a single intraperitoneal injection of 1.5 M/L NaCl. Since Fos may be induced by the stress of handling of animals, non-injected and isotonic saline-injected rats were used as controls. Faint nuclear Fos immunostaining was found in the organum vasculosum of the lamina terminalis (OVLT), the median preoptic nucleus (MnPO), subfornical organ (SFO), and SON of non-injected and isotonic saline-injected Brattleboro but not Long-Evans rats. Hypertonic saline injection specifically induced Fos-IR in neurons located in the SFO, OVLT, MnPO, PVN, SON, hypothalamic accessory nuclei (including the nucleus circularis), and arcuate hypothalamic nucleus (Arc) in both Long Evans and Brattleboro rats. No differences in distribution of the induced immunostaining were found between the strains. Stress of handling and (isotonic saline) injection induced Fos-IR in the lateral septal nuclei, central amygdaloid nuclei, medial amygdaloid nucleus, medial preoptic area, the bed nucleus of the stria terminalis, cingulate- and piriform cortex, the lateral hypothalamic area, ventromedial hypothalamic nucleus, and the habenular nucleus. The data are consistent with a role for Fos in the regulation of vasopressin gene expression during acute hyperosmotic stimulation. In addition, this study demonstrated that during chronic osmotic stimulation, as experienced by homozygous Brattleboro rats, Fos-IR is limited but apparently present constantly and that it increased in these animals following acute osmotic challenge. Our observations suggest that c-fos regulatory controls in homozygous Brattleboro rats are different from those in Long-Evans rats.
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PMID:Fos-like immunoreactivity in the brain of homozygous diabetes insipidus Brattleboro and normal Long-Evans rats. 151 86

In isolated rat hepatocytes PMA, angiotensin II and to a lesser extent other hormones induce an early genetic response (increased expression of c-fos, c-mos, c-myc and beta-actin) without altering the expression of the glyceraldehyde 3-phosphate dehydrogenase gene. PMA, PDB and O-met-PMA, but not alpha-phorbol, stimulated c-fos expression. The effect of angiotensin II was inhibited by the AT1 antagonist, Losartan (DuP 753) (Ki approx. 25 nM), but not by the AT2 antagonist PD123177. Angiotensin II was much more effective than vasopressin or epinephrine in inducing proto-oncogene expression which suggests that angiotensin II receptors may exert actions in addition to those shared with the receptors for the other calcium-mobilizing hormones. The effect of PMA and angiotensin II on c-fos expression took place rapidly, with half times of 7 and 12 min, respectively. Actinomycin D markedly diminished basal c-fos expression whereas cycloheximide had the opposite effect. Actinomycin D diminished the effect of PMA and angiotensin II but it did not block them. PMA and the calcium-mobilizing hormones increased c-fos expression above the level observed with cycloheximide alone. These data suggest that PMA and the calcium-mobilizing hormones increased both transcription of the c-fos gene and stabilization of the proto-oncogene mRNA.
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PMID:Angiotensin II and active phorbol esters induce proto-oncogene expression in isolated rat hepatocytes. 152 Jul 5

Conscious rats were given an intraperitoneal (i.p.) injection of isotonic or hypertonic saline, and killed 10-240 min later. In the hypothalamus of hypertonic saline-injected rats, c-fos-mRNA positive cells were mainly restricted to the supraoptic and paraventricular nuclei and to structures associated with the lamina terminalis of the third ventricle, including in particular the subfornical organ, the organum vasculosum of the lamina terminalis (OVLT) and the median preoptic nucleus. These structures comprise the proposed anterior hypothalamic 'osmoreceptor complex' for regulation of vasopressin release. The time course of the appearance and disappearance of c-fos mRNA signals was similar in all regions. Thus c-fos protein (Fos) may be a common transcription factor in the hypothalamic neural circuits involved in osmoregulation.
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PMID:c-fos may code for a common transcription factor within the hypothalamic neural circuits involved in osmoregulation. 161 36

Prolonged treatment of quiescent Swiss 3T3 cells with vasopressin induced heterologous desensitization of specific early signals stimulated by platelet-derived growth factor (PDGF). PDGF caused a striking dose-dependent release of [3H]arachidonic acid (EC50 = 2 ng/ml) and prostaglandin E2 (EC50 = 5 ng/ml). These responses are severely attenuated (greater than 85%) by prior exposure to vasopressin in a dose-dependent manner (IC50 = 1.5 nM). Maximal loss of responsiveness occurred after 40 h of vasopressin treatment with a half-maximal desensitization after 11-13 h. The desensitization is dependent upon binding to the V1 receptor, since it can be prevented by the antagonist [Pmp1,O-Me-Tyr2,Arg8]vasopressin. In contrast, stimulation of inositol phosphate accumulation and production of diacylglycerol and phosphatidic acid by PDGF are unchanged. Thus, the observed heterologous desensitization cannot be attributed to an inability to activate phospholipase C. Furthermore, prior exposure to vasopressin did not affect the ability of PDGF to evoke tyrosine phosphorylation of cellular substrates, demonstrating that vasopressin-induced heterologous desensitization causes a block at a point distal to activation of receptor tyrosine kinase activity. Other downstream responses including transient induction of c-fos expression and stimulation of DNA synthesis were attenuated by vasopressin pretreatment. The findings demonstrate a novel mechanism of heterologous cellular desensitization namely, persistent occupancy of a guanine nucleotide-binding protein-coupled receptor, like the V1 type vasopressin receptor, attenuates responsiveness to a polypeptide growth factor like PDGF that initiates responses through a tyrosine kinase receptor.
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PMID:Heterologous desensitization of platelet-derived growth factor-mediated arachidonic acid release and prostaglandin synthesis. 163 51

Using immunofluorescence histochemistry, the paraventricular and supraoptic hypothalamic nuclei of normal control and hypophysectomized rats were studied in double labelling experiments with antibodies against the protein c-fos (Fos) and against vasopressin or oxytocin in order to characterize the activated neurons chemically. Normal controls showed no expression of Fos, whereas in hypophysectomized animals an intense induction of Fos-like immunoreactivity (-LI) was observed 12 h and 24 h post hypophysectomy but not beyond this survival time. Both vasopressinergic and oxytocinergic magnocellular neurons were labelled with Fos-LI. Thus Fos-LI can be induced in magnocellular hypothalamic neurons by injury, suggesting that this protein may be involved in adaptive mechanisms following axotomy.
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PMID:Transient induction of c-fos in rat magnocellular hypothalamic neurons after hypophysectomy. 181 Apr 61

1. The expression of c-fos mRNA in the rat hypothalamus was examined by in situ hybridization following systemic administration of cholecystokinin (CCK), a procedure known to activate magnocellular oxytocin neurons but not magnocellular vasopressin neurones. 2. Conscious male rats were given a single I.P. injection of 50 micrograms/kg CCK, c-fos mRNA signal was apparent in the supraoptic and paraventricular nuclei in rats killed 10 min after injection but not in uninjected or saline-(vehicle) injected rats. The density of c-fos mRNA at both sites was further elevated in rats killed 30 min or 60 min following injection, and was absent in rats killed 4 h after injection. 3. In the paraventricular nucleus the most dense expression of c-fos mRNA following CCK administration was in the medial, mainly parvocellular portion of the nucleus, in an area corresponding to the distribution of corticotrophin-releasing factor mRNA determined by in situ hybridization in adjacent sections. 4. The I.P. injection of CCK increased plasma oxytocin concentrations, measured by specific radioimmunoassay from 13 +/- 5 pg/ml in control rats to 107 +/- 9 pg/ml in the rats killed 10 min after injection, a similar response to that observed previously in urethane-anaesthetized rats. 5. In each of six urethane-anaesthetized rats, recordings were made from single neurones in the supraoptic nucleus, identified antidronomically as projecting to the posterior pituitary and identified electrophysiologically as putative oxytocin neurones. Following I.P. injection of 50 micrograms/kg CCK, the neurones increased their firing rate by a mean of 1.3 +/- 0.2 spikes/s averaged over the 10 min following injection. 6. From the appearance of c-fos mRNA in supraoptic neurones following CCK administration we conclude that this message is expressed in magnocellular oxytocin neurones, since vasopressin neuronal activity and vasopressin release is known to be unaffected by this stimulus, and since the supraoptic nucleus contains essentially only oxytocin neurones and vasopressin neurones. 7. We conclude that c-fos mRNA expression can be induced in supraoptic oxytocin neurones following brief and modest episodes of electrical activation, suggesting that c-fos may be involved in the gene regulation of these neurones under physiological conditions.
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PMID:Electrical activation and c-fos mRNA expression in rat neurosecretory neurones after systemic administration of cholecystokinin. 182 61


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