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 adrenocortical cells of the amphibian interrenal (adrenal) gland are controlled by multiple factors including neuropeptides and classical neurotransmitters. In particular, it has recently been shown that vasotocin (AVT), the amphibian counterpart of vasopressin, is a potent stimulator of frog corticosteroidogenesis. In the present study, we have investigated the possible interactions between AVT and other regulatory factors on frog interrenal tissue. When AVT (10(-9) M) and serotonin (10(-6) M) were infused together, a strict addition of the individual effects was observed. Similar results were obtained with concomitant infusion of AVT and vasoactive intestinal peptide or AVT and ACTH. In contrast, when AVT (10(-9) M) and acetylcholine (5 x 10(-5) M) were added together, the increase in corticosteroid secretion was less than additive. Dopamine induced a significant reduction of AVT-evoked stimulation of corticosterone production. These results indicate that regulatory peptides or classical neurotransmitters which participate in the control of adrenal steroidogenesis may interact on their target cell to modulate the activity of their congeners.
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PMID:Interactions between vasotocin and other corticotropic factors on the frog adrenal gland. 131 84

The hypothalamo-neurohypophyseal tract is known to contain the classical neurohypophyseal hormones vasopressin and oxytocin. Additionally, dynorphin, methionine- and leucine-enkephalin, cholecystokinin (CCK), corticotropin-releasing factor (CRF), and galanin are co-stored with vasopressin and/or oxytocin. Recent immunohistochemical studies have revealed the existence of a low to moderate number of substance P-, vasoactive intestinal peptide (VIP)-, neuropeptide Y (NPY)- and somatostatin-immunoreactive nerve fibers within the rat neurohypophysis. VIP-, substance P- and NPY-immunoreactive fibers were distributed throughout the organ, whereas somatostatin-immunoreactive fibers were present in the proximal part of the organ. The positive nerve endings were either large in size resembling classical nerve terminals related to perivascular spaces, or smaller similar to peptidergic fibers as described in the CNS. These results indicate that these neuropeptides may be either co-stored with the classical neurohypophyseal hormones or contained in another system of afferents to the organ. The probably distinct functional roles of these neuropeptides in the physiology of the neurohypophysis are discussed.
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PMID:Non-vasopressinergic, non-oxytocinergic neuropeptides in the rat hypothalamo-neurohypophyseal tract: experimental immunohistochemical studies. 138 83

The aims of this study were: (1) to examine whether the posterior pituitary contains prolactin releasing factor (PRF) activity, (2) to determine to what extent known neurohypophyseal peptides contribute to this activity, and (3) to compare posterior pituitary PRF activities of hens in different reproductive stages. Anterior pituitary cells derived from juvenile female turkeys were incubated with posterior pituitary extracts or test substances for 3 hr. Posterior pituitary extracts (0.1-0.8 equivalent) contained a potent substance(s) which stimulated PRL release in a concentration-dependent manner (2.4 +/- 0.08 to 6.5 +/- 0.23 micrograms/500 k cells). Arginine vasotocin (AVT) and vasoactive intestinal peptide (VIP) antisera (1:500) completely abolished the PRL-releasing activities of their respective peptides but partially reduced (P less than 0.05) the PRF activity of the posterior pituitary (AVT, 19.9%; VIP, 55.1%). Mesotocin antiserum did not alter (P greater than 0.05) PRL release induced by posterior pituitary extract. Posterior pituitary extract (0.01-0.5 equivalent) from hens in each of the various stages of the reproductive cycle induced a concentration dependent PRL release. The 0.5 posterior pituitary equivalent dose from reproductively quiescent (nonphotostimulated), laying, photorefractory, and incubating hens increased PRL release 2.4-, 2.9-, 3.8-, and 11.1-fold, respectively. The turkey posterior pituitary contains a potent PRF activity, partially accounted for by VIP and AVT, at the assayed concentrations, which varies with the reproductive cycle.
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PMID:Evidence of a role for the turkey posterior pituitary in prolactin release. 142 46

The distribution of vasoactive intestinal peptide (VIP) was analysed in perikarya of the mink hypothalamus with immunohistochemistry and, surprisingly, a large population of magnocellular VIP-immunoreactive neurons was present in the paraventricular and supraoptic nuclei as well as in accessory hypothalamic nuclei. From perikarya in the paraventricular as well as supraoptic nuclei, a large number of VIP immunoreactive nerve fibers was observed to enter the hypothalamo-neurohypophysial tract. Within the median eminence, a high density of VIP-immunoreactive nerve fibers was present in the external and internal zones. Fibers in the external zone of the median eminence were endowed with varicosities and perivascular terminals, while fibers in the internal zone were smooth and without terminal specializations. From the internal zone of the median eminence, fibers coursed via the infundibular stalk to terminate in perivascularly situated terminals in the neurohypophysis. In addition, a substantial number of small VIP-immunoreactive perikarya was observed within the suprachiasmatic nucleus. These perikarya were immunoreactive to neither vasopressin nor neurophysin. To elucidate the co-existence of VIP-immunoreactivity with vasopressin, oxytocin or neurophysin, a sequential double immunoperoxidase procedure to localize antigens with diaminobenzidine and benzidine dihydrochloride as chromagens was performed. From these experiments it was evident that VIP in nearly all magnocellular hypothalamo-neurohypophysial neurons co-existed with neurophysin. Based on a semi-quantitative estimate, half the VIP-immunoreactive magnocellular perikarya co-stored vasopressin, while another half co-stored oxytoxin. The present study describes the presence of a large population of VIP-containing neurons in the hypothalamo-neurohypophysial system of the mink. These findings raise evidence that within the mink, VIP may be involved in neurohypophysial physiology.
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PMID:Vasoactive intestinal peptide (VIP) in magnocellular neurons of the hypothalamo-neurohypophysial system of the mink (Mustela vision) is co-localized with vasopressin or oxytocin. 147 74

In chronic heart failure, neurohumoral mechanisms play an important role in the regulation of cardiac performance directly, by influencing systolic and diastolic function of the myocardium, and indirectly, by modulating pre- and afterload. The important vasoconstrictor, fluid and sodium retaining factors are the renin-angiotensin-aldosterone system, sympathetic nerve activity and vasopressin; the vasodilator, volume and sodium eliminating factors are atrial natriuretic peptide, vasodilator prostaglandins, such as prostacyclin and prostaglandin E2, dopamine, bradykinin and, possibly, endothelium-derived relaxing factor and vasoactive intestinal peptide. There is evidence from experimental and clinical studies that sympathetic nerve activity is stimulated in the early phase of the disease, as is the secretion of atrial natriuretic peptide, which increases in proportion to an increased preload. In early or mild heart failure, atrial natriuretic peptide suppresses the activity of the renin-angiotensin-aldosterone system, may prevent an increase in peripheral vascular resistance and preserves renal blood flow. In more severe heart failure, the renin-angiotensin-aldosterone system is activated, leading to an increase of peripheral and renal vascular resistance and fluid and sodium retention. This is associated with an increased production of vasodilator prostaglandins. In severe heart failure, mostly in connection with hyponatraemia, a non-osmolar inappropriately high secretion of vasopressin can be demonstrated. These findings suggest that early therapeutic intervention to suppress unfavourable neurohumoral mechanisms or to support protective factors, such as atrial natriuretic peptide, may be of particular importance in the treatment of congestive heart failure, delaying progression of the disease, which would improve survival.
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PMID:Hormones in heart failure--regulation and counterregulation. 183 97

Data are presented to show that vasoactive intestinal peptide (VIP) is synthesized and secreted by the hypothalamus and anterior pituitary and that it participates in the regulation of pituitary functions. Immunoreactive VIP in the hypothalamus and pituitary is increased following estrogen treatment and adrenalectomy and is reduced in hyperprolactinemic states. The level of VIP mRNA in the hypothalamus is increased during lactation and sexual maturation, while that in the anterior pituitary shows a sexual dimorphism and is increased with estrogen treatment and hypothyroidism. All these findings suggest a physiological regulation of hypothalamic and pituitary VIP gene expression in relation to its potential role as a neuroendocrine hormone. Furthermore, VIP stimulates prolactin (PRL) release at concentrations attainable in the hypophyseal-portal blood. Passive immunoneutralization studies with anti-VIP antisera suggest that endogenous VIP acts at multiple loci in the hypothalamic-pituitary axis to regulate PRL secretion, interacting possibly with other regulators of PRL secretion such as estrogen, serotonin, cholecystokinin, prostaglandins, galanin and oxytocin. Regarding other pituitary functions, although VIP has been shown to release growth hormone, ACTH, and vasopressin in vivo and in vitro, the physiological significance of these findings remains to be determined.
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PMID:Vasoactive intestinal peptide in the hypothalamus and pituitary. 190 91

Primary monolayer cultures of rat epididymal cells have been shown to secrete chloride and bicarbonate when stimulated with beta-adrenergic agents, humoral agents and vasoactive peptides. The intracellular messengers mediating the secretory response are unknown. In this study intracellular AMP, Ca2+ and inositol phosphates were measured in epididymal monolayers at rest and upon stimulation with various secretory agonists. Adrenaline, forskolin, lysylbradykinin, prostaglandin, endothelin, angiotensin II, antidiuretic hormone and vasoactive intestinal peptide at concentrations that stimulate anion secretion caused a rise in intracellular cyclic AMP. The increase in cyclic AMP by adrenaline was blocked by propranolol but not by phentolamine. Studies of the concentration-effect relationships showed that for adrenaline and endothelin the EC50 for stimulation of cyclic AMP was higher than that for stimulation of anion secretion. None of these agonists affects intracellular Ca2+ concentration and inositol phosphate contents in epididymal monolayers. Ca2+ ionophores A21387, ionomycin and erythrosin B (with irradiation with white light), at concentrations that stimulate anion secretion, also stimulated a rise in intracellular cyclic AMP and concomitantly increased intracellular Ca2+. The increase in cyclic AMP was dependent on extracellular Ca2+. It is not known whether the secretory response to Ca2+ ionophores was mediated by an increase in cell Ca2+ per se, or cyclic AMP. However, it can be concluded that cyclic AMP is the second messenger which mediates the secretory responses to physiological stimuli.
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PMID:Secretory agonists stimulate a rise in intracellular cyclic AMP but not Ca2+ and inositol phosphates in cultured rat epididymal epithelium. 197 25

The central nervous system effects of somatostatin-28 on proximal duodenal bicarbonate secretion were studied in freely moving rats. Cerebroventricular administration of somatostatin-28 (0.2-2.0 nmol) significantly stimulated duodenal bicarbonate secretion in a dose-dependent fashion. Somatostatin-28 was approximately twice as effective as somatostatin-14. Intravenous administration of somatostatin-28 or somatostatin-14 did not significantly alter the bicarbonate response. Ganglionic blockade with chlorisondamine and truncal vagotomy abolished the stimulatory effect of somatostatin-28 while bretylium, naloxone, indomethacin, and adrenalectomy did not. Furthermore, atropine methylnitrate significantly attenuated and the vasoactive intestinal peptide antagonist 4Cl-D-Phe6, Leu17-vasoactive intestinal peptide abolished the bicarbonate response produced by cerebroventricular somatostatin-28. In contrast, hypophysectomy and pretreatment with the vasopressin V1-receptor antagonist [1-deaminopenicillamine, 2-(0-methyl)Tyr, 8-Arg]-vasopressin significantly enhanced the bicarbonate response produced by cerebroventricular somatostatin-28. These findings indicate that somatostatin-28 acts within the central nervous system to stimulate duodenal bicarbonate secretion in freely moving rats via vagal efferents by release of vasoactive intestinal peptide and, in part, by a muscarinic pathway and not by catecholamine, opiate, or prostaglandin release.
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PMID:Stimulation of duodenal bicarbonate secretion in conscious rats by cerebral somatostatin-28. Role of neurohumoral pathways. 197 31

Histamine (HA), which acts as a neurotransmitter in the central nervous system, participates in the neuroendocrine regulation of prolactin (PRL) secretion. HA has a predominant stimulatory effect which is mediated via H2-receptors following central administration and via H1-receptors following systemic infusion of the amine. In addition, HA seems to exert a minor inhibitory effect on PRL secretion, an effect unmasked only during blockade of the receptor mediating the stimulatory effect. Following central administration the inhibitory effect is mediated via H1-receptors, while following systemic administration this effect is mediated via H2-receptors. In accordance with these findings, the H2-receptor antagonist cimetidine (CIM) has an inhibitory (following central administration) or stimulatory (following systemic administration) effect on PRL secretion. However, high doses of CIM possess an additional PRL stimulatory action not related to blockade of H2-receptors. This non-specific action is not exerted by the chemically different H2-receptor antagonist ranitidine. Since HA has no effect directly at the pituitary level, the actions of the amine may occur at different sites within the hypothalamus by an effect on hypothalamic transmitters regulating PRL secretion. Dopaminergic as well as serotoninergic neurons are involved in the mediation of the action of HA, since the dopamine (DA) concentration in the pituitary portal vessels is decreased by central or systemic infusion of HA, and since blockade of DA synthesis and of DA or serotonin (5-HT) receptors inhibit or prevent the PRL stimulatory action of HA infused centrally or systemically. However, other factors regulating PRL secretion (e.g. beta-endorphin, vasoactive intestinal peptide, vasopressin or TRH) may be involved in the mediation of the PRL response to HA. In men the effects of HA on PRL secretion are similar to the effects in male rats. Systemic infusion of HA stimulates PRL secretion via H1-receptors and inhibits PRL secretion via H2-receptors. The PRL-stimulatory effect of HA is caused by an inhibition of the dopaminergic system, while the PRL-inhibitory effect of HA may involve other transmitters than DA. In contrast to its stimulatory effect in men, HA had no effect on basal PRL secretion in women, but enhanced the PRL response to TRH. In rats or in humans the PRL stimulatory effect of HA is not caused by the cardiovascular actions of the amine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Histaminergic regulation of prolactin secretion. 218 99

To evaluate the possibility that the proopiomelanocortin (POMC)-derived peptide gamma 2-melanocyte stimulating hormone (gamma 2-MSH) has a role in circulatory regulation in man we studied circulating levels of this peptide at three different stages of physical activity in 10 young healthy subjects. The results were compared to simultaneously measured plasma levels of catecholamines, neuropeptide Y, vasopressin, renin activity, aldosterone and human alpha-atrial natriuretic peptide (alpha-hANP) and of the vasodilatory peptides calcitonin gene-related peptide, substance P and vasoactive intestinal peptide. The plasma levels of gamma 2-MSH-LI (like immunoreactivity) increased from 1009 +/- 101 pmol l-1 at supine rest to 1281 +/- 79 pmol l-1 when measured after 10 min walking (P less than 0.05), and remained at this increased level also after a consecutive further increase of physical activity (4 min stair rush), 1293 +/- 87 pmol l-1 (P less than 0.05 vs. at rest). The increase in circulating gamma 2-MSH-LI levels preceded the elevation of the venous plasma noradrenaline level, but did not rise further with more pronounced activation of the sympathetic nervous system at the highest grade of physical activity examined.
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PMID:Gamma 2-MSH increases during graded exercise in healthy subjects: comparison with plasma catecholamines, neuropeptides, aldosterone and renin activity. 220 97


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