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)

The hypothalamus receives neuronal afferents from numerous sources including inputs from limbic structures, such as the amygdala and hippocampus, and from brainstem regions involved in the regulation of the cardiovascular system and other autonomic functions. These afferents using a vast array of neurotransmitters and neuropeptides influence the activity of the hypothalamic neurons which synthesize and secrete the hypothalamic releasing and release-inhibiting factors into the hypophyseal portal circulatory system. The afferents can modulate the activity of the hypothalamic neurons by forming synapses on the neuronal cell body, on the nerve terminals in the median eminence or both. The chemicals most frequently used as neurotransmitters are the biogenic amines, including the catecholamines (norepinephrine, dopamine and epinephrine), serotonin, acetylcholine and gamma-aminobutyric acid (GABA). The stimulatory influence of norepinephrine, serotonin, and acetylcholine on the secretion of corticotropin (ACTH) in rodents and man will be discussed, whereas GABA exerts an inhibitory effect on the secretion of ACTH in both man and rodents. These effects appear to be mediated by changes in the secretion of the corticotropin-releasing hormone (CRH) and vasopressin into the hypophyseal portal circulation. Numerous neuropeptides appear to alter the secretion of ACTH in the rat. We will discuss the stimulatory actions of neuropeptide Y (NPY), angiotensin II, and peptides of immune cell origin on the secretion of ACTH and CRH. The opioid peptides inhibit the secretion of CRH into the portal blood, however, they exert a potent stimulatory effect on prolactin secretion in the rat and man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pituitary gland: neuropeptides, neurotransmitters and growth factors. 257 Nov 83

Neurophysins have been considered to be physiologically inert carrier proteins for the neurohypophysial hormones, oxytocin and vasopressin. We have observed that bovine neurophysin-II indirectly stimulates prolactin release in estradiol-primed male rats. The release of prolactin is regulated by a dual hypothalamic control system, the prolactin-release-inhibiting factor and the prolactin-releasing factor. We have tried to clarify whether neurophysin-II is acting through stimulation of prolactin-releasing factor by eliminating the possibility of dopaminergic prolactin release-inhibiting factor release. Male rats were primed with estradiol and functional dopaminergic prolactin release-inhibiting factor receptors were completely blocked by pretreatment with a large dose of pimozide (3 mg/kg), a dopaminergic receptor blocking agent. The neurophysin-II stimulated prolactin release in the rats which did not have any functional dopaminergic prolactin release-inhibiting factor receptors suggesting that neurophysin-II likely initiates a chain of events which eventually stimulates prolactin-releasing factor release since the possibility of involvement of the dopaminergic prolactin release-inhibiting factor system is eliminated. Opioids are known to be one of a chain of events which transmit external stress into a stimulation of prolactin release. Naloxone, a mu-receptor antagonist, was injected 20 min before neurophysin-II administration into rats which were primed with estradiol and pretreated with pimozide (3 mg/kg), but the naloxone administration did not block the prolactin release stimulated by neurophysin-II injection. This result indicates that opioids are not one of the chain of events between initiation of stimulation by neurophysin-II and prolactin release.
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PMID:Bovine neurophysin-II stimulates prolactin release without involvement of dopaminergic prolactin-release inhibiting factor receptor in the estradiol-primed male rat. 257 26

It has been clearly demonstrated that chlordecone exerts estrogen-like effects on the reproductive system. However, the extent to which the estrogenic activity of this neurotoxicant may contribute to its central nervous system effects is not clear. The purpose of this study was to compare the estrogenic activity of chlordecone and estrogen on the rat hypothalamo-pituitary axis (HPA) by using the pituitary enkephalin system as a model. It was found that the enkephalin system of the anterior pituitary is regulated by circulating estrogen. Ovariectomy caused an increase in the pituitary content of enkephalin and this increase was prevented by estrogen treatment. Administration of estrogen reduced the pituitary content of this peptide in intact male rats. Similarly, chlordecone treatment reduced the pituitary content of enkephalin in a manner identical to that of estrogen. A single injection of chlordecone (75 mg/kg; i.p.) caused a delayed decrease in the enkephalin level of the anterior lobe (but not the posterior lobe) of the pituitary. This effect of chlordecone was selective to male rats since the pituitary enkephalin level of females was not altered by such treatment. Levels of other pituitary hormones such as beta-endorphin, vasopressin, etc., were not decreased. Further studies revealed that the similarities between chlordecone and estrogen could be extended to other pituitary hormones. For example, implantation of estrogen or of chlordecone in ovariectomized rats caused similar changes in serum prolactin and luteinizing hormone levels. Thus, this study demonstrates a clear estrogen-like action of chlordecone on the HPA. Moreover, due to the similarity of both estrogen and chlordecone to anti-dopaminergic agents in altering [Met5]-enkephalin levels in both the pituitary and caudate nucleus it is speculated that a dopaminergic mechanism is responsible for their actions on the enkephalin system.
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PMID:Effects of chlordecone administration on brain and pituitary peptide systems. 258 Nov 93

Two genes each encoding a distinct precursor protein to the hormone isotocin and a neurophysin-related protein are present in the teleost fish Catostomus commersoni. These precursors are referred to as isotocin 1 and 2. As shown by the polymerase chain reaction technique, both genes lack introns in their protein-coding sequences. Both genes are transcribed giving rise to mRNAs of 920 (isotocin 1) and 1020 (isotocin 2) bases, respectively. Based on the nucleotide sequences, the predicted isotocin precursors contain, besides the hormone moiety, a neurophysin-like protein that, in contrast to its mammalian counterpart, is extended at its C-terminus by a peptide which includes a leucine-rich core segment. This segment shows similarities to the copeptin of the mammalian vasopressin precursor that is known to possess prolactin-releasing activity. The data imply that the mammalian copeptin sequence was initially part of a larger ancestral neurophysin molecule.
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PMID:Two isotocin genes are present in the white sucker Catostomus commersoni both lacking introns in their protein coding regions. 258 84

Suckling stimulus did not induce significant release of prolactin (PRL) in lactating homozygous Brattleboro rats, whereas it did it in heterozygous animals. Daily treatment of homozygous rats with vasopressin partly restored the PRL response to suckling. Findings suggest that vasopressin-neurophysin-glycopeptide precursor missing in homozygous Brattleboro rats may play a role in suckling-induced PRL release.
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PMID:Lack of the suckling-induced prolactin release in homozygous Brattleboro rats: the vasopressin-neurophysin-glycopeptide precursor may play a role in prolactin release. 259 13

In connection with measurement of the binding of growth hormone and prolactin to rat hepatocytes we investigated whether such binding is associated with changes in the cytoplasmic Ca2+ concentration. Whereas hepatocytes from male animals were found to have essentially only somatogenic receptors, lactogenic receptors were dominant in females. All hepatocyte preparations responded to epinephrine and vasopressin with transient peaks of cytoplasmic Ca2+. However, no effects on cytoplasmic Ca2+ were obtained when cells from female or male animals were exposed to growth hormone or prolactin. We therefore conclude that signal transduction of the growth hormone and prolactin responses in the rat liver does not involve an early messenger function for Ca2+.
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PMID:The actions of growth hormone and prolactin on rat hepatocytes are not mediated by changes in cytoplasmic Ca2+. 260 72

As is obvious from the previous discussions, obesity is associated with a wide variety of changes in endocrine parameters (Table 1). Some of these changes, such as the reduction in SHBG without change in serum free testosterone levels, reflect merely laboratory abnormalities that may influence interpretation of diagnostic tests but have no important physiologic relevance. Other abnormalities have major clinical impact, such as hyperestrogenemia-endometrial carcinoma and hyperlipidemia-coronary artery disease. In some cases, endocrine changes in obesity are beneficial--that is, hyperestrogenemia leading to lower incidence of osteoporosis. In other cases, such as the profound suppression of growth hormone output in obesity, the physiologic relevance is unknown. Several endocrine changes in obesity, such as the impaired response of many hormones (growth hormone, prolactin, vasopressin, corticotropin) to insulin-induced hypoglycemia and elevated endorphin levels, suggest hypothalamic dysfunction. Furthermore, the failure of all of these abnormalities to be normalized after weight reduction raises the possibility of an underlying disorder leading to both endocrine dysfunction and obesity, rather than the endocrine dysfunction being simply a consequence of the obesity. Successful elucidation of the pathogenesis of obesity, which might then lead to much needed specific treatment modalities, may be advanced if we can solve some of these puzzles.
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PMID:Endocrine aspects of obesity. 264 1

Over many years a large number of studies have demonstrated that nicotine and exposure to cigarette smoke produce marked neuroendocrine changes in animals and in man. The initial effects of nicotine are characterized by a marked hypersecretion of ACTH, vasopressin, beta-endorphin, prolactin and LH. Many of these very acute stimulatory effects of nicotine rapidly disappear, probably due to a desensitization of the central nicotinic cholinergic receptors involved. Instead, upon acute intermittent treatment with nicotine or exposure to cigarette smoke, an inhibition of prolactin, LH and TSH secretion occurs, which is associated with maintained hypersecretion of corticosterone. These effects are probably mediated via activation of central cholinergic receptors of the ganglionic type. Evidence indicates that the inhibitory effects of nicotine on LH and prolactin secretion are produced via an activation by these nicotinic receptors of the tubero-infundibular dopamine neurons, releasing dopamine as a prolactin inhibitory factor. Dopamine inhibits LHRH release via an axonic interaction involving D1-like dopamine receptors in the median eminence. It therefore seems possible that the reduced fertility found in heavy smokers may be counteracted by D1 receptor antagonists. The symptoms associated with glucocorticoid hypersecretion induced by nicotine is discussed considering not only the peripheral side effects but also permanent deficits in hippocampal glucocorticoid receptors and loss of hippocampal neurons. In view of the important influence of hormones on immune functions, it seems likely that smoking will cause disturbances in immune responsiveness. Finally, the nicotine-induced alterations of neuroendocrine function, especially in the pituitary-adrenal axis and in vasopressin release, may also lead to behavioural consequences in smokers, especially in the withdrawal phase.
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PMID:Neuroendocrine actions of nicotine and of exposure to cigarette smoke: medical implications. 266 Jan 82

The endocrine and neurochemical actions of cocaine in human and animal studies are reviewed. In humans, cocaine has been shown to influence plasma prolactin and growth hormone, as well as the dexamethasone suppression of cortisol and the thyroid-stimulating hormone response to thyroid-releasing hormone. In rats, cocaine affects plasma prolactin, luteinizing hormone, and testosterone, and can lead to adrenocortical hypertrophy. Behavioral sensitization to cocaine in rats has been shown to be related to the gender of the animals and appears to be modulated by vasopressin. A review of the neurochemical actions of cocaine indicates the important role of dopamine systems in the euphoric effects of the drug, as well as its withdrawal symptoms. Cocaine is a potent dopamine uptake inhibitor, as shown by its competition with [3H]GBR-12935 (a specific ligand for the dopamine uptake sites) for striatum binding sites. However, it does not acutely affect the high-affinity agonist sites of the D-2 dopamine receptors, which are suggested to be the active form of the presynaptic receptor. Using microdialysis techniques, cocaine is shown to rapidly cause a large increase of rat striatal dopamine levels, while its metabolites dihydroxyphenylacetic acid and homovanillic acid are slightly decreased and increased, respectively.
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PMID:Endocrine and neurochemical actions of cocaine. 268 66

This review examines the role of serotonin (5-HT) in depression. Dysfunction of serotonergic neurons has been implicated as one of the causes of endogenous depression. Since serotonergic neurons innervate the hypothalamus and these neurons send collaterals to several other brain areas, it is possible that hypothalamic sites which control hormone secretion receive the same serotonergic afferents that innervate other limbic areas in the brain. Several investigators have devised neuroendocrine challenge tests measuring the effect of 5-HT agonists on plasma cortisol and prolactin in depressed patients. These tests help to identify dysfunctional 5-HT neurons, and are a "window into the brain." The secretion of cortisol and prolactin is increased predominantly by 5-HT1 receptors. However, changes in 5-HT2 receptors have also been implicated in depression. Results from our laboratory and by others suggest that brain serotonergic neurons stimulate renin and vasopressin secretion by activation of 5-HT2 receptors. Therefore, the renin and vasopressin response to 5-HT agonists should be included in neuroendocrine tests of serotonergic function in affective disorders. Since antidepressants produce a decrease in the density of 5-HT2 receptors, renin and vasopressin could be used to evaluate the antidepressant potential of new drugs.
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PMID:Neuroendocrine aspects of the serotonergic hypothesis of depression. 269 29


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