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)

A number of candidate mammalian prohormone processing enzymes related to the yeast Kex2 endoprotease have been cloned and demonstrated to cleave several prohormone precursors at single, pairs and tetra basic amino acid processing sites. We have mapped the distribution of the mRNAs encoding two of these endoproteases in adult rat brain. SPC3 message levels showed a more restricted distribution and generally lower levels than SPC2 transcripts. The highest levels of SPC2 mRNA were found in the pyramidal cells of the hippocampus, several thalamic nuclei, the habenula and selected nuclei in the hypothalamus. SPC3 mRNA was most abundant in dentate gyrus granule cells, the habenula and selected hypothalamic nuclei. In the hypothalamus overlapping and unique distributions of the two transcripts were seen in the paraventricular nucleus with SPC3 mRNA predominantly expressed in lateral magnocellular cells. Both SPC2 and SPC3 mRNA were upregulated in the paraventricular and supraoptic hypothalamic nuclei following chronic salt loading. Combined immunocytochemistry/in situ hybridization histochemistry demonstrated that SPC2 and SPC3 transcripts were both expressed in the vasopressinergic subpopulation of magnocellular neurons in the supraoptic nucleus. SPC3 mRNA, but not SPC2 transcripts, also colocalized with immunoreactive vasopressin-associated neurophysin in the suprachiasmatic nucleus. These results remain consistent with roles for SPC2 and SPC3 in the biosynthesis of neuropeptides and for a specific role for SPC3 in the processing of provasopressin. Increased levels of SPC2 and SPC3 transcripts following a chronic osmotic stimulus suggests these proteases are coregulated with prohormone substrates and may be useful as an indicator of peptidergic activity.
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PMID:Distribution and regulation of the candidate prohormone processing enzymes SPC2 and SPC3 in adult rat brain. 789 39

Simultaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg) results in short-latency thirst and sodium appetite (i.e., the rapid ingestion of water and NaCl solution). To elucidate potential mechanisms for mediating this behavior, changes in plasma levels of key hormones involved in fluid intake and balance were characterized in rats subjected to this treatment protocol. Rats treated jointly with furosemide and low-dose captopril had exaggerated increases in plasma renin activity and angiotensin I but equivalent increases in plasma aldosterone compared with rats treated with either agent alone. Treatment with furosemide plus low-dose captopril increased plasma vasopressin but not plasma oxytocin. The administration of a higher dose of captopril (100 mg/kg) with furosemide, a combination of drugs that does not stimulate fluid intake (29), further increased plasma renin activity and angiotensin I but prevented the rise in plasma vasopressin. The results support the hypothesis that thirst and salt appetite generated by this protocol depend on angiotensin II formed within brain circumventricular organs rather than the systemic circulation.
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PMID:Endocrine changes associated with a rapidly developing sodium appetite in rats. 797 42

The effects of acute ethanol administration on the ingestion of NaCl and food were assessed in adult rats subjected to 1-hr drinking and feeding tests 30 min after intraperitoneal administration of ethanol. Ethanol pretreatment did not induce spontaneous NaCl ingestion, but significantly potentiated angiotensin II-stimulated salt appetite, but not water intake, in a dose-dependent manner. Similarly, ethanol pretreatment significantly potentiated neuropeptide Y-stimulated food intake in nonfasted rats, but did not, by itself, cause spontaneous food ingestion. Ethanol pretreatment also significantly blunted pituitary secretion of oxytocin in response to multiple excitatory stimuli. Finally, administration of oxytocin intracerebroventricularly prevented the ethanol-induced potentiation of salt appetite elicited by angiotensin II. In view of our previous findings that central oxytocin secretion inhibits both NaCl and food intake, we propose that ethanol potentiates the ingestion of various solutes in rats, in part, by inhibiting brain-projecting oxytocinergic pathways concurrently with its well-known effects to inhibit pituitary oxytocin secretion.
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PMID:Acute effects of ethanol on ingestive behavior in rats. 797 5

I.c.v. injection of CCK-8 (50 ng/day) to euhydrated rats significantly decreased vasopressin and oxytocin content in the hypothalamo-neurohypophysial system. In rats drinking hypertonic saline and simultaneously treated with CCK-8, the decrease of vasopressin content was more marked in hypothalamus but somewhat restrained in the neurohypophysis. The decrease of hypothalamic and neurohypophysial oxytocin content (as brought about by the salt load) was significantly less marked in animals treated simultaneously with CCK-8. Incubation of neurointermediate lobes in medium enriched with CCK-33/CCK-39 or CCK-8 did not change significantly the vasopressin and oxytocin release from the neurointermediate lobes both under basal conditions and during potassium stimulation. It is suggested that afferent impulses of osmoreceptor origin may modify the response of vasopressinergic and oxytocinergic neurons to CCK-8. The events, related to the influence of CCK peptides on vasopressin or oxytocin release, do not seem to be localized at the neurohypophysial level.
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PMID:Neurohypophysial response to peptides of the cholecystokinin family: in vivo and in vitro studies. 806 68

The arginine vasopressin (AVP) gene was sequenced in a pedigree with familial central diabetes insipidus (DI). When polymerase chain reaction-amplified DNAs from affected subjects were subjected to polyacrylamide gel electrophoresis, fragments including exon 2 displayed two additional, slower migrating bands. These extra bands represented DNA heteroduplexes, indicating that there was a deletion or insertion mutation in exon 2. As the region with such a mutation was identified by direct sequence analysis, polymerase chain reaction-amplified fragments including the region were subcloned and sequenced. A 3-basepair deletion (AGG) out of two consecutive AGG sequences (nucleotides 1824-1829) was identified in one of two alleles. The cosegregation of the mutation with the DI phenotype in the family was confirmed by restriction enzyme analyses. This mutation should yield an abnormal AVP precursor lacking Glu47 in its neurophysin-II (NP) moiety. Since Glu47 is essential for NP molecules to form a salt bridge with AVP, it is very likely that the function of NP as a carrier protein for AVP would be impaired. We suggest that AVP would undergo accelerated proteolytic degradation, and this mechanism would be involved in the pathogenesis of DI in this pedigree.
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PMID:Glu-47, which forms a salt bridge between neurophysin-II and arginine vasopressin, is deleted in patients with familial central diabetes insipidus. 837 Jun 80

Dietary NaCl deprivation stimulates a robust salt appetite in Wistar rats but has little influence on this behavior in rats of the Fischer 344 (F344) strain. To examine physiological substrates of attenuated salt appetite in F344 rats, several pertinent measures of renal function and fluid homeostasis were made in Wistar and F344 rats eating normal and NaCl-deplete diets. Physiological adjustments to NaCl deprivation were similar between the two strains; however, F344 rats showed smaller increases in plasma renin activity (PRA) than their Wistar counterparts. In addition, F344s decreased urinary sodium excretion more rapidly than Wistar rats in response to deprivation. The present studies also revealed several strain differences in baseline fluid and electrolyte regulation. Relative to the Wistar strain, F344 rats were characterized by high baseline PRA, increased arginine vasopressin (AVP) excretion, decreased urine volume, and diminished thirst. We propose that AVP and oxytocin activation may reduce salt preference and suppress the development of salt appetite in F344 rats.
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PMID:Physiological correlates of attenuated salt appetite in Fischer 344 rats. 814 Jan 78

Sodium chloride ingestion is stimulated during conditions of sodium deficiency to maintain body fluid and electrolyte balance. Recent studies have indicated that salt appetite in rats is often inversely related to peripheral and central secretion of the hormone oxytocin (OT). We studied the potential role of central OT on salt and water ingestion by treating rats intracerebroventricularly with OT conjugated to the A chain of the plant cytotoxin ricin (rAOT) to produce a chronic selective inactivation of brain cells containing OT-receptive elements. The rats treated with rAOT and control rats treated with the ricin A chain alone were given 5-hr two-bottle (water and 0.5 M NaCl) drinking tests 30 min after they were made hyperosmolar by injections of hypertonic (2M) mannitol solution, which elevated plasma osmolality but reduced plasma Na+ concentration. In the control rats only water intake was stimulated in response to the induced hyperosmolality, but in the rAOT-treated rats hypertonic mannitol caused a robust salt appetite as well as thirst. Analogous results were obtained in rats treated with two different OT-receptor antagonists prior to induction of hyperosmolality with mannitol. In contrast to these results, when hyperosmolality was induced by administration of equivalently hypertonic (1M) NaCl, which elevated both plasma osmolality and plasma Na+ concentration, only water intake but not salt intake was stimulated in both control and OT-receptor antagonist-treated rats. When salt appetite was stimulated by the physiological stimulus of polyethylene glycol-induced hypovolemia, hypertonic mannitol similarly inhibited salt ingestion in control animals but not in rAOT-treated rats, whereas hypertonic NaCl inhibited subsequent salt ingestion in both groups. These results suggest that salt appetite is regulated by both Na(+)- and osmolality-sensing mechanisms in rats. In addition, they indicate that central OT likely mediates a significant component of osmolality-related inhibition of salt appetite but does not appear to be essential for Na(+)-related inhibition of this important homeostatic behavior.
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PMID:Central oxytocin inhibition of salt appetite in rats: evidence for differential sensing of plasma sodium and osmolality. 823 2

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

The promoter regions of the rat corticotropin-releasing factor (CRF), oxytocin (OT), and vasopressin (AVP) genes contain sequences similar to the cis-acting response element identified for NGFI-B, an immediate-early gene structurally related to the steroid hormone receptor superfamily. Combined immuno- and hybridization histochemical approaches were used to determine whether challenges that influence the synthesis and secretion of CRF, OT, and/or AVP result in altered expression in neurosecretory neurons of NGFI-B and another immediate-early gene, c-fos, which is widely used as a marker for functionally activated neurons. NGFI-B mRNA was found to be expressed at constitutively high levels in the telencephalon, but not in the endocrine hypothalamus, of unperturbed controls; basal levels of c-fos expression were uniformly low throughout the CNS. NGFI-B and c-fos mRNAs, and Fos protein, were induced with a similar time course and in similar neuroendocrine cell types in response to acute hypotensive hemorrhage (15% reduction in blood volume), intravenous injection of interleukin-1 beta (IL-1 beta; 1.87 micrograms/kg), chronic salt loading (7 d maintenance on 2% saline), and acute bilateral adrenalectomy. c-fos mRNA and Fos protein were readily demonstrable in afferent pathways that have been implicated as mediating the neuroendocrine responses in the three stress paradigms; these include medullary catecholaminergic cell groups in response to IL-1 beta and hemorrhage, and cell groups lining the lamina terminalis in response to salt loading. Challenge-specific induction of NGFI-B expression was detectable in these extrahypothalamic cell groups, though with a lesser sensitivity than that required to reveal NGFI-B induction in the hypothalamus, or c-fos expression in these related afferents. These results establish NGFI-B as a useful adjunct to c-fos, for revealing synaptic and/or transcriptional activation in the magno- and parvocellular neurosecretory systems. Differences in the sensitivity of the two markers in revealing functionally related activation in extrahypothalamic regions speak to general issues concerning the use of immediate-early genes in mapping functional circuitry in the CNS.
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PMID:A comparison of two immediate-early genes, c-fos and NGFI-B, as markers for functional activation in stress-related neuroendocrine circuitry. 825 63

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


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