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)

The cellular actions of vasopressin (AVP) in the anterior pituitary were investigated. HPLC analysis of [3H]inositol-labeled cells indicated that AVP stimulated a rapid increase in inositol-1,4,5 trisphosphate (IP3), inositol-1,4 bisphosphate, and inositol-4 monophosphate levels. While CRF had no effect on basal IP3 levels, it blocked their stimulation by AVP. CRF-stimulated ACTH secretion and cAMP accumulation were potentiated by AVP. AFter dexamethasone (DEX) treatment (20 nM, 18 h), CRF-dependent ACTH secretion and cAMP accumulation were attenuated but AVP was still able to potentiate both of these actions of CRF suggesting that cellular actions of AVP may be resistant to DEX effects. Therefore, [3H]AVP binding was determined in control and DEX-treated cells. Pretreatment with DEX had no effect on either AVP receptor affinity or on the number of available binding sites. Consistently, stimulation of IP3 production by AVP in DEX-treated cells was comparable to that of control cells. Protein kinase C activators such as 12-O-tetradecanoyl-phorbol-13-acetate and dioctanoylglycerol were either near additive with CRF or also potentiated the action of CRF on ACTH secretion, respectively, even after DEX pretreatment. These results indicate that, in the anterior pituitary, distinct intracellular signaling pathways mediate the actions of CRF and AVP; cAMP mediates CRF actions and IP3/protein kinase C mediate the effects of AVP. Neuromodulation of ACTH secretion by dual effector mechanisms which exhibit a complex mode of interaction and only one of which is negatively influenced by glucocorticoids, provides these cells a mechanisms by which appropriate responses can be elicited under various physiological states.
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PMID:The cellular actions of vasopressin on corticotrophs of the anterior pituitary: resistance to glucocorticoid action. 315 72

The role of protein kinase C (PKC) in the multihormonally regulated ACTH secretory responses of rat anterior pituitary cells was examined in control cells or after pretreatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), an activator of PKC. Using affinity-purified polyclonal antiserum raised against purified rat brain PKC, immunoprecipitable PKC was demonstrated in [35S]methionine-labeled cells appearing as a doublet of 78/80 kilodaltons. Long-term treatment (24 h) of cells with 0.6 microM TPA caused the specific loss of immunologically reactive PKC. Consistently, TPA pretreatment decreased the amount of phosphatidylserine-dependent protein kinase activity measured in vitro by 90%. In control cells, vasopressin (AVP) stimulated ACTH secretion and potentiated ACTH secretion stimulated by CRF. After a 24-h treatment with 0.6 microM TPA, secretory responses to AVP and the potentiating effect of AVP on CRF action were completely abolished. In contrast, CRF action on ACTH secretion, thought to be mediated by cAMP, was unaffected. Similarly, forskolin- and 8 bromo-cAMP-induced ACTH secretion remained unchanged after TPA pretreatment. These results indicate a crucial role for PKC in mediating the effects of AVP on ACTH secretion and on the potentiating action of AVP on CRF-induced secretion from corticotropic cells of the anterior pituitary.
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PMID:Phorbol ester-induced down-regulation of protein kinase C abolishes vasopressin-mediated responses in rat anterior pituitary cells. 315 77

Previous studies in vitro have shown that prostaglandin (PG) E2 is formed in rat adenohypophysis upon stimulation by arginine-vasopressin (AVP) and synthetic ovine corticotropin-releasing factor (CRF-(1-41]. The aim of the present study was to examine whether long-term changes in the hypothalamic stimulation of the pituitary corticotrophs in vivo may influence PG synthesis in subsequent in vitro incubations of rat anterior pituitary quarters. The release of PGE2 from adenohypophyses obtained from adrenalectomized rats was increased to about 300% of controls both under basal conditions and after stimulation by AVP; by contrast, the release of PG D2 was changed neither by adrenalectomy nor by AVP. Simultaneously, basal release of beta-endorphin-like immunoreactivity (beta-EI) was increased after adrenalectomy to about 300% of controls, parallel to the increase in the tissue content, whereas AVP-induced beta-EI release was unchanged. Addition of PG E2 inhibited, whereas blockade of PG formation by indomethacin enhanced AVP-induced beta-EI release both in controls and after adrenalectomy. When anterior pituitary glands were taken from rats with lesions of the paraventricular nuclei, release of PG E2 was decreased as compared to controls both under basal conditions and after stimulation by AVP or CRF-(1-41). Simultaneously, basal and evoked release of beta-EI was unchanged. We conclude that the formation of PG E2 in the adenohypophysis varies according to long-term changes in the hypothalamic stimulation of adrenocorticotropin and beta-endorphin release supporting the view that PG E2 synthesis is related to, and may be involved in mechanisms controlling peptide hormone release from the corticotrophs.
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PMID:Release of prostaglandin E2 and beta-endorphin-like immunoreactivity from rat adenohypophysis in vitro: variations after adrenalectomy or lesions of the paraventricular nuclei. 315 85

In the present study we report the properties of vasopressin (VP) receptors in the anterior pituitary gland and show that the number of these receptors is markedly affected by adrenalectomy and hypothalamic lesions. VP-binding activity was assayed in particulate fractions of rat anterior pituitary glands using tritium-labeled arginine VP ([3H] AVP) as tracer. In the presence of Mg2+ the radioligand interacted with a single class of high affinity, low capacity binding sites. Magnesium ions modulated the affinity of the receptors but had no effect on binding capacity. Guanine nucleotides decreased the amount of tracer bound in a dose-dependent manner by increasing the dissociation constant (Kd) of the binding reaction by approximately 2-fold. Increasing the concentration of Mg2+ did not prevent this effect. Bilateral adrenalectomy (ADX) decreased pituitary AVP-binding activity: binding fell by 30% 4 h after surgery and declined further to 10% or less of control at 4 days. The decrease in binding was primarily due to a reduction in the number of receptors. Daily administration of corticosterone inhibited the reduction of binding activity at 4 days in a dose-dependent manner. Destruction of hypophyseotropic VP neurons by means of surgical lesioning of the hypothalamic paraventricular nucleus or the medial basal hypothalamus abolished the effect of ADX on pituitary AVP binding at 24 h but only attenuated the degree of receptor loss at 4 days. Furthermore, the lesions themselves caused a significant (approximately 30%) reduction in receptor number 4-7 days after hypothalamic surgery. Adrenalectomy reduced pituitary AVP-binding activity in homozygous (di/di) Brattleboro rats. The extent as well as the time course of the loss of receptor activity resembled that in normal rats. Rat anterior pituitary segments were exposed to synthetic CRF, AVP, or oxytocin (all 10(-7) M) for 4 h in vitro, and [3H] AVP-binding activity was subsequently determined. Both AVP and oxytocin reduced the amount of radioligand bound, while CRF had no effect. These observations allow the following conclusions: Magnesium ions and guanine nucleotides modulate the affinity of pituitary AVP receptors by different mechanisms and have no effect on binding capacity; Pituitary receptors for AVP are regulated by the amount of AVP released by paraventricular nucleus neurons as well as through a mechanism that requires the presence of corticosterone; Homozygous Brattleboro rats may respond to ADX by increased hypothalamic release of an endogenous ligand for pituitary AVP receptors.
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PMID:Pituitary binding of vasopressin is altered by experimental manipulations of the hypothalamo-pituitary-adrenocortical axis in normal as well as homozygous (di/di) Brattleboro rats. 316 22

The hypothalamic systems secreting corticotropin-releasing hormone (CRF), somatostatin, oxytocin, vasopressin and luteinizing hormone-releasing hormone (LHRH) were characterized using immunochemistry, and variations were studied in relation to the recrudescence of testicular activity in the ferret and the mink, two species with opposite photoregulation of their annual reproductive cycles. Under the present conditions of study, the immunoreactivity of the CRF, somatostatin, and oxytocin systems showed no significant variation in either species. In contrast, in these two species, the immunoreactivity of the LHRH system varied considerably depending on the date of observation. The increase in the number and immunoreactivity of the LHRH-secreting neurons that occurred in November in the mink and in January in the ferret, is in agreement with previous results showing that the photoperiod plays an essential role in regulating the annual activity of the testis and that the photoperiodic environmental conditions required for the activation of the LHRH system differ between the species. Similarly, correlations could be found between an increase in immunoreactivity of the vasopressinergic axons projecting to the external median eminence and the recrudescence of testicular activity.
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PMID:Peptidergic neurohormonal systems in the basal hypothalamus of the ferret and the mink: immunocytochemical study of variations during the annual reproductive cycle. 334 34

A reduced duration of activity of local anesthetic drugs in patients with chronic renal failure has been described by several authors. Because surgical duration is not always predictable and these patients must be classified as high-risk patients (ASA physical status III-IV), reduced effectiveness may be a significant problem in clinical practice. Various reasons have been discussed as possible explanations for this phenomenon such as: (1) uremia-induced changes in acid-base status of blood and tissue, (2) alterations in protein-binding; and (3) changes in hemodynamic parameters. However, we have not been able to find any severe changes in electrolyte or acid-base status in patients with chronic renal failure after adequate hemodialysis. We wondered, therefore, whether changes in tissue pH might be one cause of the shorter duration of action of anesthetic drugs. We also examined some other pharmacokinetic parameters after administration of the anesthetic drug in order to find differences in comparison to healthy patients. Supraclavicular brachial blockade (3 mg/kg bupivacaine 0.5% + 0.1 IU vasopressin/ml) was performed in 11 patients with chronic renal failure requiring hemodialysis who were admitted to the hospital for a shunt operation in the forearm. The control group consisted of 11 healthy patients who were admitted for minor hand surgery. Preoperative blood samples were taken for measurement of blood urea nitrogen, serum creatinine, serum electrolytes, lactate, hemoglobin and hematocrit, and an arterial blood gas duration of action was defined as the time to full recovery of sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The action of bupivacaine-HCl following supraclavicular plexus block in patients with chronic kidney insufficiency]. 341 3

CRF-containing parvocellular axons in the external zone of the rat median eminence were classified as vasopressin-containing (CRF+/AVP+) and vasopressin-deficient (CRF+/AVP-) subpopulations based on post-embedding electron microscopic immunocytochemical staining of serial ultrathin sections for CRF, AVP and the other peptides derived from the AVP precursor: AVP-associated neurophysin (NP-AVP) and the C-terminal glycopeptide (GP). In normal animals, the CRF+/AVP+ and CRF+/AVP- subpopulations were approximately equal in terms of detectable axonal swellings. Three to 14 days after adrenalectomy (ADX), the CRF+/AVP+ and CRF+/AVP- subpopulations represented about 95% and 5%, respectively, of total CRF+ swellings. This change was due to a 90% decrease in the absolute number of detectable CRF+/AVP- swellings after ADX, whereas the absolute number of detectable CRF+/AVP+ swellings rose by less than 20%. These changes were completely blocked by administering the glucocorticoid agonist dexamethasone throughout the period after ADX. The results suggest that the CRF+/AVP+ and CRF+/AVP- subpopulations of neurosecretory axons in the external zone of the median eminence respond differently to ADX, indicating that they are independently regulated by glucocorticoids.
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PMID:Vasopressin-containing and vasopressin-deficient subpopulations of corticotropin-releasing factor axons are differentially affected by adrenalectomy. 349 95

Intact rats exposed to low or moderate intensity electroshocks for 3-5 h showed a marked increase in plasma ACTH levels 10 min after the beginning of the stress, followed by a decline despite continuous exposure to the stimulus. We have explored the role of steroid feedback, desensitization of the pituitary response to CRF, or changes in pituitary ACTH content in mediating this phenomenon. The following results were obtained. Exposure of adrenalectomized rats to shocks showed that removal of steroid feedback did not restore the ability of the animals to maintain elevated levels of circulating ACTH during electroshocks. To determine whether prolonged stress caused changes in pituitary sensitivity to CRF, intact rats received CRF, epinephrine, vasopressin, or phorbol ester at the end of the 3-h shock session; all secretagogues caused a significantly smaller increase in the plasma ACTH levels in intact rats subjected to low or moderate intensity shocks compared to that of control animals, which suggested that there was no specific desensitization to CRF. By contrast, pituitary responsiveness to CRF was not significantly altered in adrenalectomized rats submitted to low intensity shocks for 1-3 h; however, when moderate intensity shocks were used, adrenalectomized rats showed a blunting of the response to CRF comparable to that in intact animals. Finally, we observed a comparable decrease in the pituitary ACTH content of intact or adrenalectomized rats exposed to electroshocks; this decrease was proportional to the length and intensity of the shocks. We conclude that the inability of continuously stressed rats to maintain elevated plasma ACTH levels appears to be mediated through both the temporary decrease in a readily releasable pituitary ACTH pool and the negative feedback exerted by corticosterone.
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PMID:Diminished responsiveness of the hypothalamic-pituitary-adrenal axis of the rat during exposure to prolonged stress: a pituitary-mediated mechanism. 349 26

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

The development of shock initiates a cascade of responses in an effort to reestablish homeostasis. Three of the most important hormonal and neurohumoral changes are the secretion of glucocorticoids, catecholamines, and vasopressin. Regulation of adrenal function is much more complex than originally thought. Hemorrhage is a potent stimulus for cortisol release, and both ACTH and ACTH-independent mechanisms have been described. The ACTH response to its releasing hormone, corticotropin releasing hormone (CRF), is itself amplified by vasopressin, which appears to have intrinsic CRF properties. Because ACTH is synthesized as part of a large precursor molecule (pro-opiomelanocortin) containing the amino acid sequences for several important proteins, stimulation of ACTH release has far-ranging effects, the specifics of which are just being clarified. Norepinephrine and epinephrine levels increase manyfold above baseline within minutes of the onset of hemorrhagic shock. Only patients experiencing cardiac arrest or the rare patient with a very active pheochromocytoma have higher concentrations. The levels reached are far in excess of those required to cause both cardiovascular and metabolic alterations. Because of the presence of the endogenous opiates leucine and methionine enkephalin in the neurosecretory granule, it is very likely that the enkephalins are coreleased with the catecholamines, modifying their cardiovascular effects and producing analgesia. Hypovolemia is also a potent stimulus for vasopressin secretion, which overrides hypotonicity, presenting a clinical picture quite compatible with the syndrome of inappropriate antidiuretic hormone secretion, from which it must be differentiated. Vasopressin also is released by pain, nausea, and hypoxia, all of which are likely to be present in the patient with shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of shock. 353 88

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