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)

Dopamine stimulates the phosphorylation of the neuron-specific synaptic vesicle proteins Synapsin I, Protein IIIa and Protein IIIb in the posterior pituitary gland of the rat [Tsou and Greengard (1982) Proc. natn. Acad. Sci. U.S.A. 79, 6075-6079]. This effect has been characterized in the present investigation. The stimulatory effect of dopamine was mimicked by the selective D-1 receptor agonist SKF 38393 and was competitively and potently inhibited by the selective D-1 receptor antagonist SKF 83509 as well as by the mixed D-1/D-2 antagonist fluphenazine. Conversely, the effect of dopamine was attenuated by a D-2 receptor agonist (LY 141865) and potentiated by a D-2 receptor antagonist (sulpiride). Norepinephrine also stimulated phosphorylation of the synaptic vesicle proteins, apparently through activation of the D-1 receptor. D-1 and D-2 dopaminergic receptors may play a role in the regulation of hormone secretion from the neurohypophysis. Evidence exists that in the isolated neurophypophysis activation of D-1 receptors facilitates, while activation of D-2 receptors inhibits, release of vasopressin. Further work will be required to determine whether the regulation by D-1 and D-2 receptors of the protein phosphorylation in the neurohypophysial peptidergic terminals is related to the regulation by those receptors of the neurohypophysial hormone secretion.
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PMID:D-1 and D-2 dopaminergic receptors regulate protein phosphorylation in the rat neurohypophysis. 241 70

The release of beta-endorphin-immunoreactivity (beta E-IR) from rat pituitary anterior lobe (AL) quarters, neurointermediate lobes (NILs), and hypothalamic fragments was investigated in vitro. The beta-adrenoceptor agonist isoproterenol (ISO) and the hypothalamic neurohormone corticotropin-releasing factor (CRF) concentration-dependently stimulated the release of beta E-IR from superfused AL quarters and NILs, but not from incubated hypothalamic fragments. Dopamine (DA) inhibited the release of beta E-IR from NILs and hypothalamic tissue in a concentration-dependent manner, whereas it did not affect the release from AL quarters. Arginine8-vasopressin (AVP) stimulated the release of beta E-IR from AL quarters and hypothalamic fragments, but did not affect the release from NILs. The data indicate that the release of beta E-IR from cells in the pituitary lobes and in the hypothalamus is differentially regulated, but that common principles are involved. In particular, the results provide first direct evidence for an action of vasopressin as a stimulator of the release of POMC-derived peptides in the hypothalamus.
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PMID:Release of beta-endorphin-immunoreactivity from rat pituitary and hypothalamus in vitro: effects of isoproterenol, dopamine, corticotropin-releasing factor and arginine8-vasopressin. 252 39

Dopamine, like other neurotransmitters, exerts its biological effects by occupation of specific receptor subtypes. The dopamine receptors in the central nervous system and certain endocrine organs are classified into the D1/D2 subtypes. Outside the central nervous system, the dopamine receptors are classified into the DA1/DA2 subtypes. The D1/D2 and DA1/DA2 receptor have marked similarities and some differences, the most notable of which is the lower affinity of the DA dopamine compared with the D dopamine receptor. DA1 receptor activation increases renal blood flow (RBF); stimulation of DA1 and DA2 receptors may also increase glomerular filtration rate (GFR). DA1 agonists inhibit fluid and electrolyte transport indirectly via hemodynamic mechanisms and directly by occupation of DA1 receptors in specific nephron segments. In the proximal tubule, DA1 agonists simulate adenylate cyclase and inhibit Na+-H+ antiport activity. They also increase phospholipase C and inhibit Na+-K+-ATPase activity (presumably as a consequence of protein kinase C activation). The latter effects may be facilitated by DA2 agonists. In cortical collecting ducts, dopamine antagonizes the effects of mineralocorticoids and the hydrosomotic effect of antidiuretic hormone. It has also been suggested that DA1 may also decrease sodium transport by influencing other hormones, such as atrial natriuretic peptide. Studies of dopamine in the young are complicated because of the propensity for dopamine to stimulate alpha-adrenoceptors. Dopamine alone may actually decrease RBF in the perinatal period. In some animals, the renal vasodilatory and natriuretic effects of dopamine increase with age. Renal tubular DA1-stimulated adenylate cyclase activity increases, whereas renal tubular DA1 receptors decrease with age. Renal DA2 receptor density is greater in the fetus; after birth renal DA2 receptors do not change. Endogenous dopamine may regulate sodium excretion in the young differently than in the adult. In the adult, sodium surfeit is associated with an increase in urinary dopamine; the opposite occurs in the young. A decrease in dopamine production or blockade of dopamine receptors results in an antinatriuresis in the adult; dopamine blockade in the young results in a natriuresis. It remains to be determined whether these age-related differences in dopamine effects are due to changes in receptor DA subtype density, second messengers, and/or interaction with other receptors.
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PMID:The dopamine receptor in adult and maturing kidney. 257 2

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 effectiveness and reliability of long-term control of circulatory stability in brain-dead patients by combined administration of vasopressin and catecholamine was examined in detail. Twenty-five patients were divided into three groups according to the dose of vasopressin. The first group (n = 10) received no vasopressin, the second group (n = 2) an antidiuretic dose (0.1-0.4 U/hr), and the third group (n = 13) a pressor dose (1-2 U/hr), respectively. Patients given no vasopressin or an antidiuretic dose demonstrated circulatory deterioration and cardiac arrest within a short time after brain death, despite administration of a large dose of epinephrine. All patients with a pressor dose of vasopressin, however, demonstrated stable circulation as long as vasopressin and epinephrine were administered. Five patients in whom stable circulation was maintained by this technique were randomly chosen from the third group and studied under the following four conditions: (1) neither vasopressin nor epinephrine; (2) vasopressin only; (3) epinephrine only; and (4) both vasopressin and epinephrine. Compared with the controls (neither vasopressin nor epinephrine), vasopressin only increased the total peripheral resistance index, whereas epinephrine alone increased the cardiac index. Combined administration, however, raised the mean arterial blood pressure significantly by markedly increasing the total peripheral resistance index and cardiac index. Finally, in four brain-dead patients also randomly chosen from the third group, epinephrine, norepinephrine, and dopamine were compared in their circulatory effects with a pressor dose of vasopressin. Epinephrine increased both the total peripheral resistance index and cardiac index, whereas norepinephrine increased the total peripheral resistance index, compared with the baseline (no catecholamine). The required dose of norepinephrine, however, was four times that of epinephrine. The major effect of dopamine was to increase the cardiac index. We conclude that a pressor dose of vasopressin plays a central role in circulatory stabilization of brain-dead patients, and that long-term maintenance of stable circulation for a desired length of time is possible by the combined use of vasopressin and a catecholamine. Individually, catecholamines exhibit characteristic differences. Epinephrine has significant effects on both peripheral vessels and the heart, whereas norepinephrine keeps the circulation stable by increasing the total peripheral resistance index, with a much larger dose than epinephrine. Dopamine acts primarily on the heart.
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PMID:Effects of vasopressin and catecholamines on the maintenance of circulatory stability in brain-dead patients. 279 13

To characterize the functional aspect of prolactin (Prl) cells coexisting with corticotroph adenomas, pituitary adenoma cells obtained from a patient with Cushing's disease and a patient with Nelson's syndrome, who were associated with hyperprolactinaemia, were cultured in monolayer and their Prl responses to various secretagogues were compared with those of prolactinoma cells in culture. Immunohistochemistry performed in one of these two adenomas demonstrated the presence of Prl-containing cells in addition to ACTH cells. When ACTH-Prl adenoma cells were exposed to ovine corticotrophin-releasing factor (CRF), a dose-dependent increase in both ACTH and Prl secretion was observed, which was blocked by coincubation with hydrocortisone. In contrast, no stimulatory effect of CRF on Prl release was observed in all of the experiments using prolactinoma cells. Thyrotrophin-releasing hormone, which consistently stimulated Prl secretion in ACTH-Prl adenomas, was effective in triggering Prl release in only 25% of the prolactinomas. Exposure of the cultured cells to lysine vasopressin, growth hormone-releasing factor and vasoactive intestinal peptide resulted in an increase in ACTH and Prl secretion in one ACTH-Prl adenoma, however, none of the prolactinomas responded to these stimuli to secrete Prl. Dopamine and somatostatin, on the other hand, uniformly suppressed Prl secretion from ACTH-Prl adenomas as well as from prolactinoma cells. These results suggest that the mode of Prl secretion by mixed ACTH-Prl pituitary adenomas is not identical to that by pure prolactinomas and is, at least in part, common to that of ACTh secretion.
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PMID:Prolactin secretion by mixed ACTH-prolactin pituitary adenoma cells in culture. 285 25

Dopamine inhibits and serotonin stimulates adenylate cyclase activity in a neuroblastoma X Chinese hamster brain explant cell line (NCB-20). The inhibition of cyclic AMP accumulation by dopamine was blocked by pretreatment of the cells with pertussis toxin. Carbachol and bradykinin stimulated the accumulation of water-soluble inositol phosphates whereas thyrotropin-releasing hormone, vasopressin, neurotensin, and phenylephrine were without effect. Dopamine and serotonin had no significant effect on carbachol-induced phosphoinositide hydrolysis or the levels of the parent lipids within the membrane. Forskolin induced a much larger stimulation of cyclic AMP than did serotonin, and caused an increase in the levels of phosphatidylinositol-4-phosphate and phosphatidyl inositol-4,5-bisphosphate in the cell membrane.
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PMID:Activation of dopamine receptors does not affect phosphoinositide turnover in NCB-20 cells. 303 93

The changes in plasma levels of arginine-vasopressin (AVP) and oxytocin (OXT) of rabbits by intraventricular administration of various drugs and their effects on the release of both hormones from the isolated posterior pituitary of rats were examined. An intraventricular injection of hypertonic saline, carbachol, angiotensin II, prostaglandin E2 or histamine to a rabbit increased the concentrations of plasma AVP and OXT, whereas serotonin decreased their plasma levels. Noradrenaline increased the concentration of OXT, but not that of AVP. Dopamine did not significantly affect the plasma level of either hormone. The release of AVP and OXT from the posterior pituitary fragments of rats was stimulated by changing the osmolality of the perfusion medium in vitro. Perfusion with medium containing dopamine suppressed the release of both hormones. However, the other bioactive amines and the drugs mentioned above did not affect the release of AVP and OXT.
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PMID:A study on the release mechanism of vasopressin and oxytocin. 323 19

To evaluate the roles for catecholamines in angiotensin II (ANG II)-induced vasopressin (AVP) release, we examined in conscious rats the effects of intraventricular (ivt) administrations of catecholamine antagonists on plasma AVP responses to ivt applications of its agonists and ANG II. Plasma AVP was determined by RIA using trunk blood collected after decapitation. Dopamine (0.15 mumol), phenylephrine (an alpha-adrenergic agonist, 0.15 mumol) or ANG II (48.2 pmol) augmented plasma AVP 90 sec after the injection, whereas after isoproterenol (a beta-adrenergic agonist, 0.15 mumol) plasma AVP was unaffected. The plasma AVP responses to both dopamine and ANG II were significantly (P less than 0.01) inhibited by haloperidol (a dopamine blocker, 0.15 mumol) given 10 min before administration of these agents. Pre-administration of phenoxybenzamine (an alpha antagonist, 0.15 mumol) which was confirmed to abolish the effect of phenylephrine, or propranolol (a beta antagonist, 0.15 mumol) did not block the effect of ANG II. Administration of haloperidol, phenoxybenzamine or propranolol alone was without effect on plasma AVP level. On the basis of these results, we concluded that ANG II-induced AVP secretion may be mediated and/or modulated by dopamine.
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PMID:Central effects of catecholamine antagonists on angiotensin-induced vasopressin secretion in conscious rats. 338 51

Since neuroimmunomodulation is brought about in part, at least, by secretion of pituitary hormones involved in stress and immune responses, we review briefly the hypothalamic control of the release of ACTH, growth hormone, and prolactin. The release of ACTH is controlled particularly by corticotropin-releasing factor (CRF), but vasopressin has intrinsic releasing activity and potentiates the action of CRF at both hypothalamic and pituitary levels. Oxytocin may even potentiate the action of CRF, but has little, if any, ACTH-releasing activity by itself. In addition, epinephrine may augment responses to the CRFs. In contrast, growth hormone is under dual control by growth-hormone-releasing factor (GRF) and somatostatin, and prolactin is under multifactorial control by a series of inhibitors and stimulators. Dopamine is accepted as a physiological prolactin-inhibiting factor (PIF), but probably GABA and possibly acetylcholine as well are PIFs. There is good evidence for a peptide PIF as well. There are a number of prolactin-releasing factors (PRFs) which include oxytocin, vasoactive intestinal polypeptide, PHI and TRH. Several other peptides can also release prolactin, including angiotensin II. In response to stress there is a complex interaction of peptides intrahypothalamically. CRF augments its own release by an ultra short-loop positive feedback, and there is negative ultra short-loop feedback of GRF and somatostatin. Vasopressin appears to augment CRF release as well as to act directly on the pituitary, and there are complex interactions of various peptides to influence prolactin and GH release.
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PMID:The role of brain peptides in neuroimmunomodulation. 347 67


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