UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A highly sensitive and specific radioimmunoassay for LRF was applied to the measurement of endogenous LRF in various hypothalamic extracts. Specific antiserum was obtained by injecting LRF conjugated to human serum albumin with glutaraldehyde. Thyrotropin-releasing hormone, lysine vasopressin, oxytocin, noradrenaline, LH, FSH and cortical extracts did not appear to affect the assay, and the maximum cross-reaction observed with the LRF analogs tested was 8.5 p. 100 with LRF 2-10. The best detection limit (0.4 pg/tube) was usually obtained when the labelled LRF had been purified by polyacrylamide gel electrophoresis. Within and between-assay coefficients of variation were 8.0 and 12.6 p. 100, respectively (from B/Bo = 20 to 80 p. 100). Synthetic LRF administered to rams by intravenous injection was readily detectable in the peripheral plasma. However, the direct measurement of plasma endogenous LRF may give misleading results due to non-specific interference by plasma factors. No endogenous LRF could be detected in plasma methanol or acetone extracts obtained from rats and rams in various physiological conditions. The inhibition curves parallel to the synthetic LRF curve were obtained by diluting the crude hypothalamic extracts of rams and rats, and a good correlation (r = 0.997) with the Ramirez-McCann bioassay resulted, indicating that using radioimmunoassay to determine hypothalamic LRF content may be fruitful in studying hypothalamo-pituitary gonad interactions. The LRF content of rat and ovine hypothalami ranged from 2-8 to 20-80 ng of LRF, respectively.
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PMID:Reassessment of LRF radioimmunoassay in the plasma and hypothalamic extracts of rats and rams. 676 Feb 82

Interleukin-1 alpha (IL-1 alpha) exerts numerous neuroendocrinological and immunological actions. In the ovariectomized (OVX) monkey, intracerebroventricular (icv) infusion of IL-1 alpha stimulates the hypothalamo-pituitary-adrenal (HPA) axis and inhibits pulsatile LH and FSH secretion. This inhibitory effect of IL-1 alpha on the gonadotropins is prevented by coadministration of corticotropin releasing hormone (CRH) and vasopressin (AVP) antagonists, suggesting a role of these two HPA neuropeptides. In order to understand the central mechanisms by which "stress" interrupts the menstrual cycle, we have also investigated the modulatory role of estradiol. When early follicular phase estradiol concentrations are reproduced, there was a complete prevention of HPA activation and of the consequent inhibition of gonadotropin by IL-1 alpha. The mechanisms regulating this unexpected action remain to be elucidated. In contrast, in the presence of late follicular phase estradiol concentrations, the HPA response to IL-1 alpha is restored, but there is a stimulation of LH release. These data demonstrate interactions between the adrenal and gonadal endocrine axes, and highlight the role of estradiol in modulating these effects.
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PMID:The antireproductive role of corticotropin releasing hormone and interleukin-1 in the female rhesus monkey. 767 2

1. The sympathetic superior cervical ganglia (SCG) provide innervation to the pineal gland and median eminence through the internal carotid nerve and to the thyroid and parathyroid glands through the external carotid nerve. 2. Postsynaptic activation in median eminence nerve endings shortly after superior cervical ganglionectomy (SCGx) was accompanied by a depression of LH and FSH release and by a 3-5 day delay in rat estrous cyclicity. A decrease in TSH and GH release and an increase in ACTH and prolactin release were also found. These effects were accompanied by a) an increase in medial basal hypothalamic (MBH) LHRH, TRH and GHRH, b) a decrease in MBH somatostatin, AVP and CRH, and c) a normal adenohypophyseal response to hypophysiotropic hormones. Neurohypophyseal AVP release decreased during degeneration of sympathetic nerve terminals in the neurohypophyseal lobe after SCGx. The effects were generally mediated by alpha 1-adrenoceptors and were pineal gland. 3. In thyroid and parathyroid tissue the following events were observed during the wallerian degeneration phase after SCGx: a) alpha 1-adrenoceptor inhibition of thyroxine (T4) release, b) alpha 1-adrenoceptor inhibition, together with beta-adrenoceptor stimulation, of calcitonin release, and c) alpha 1-adrenoceptor inhibition of parathyroid hormone release. Thyroid sympathetic nerves also modulate slow phenomena such as compensatory thyroid growth after partial thyroidectomy. 4. In rats subjected to cholinergic decentralization of the thyroid gland, a decrease of plasma T4 and an increase of plasma TSH, as well as an impaired goitrogenic and thyroid compensatory response were detectable. The calcitonin and PTH response to changes in calcium levels increased after regional parasympathetic denervation. 5. The results indicate that cervical autonomic nerves constitute a parallel pathway through which the brain communicates with the endocrine system.
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PMID:Peripheral neuroendocrinology of the cervical autonomic nervous system. 808 Dec 83

To evaluate the significance of endogenous vasopressin and oxytocin in control of anterior pituitary hormone release, antiserum against vasopressin (AB-VP) or oxytocin (AB-OT) were microinjected into the third ventricle (3V) of conscious, ovariectomized rats to immunoneutralize endogenous VP or OT, respectively. Blood samples were collected just before and at different times after the microinjections. There were no differences in the plasma LH, FSH, PRL and TSH concentrations between control groups injected into the 3V with normal rabbit serum (NRS) and groups submitted to the intraventricular injection of AB-OT or AB-VP for 24 h after the injections. Plasma growth hormone (GH) declined significantly by 4 h after NRS injection, remained low at 6 h and had rebounded to nearly initial levels at 24 h. This pattern was not changed by microinjection of AB-VP, but plasma GH increased significantly compared to initial values in the period from 1 to 24 h after intraventricular microinjection of AB-OT. The intraventricular injection of AB-VP or AB-OT significantly decreased plasma ACTH; however, the effect of AB-VP was more prolonged and persisted for 6 rather than 4 h after injection. Thus, endogenous oxytocin may play a role in the control of basal GH release probably by stimulating somatostatin secretion and/or inhibiting GH-releasing hormone secretion or by both actions. On the other hand, both endogenous vasopressin and oxytocin play a physiologically significant stimulatory role in the control of basal ACTH release.
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PMID:Actions of endogenous vasopressin and oxytocin on anterior pituitary hormone secretion. 839 22

The testis is a complex organ in which local control is achieved by signalling between its constituent cells. Herein we describe the responses of cultured rat testicular cells and a mouse Sertoli cell-line to stimulation by endothelin and ATP, and elsewhere we have shown that rat peritubular myoid cells possess phosphoinositidase C-coupled V1a-vasopressin receptors identical to those of liver (Howl, J. et al, 1995, Endocrinology 136: 2206-2213). 1. Peritubular myoid cells from pre-pubertal rats responded through ETA receptors with PtdIns(4,5)P2 hydrolysis [EC50 for endothelin-1 (ET-1) approximately 0.4 nM], elevation of intracellular [Ca2+], and tyrosine phosphorylation of a variety of cellular proteins. They also showed enhanced adenylate cyclase activity, with an EC50 for ET-1 of approximately 3 nM, also through ETA receptors. Pharmacological elevation of [cAMP] did not immediately change the ET-1-stimulated formation of inositol phosphates, but attenuated the response after several hours. 2. Pre-pubertal rat Sertoli cells showed no detectable responses to ET-1, but responded to FSH with elevated [cAMP] and to ATP with PtdIns(4,5)P2 hydrolysis. PtdIns(4,5)P2 hydrolysis was equally responsive to ATP and UTP, and so appears to be activated by P2U-purinergic receptors. This response was enhanced by protein kinase C inhibition and attenuated by PKC activation. 3. Despite its lack of effect on rat Sertoli cells in primary culture, ET-1 provoked PtdIns(4,5)P2 hydrolysis in the TM4 murine Sertoli cell line (EC50 approximately 0.6 nM), and this response was negatively regulated by protein kinase C activation. 5. No receptor-stimulated activation of phosphoinositase C was detected in 'germ cell' populations, but the non-specific G protein activator A1F4-provoked inositol phosphate accumulation in these cells, so demonstrating their potential to respond through yet to be identified G protein-coupled receptors with phosphoinositidase C activation. 6. Immunoblotting studies showed the presence in rat testis of phosphoinositidase C-beta 1 and the alpha-subunits(s) of the G-protein(s) Gq and/or G11. These studies show that testicular myoid and Sertoli cells use at least three G protein-coupled receptors (V1a-vasopressins, ETA-endothelin and P2U-purinergic) to signal through phosphoinositidase C activation, that ET-1 can activate multiple signalling pathways in myoid cells, and that the ET-1-stimulated phosphoinositidase C responses of myoid and Sertoli cells have different regulatory characteristics.
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PMID:Inositol lipid-mediated signalling in response to endothelin and ATP in the mammalian testis. 856 25

The study was undertaken to obtain simultaneous measurements of circulating anterior pituitary hormone levels after the i.v. injection of arginine-vasopressin (AVP). Nine healthy men, mean age 31 years (range 24-41), received single blind with at least one week apart, after resting in the supine position for 30 min, AVP 0.26 microgram/kg body weight i.v. (Pitressin, Parke-Davis) or saline in randomized order. Blood samples were taken at 0, 10, 20, 30, 45 and 60 min for analyses of serum or plasma levels of ACTH, prolactin, TSH, GH, FSH, LH and AVP. The hormone responses after AVP or saline were calculated as the area under the curve (AUC) 0-60 min as well as the change in hormone levels from 0 to 10 min to pick up possible short lasting effects when there was no significant difference in AUC between AVP and control. As expected the highest plasma concentration of AVP was measured 10 min after the injection of AVP and well comparable to those in other studies where AVP was observed to release ACTH. The AUC:s for both ACTH and prolactin levels were significantly increased after AVP in comparison with saline (p = 0.008 and p = 0.038, respectively). The AUC:s for the other hormones measured were not significantly changed after AVP, but there were small but significant changes in the 0-10 min values for TSH and LH after AVP compared to saline. It is concluded that AVP has the potency to release not only ACTH but also prolactin in healthy men.
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PMID:Release of prolactin as well as adrenocorticotropin after administration of arginine-vasopressin to healthy men. 896 Sep 1

Gonadotropes synthesize and secrete LH and FSH under the control of GnRH, which acts via phosphoinositidase C (PIC)-linked G protein coupled receptors. Additionally, gonadotropin released from the pituitary is influenced by oxytocin, a peptide that has been shown to play a role in generation of the preovulatory LH surge. Although oxytocin receptors are present in the pituitary, studies have identified their presence on lactotropes but not on gonadotropes, raising the question of which cells act as the direct target of oxytocin in gonadotrope regulation. In this study, we examined effects of oxytocin on alphaT3-1 cells, a gonadotrope-derived cell line. Oxytocin, vasopressin, and vasotocin each stimulated accumulation of [3H]inositol phosphates in cells prelabeled with [3H]inositol, indicating activation of PIC. The rank order of potency (oxytocin > vasotocin > vasopressin) and sensitivity to inhibition by oxytocin and vasopressin receptor antagonists, revealed the effect to be mediated by oxytocin-selective receptors. Like other PIC activators, these nonapeptides caused biphasic (spike-plateau) increases in the cytosolic Ca2+. The spike response to oxytocin and GnRH were both retained in Ca2+-free medium, reflecting mobilization of intracellular Ca2+, and were comparably reduced by thapsigargin, implying mobilization of Ca2+ from a shared thapsigargin-sensitive intracellular pool. Brief stimulation with oxytocin, vasopressin, or vasotocin prevented subsequent Ca2+ responses to oxytocin, but not to GnRH, suggesting that the oxytocin receptor undergoes rapid homologous desensitization and reinforcing the interpretation that the nonapeptides act via the same receptor type. Oxytocin did not increase Ca2+ in cells stimulated with GnRH, whereas GnRH caused a spike Ca2+ increase even in the presence of oxytocin, implying that different mechanisms of desensitization (Ca2+ pool depletion and receptor uncoupling) are operating for two distinct PIC-coupled receptors in these cells. The demonstration that oxytocin acts directly via PIC-linked, oxytocin-selective receptors to increase cytosolic Ca2+ in a gonadotrope-derived cell line is consistent with the possibility that oxytocin has a comparable effect on nonimmortalized gonadotropes.
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PMID:Oxytocin receptor-mediated activation of phosphoinositidase C and elevation of cytosolic calcium in the gonadotrope-derived alphaT3-1 cell line. 911 4

Interferons (IFNs) are now in use worldwide for the treatment of chronic viral hepatitis. Unfortunately, various side effects of IFNs have been reported. Because cytokines, which include IFNs, can affect endocrine function, endocrinological abnormalities are sometimes observed in patients treated with IFNs. We examined the effects of IFN-beta on peripheral levels of pituitary and adrenal hormones and cytokines. Six million international units of IFN-beta dissolved in glucose solution was injected for 30 min. As a control study, glucose solution without IFN-beta was injected. Pituitary hormones (ACTH, GH, TSH, prolactin (PRL), LH, FSH, and arginine-vasopressin (AVP)), cortisol, and cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TNF), and interleukin-1 receptor antagonist (IL-1ra) were measured before and after IFN-beta injection. The study was carried out on 14 patients with chronic hepatitis type C who were under treatment with IFN-beta. All studies were performed when the patients were afebrile. None of the patients had any endocrine or autoimmune diseases. Plasma ACTH levels increased significantly at 60-120 min after IFN-beta injection compared with the levels before IFN-beta injection and in the control study using glucose injection. Plasma cortisol levels increased after IFN-beta injection, in parallel with plasma ACTH elevation. Serum GH levels increased significantly at 120 min after IFN-beta injection. All the increased hormones including ACTH, cortisol, and GH, were decreased at the end of the study-180 min after IFN-beta injection. Serum levels of TSH, PRL, LH, FSH, and AVP were not changed significantly by IFN-beta injection. Plasma IL-1 and TNF levels did not change after IFN-beta injection, while IL-6 and IL-1ra were elevated significantly. The increases in IL-6 and IL-1ra were gradual, reaching their peak levels at 180 min after IFN-beta injection. However there were no correlations between the hormones measured in this study and the levels of IL-6 or IL-1ra. It would seem that IFN-beta has direct or indirect stimulatory effects for ACTH and GH without mediation of the cytokines. These in vivo results are important for investigating the relationship between endocrine and cytokine systems in humans.
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PMID:Change of peripheral levels of pituitary hormones and cytokines after injection of interferon (IFN)-beta in patients with chronic hepatitis C. 976 84

Virusencephalitis is characterised by clinical symptoms of a parenchymatous inflammation. In addition, early mental status changes often occur as a result of virusencephalitis, beside focal neurological deficiencies, epileptic seizures, cerebral compression, even coma. Other pathological manifestations of virusencephalitis are disturbances of the neurohumoral and the endocrine system, which are often recognised and treated too late. This case report describes symptoms, treatment, and complications of a 76 year old female in-patient, who was diagnosed with virusencephalitis. The number of lymphocytes in the cerebrospinal fluid was increased to 30 cells per microliter, liquor albumin was 1705 mg/l, liquor sugar was 53 mg/dl and liquor lactat was 1.9 mmol/l. IgM antibodies against herpes viruses were found in the cerebrospinal fluid and distinct contrasting foci were found near the mammillary bodies, hypothalamus, tractus opticus, hypophyseal stalk and right parahippocampal in the magnetic resonance imaging of the head, indicating a focal herpes simplex encephalitis. Within seven days, the following symptoms developed: akinetic parkinsonian syndrome, central diabetes insipidus with hypernatremia and polyuria (6 l/die), hypothyreosis, adrenal insufficiency with adynamia, sopor, hypotension and even hypophyseal coma. Panhypopituitarism was diagnosed after measuring the basal hormone levels (ACTH, TSH, FT3, FT4, Cortisol, Prolactin, LH, FSH, ADH) and conducting the pituitary stimulation test. The severeness of all symptoms was slightly improved after substitution with antidiuretic hormone at 0.4 microgram/die and administration of hydrocortisone at 50 mg/die. Administration of amantadine sulphate at 0.6 g/die and L-dopa at 187.5 mg/die for 14 days resulted in a complete regression of the parkinsonism. After administration of aciclovir at 2.25 g/die for 21 days a complete regression of the clinical symptoms could be reached in connection with a decrease of 90% in number and size of cerebral contrasting foci in the magnetic resonance imaging of the head. Three month after therapy, clinical examination and blood serum analysis revealed persistent panhypopituitarism. The present case report is the first description of a viral infection on of the central nervous system (CNS) in combination with parkinsonism, diabetes insipidus, persistent panhypopituitarism and hyperprolactinemia. Early treatment of viral infections of the brain can improve a patient's prognosis dramatically. Early determination and early treatment of a patient's neurohumoral parameters is therefore critical to prevent or reverse early mental status changes like attention disturbances, alterations of personality and behavior, apathy, and slowed cognition.
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PMID:[Virus encephalitis with symptomatic Parkinson syndrome, diabetes insipidus and panhypopituitarism]. 1059 69

This review of the physiology of ovarian contractility cites the functions of FSH and LH and the contribution of chorionic gonadotropin (HCG) to follicular swelling and rupture. Endogenous estrogen priming seems to be needed for this response. Luteninizing hormone releasing hormone (LHRH) administered during the ovulatory phase also causes changes to occur in ovaries treated with smooth muscle stimulants. A contractile response may be induced by alpha-adrenergic receptors, which confirms the finding of smooth muscle fibers in the ovaries. Spontaneous contractions have also been observed in ovaries removed from animals at estrus. Estrogen activate, progesterone inhibits ovarian contractility. In rabbits and guinea pigs spontaneous activity of the ovary is increased during early pregnancy. Treatment with nor- epinephrine inhibits this. Quiescent ovaries show marked activation with nor-adrenergic compounds such as nor-epinephrine and phenilephrine. Pretreatment with alpha-adrenergic blocking agents such as progranolol reverses this effect. Prostaglandin F-2-alpha is a more powerful stimulant on ovarian motility than vasopressin or oxytocin. The role of ovarian contractions in the reproductive function is still unknown. Further studies may provide ways of interfering with reproduction at the ovarian level.
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PMID:Ovarian contractility and ovulation. 1225 6

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