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

Cells and fibers containing somatostain (SRIF) or SRIF-like peptides were detected immunocytochemically in the brain of the garden dormouse (Eliomys quercinus L.). The periventricular preoptic nucleus and the paraventricular nucleus encompass a component of the SRIF-immunoreactive hypothalamo-infundibular and hypothalamo-neurohypophyseal systems. The suprachiastmatic, ventromedial and arcuate nuclei contain a number of SRIF-positive cells and receive a rich SRIF innervation. The extrahypothalamic systems containing SRIF can be subdivided into the following groups: (1) Afferents, the cellular origin of which is not always clearly evident, i.e., fibers of the septum, the lateral preoptic area, the thalamus, the superior olivary nucleus, the mesencephalic gray matter, and the subfornical organ; (2) dispersed cells with short projections (neocortex, caudate nucleus, putamen); (3) scattered cells with short projections (nucleus accumbens) or innervating remote territories (nucleaus interpeduncularis); (4) vascular organ of the lamina terminalis, a neurohemal area comparable to the median eminence. These observations lead to a theory of a functional bipotentiality of the somatostatin molecule. Immunocytological results depend on the antisera employed, the type of fixation and the experimental conditions. Adrenalectomy is followed by an accumulation of immunoreactive material in all SRIF-containing systems of the brain. These results clearly indicate the SRIF participates in the function of the CRF-ACTH-adrenal axis. The endocrine disturbance induced by adrenalectomy appears to modify the activity of both the neurohormonal and neuromodulator components of the SRIF system.
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PMID:Neuronal systems immunologically related to the somatostatin system in the garden dormouse. 610 21

Light and electron microscope methods which can be used to examine the possibilities of co-occurrence of peptides are reviewed. The results obtained using some of them are exposed and discussed, concerning i/the light microscope demonstration of the CRF/vasopressin coexistence in rat and guinea-pig. ii/the electron microscope demonstration of the granular colocalization of LH-RH/C-terminal ACTH and somatostatin/enkephalin in the guinea-pig median eminence.
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PMID:[Immunohistochemical arguments in favor of co-localization of neuropeptides in hypothalamo-infundibular neuron systems]. 615 22

The present study examined the involvement of prostaglandins (PGs) in the mechanisms of ACTH and beta-endorphin release from rat anterior pituitary quarters incubated in vitro. Various cyclooxygenase inhibitors (indomethacin, diclofenac, flurbiprofen) had no effect on basal release of ACTH-like or beta-endorphin-like immunoreactivity (beta-EI), but enhanced ACTH-immunoreactivity/beta-EI release upon stimulation by arginine-vasopressin (AVP) or synthetic ovine corticotropin-releasing factor [CRF-(1-41)]. The lowest effective concentration of indomethacin was just sufficient to prevent PG synthesis. Indomethacin was similarly active after blockade of the phosphodiesterase by 3-isobutyl-1-methylxanthine. When added to the incubation media in concentrations up to 1 microM, PGE2, D2, F2 alpha, or prostacyclin (PGI2) did not alter basal beta-EI release; however, with stimulation by AVP or CRF-(1-41), PGE2 but not PGD2, F2 alpha, or I2 inhibited beta-EI release by about 60%. The concentrations of PGE2 in the incubation media, as measured by RIA, were somewhat higher than those of any other cyclooxygenase product (PGD2, F2 alpha, 6-keto-PGF1 alpha, thromboxane B2). Upon stimulation by AVP or CRF-(1-41), the concentrations of PGE2 increased, whereas those of PGD2 or F2 alpha remained unchanged. The release of beta-EI stimulated by high potassium concentration was not enhanced by indomethacin, although this release was sensitive to inhibition by PGE2. We conclude that PGE2 is formed locally subsequent to binding of the neurohormones and may act as a negative feedback-modulator of vasopressin's and CRF-(1-41)'s activity in the anterior pituitary gland.
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PMID:Adrenocorticotropin and beta-endorphin release from rat adenohypophysis in vitro: inhibition by prostaglandin E2 formed locally in response to vasopressin and corticotropin-releasing factor. 620 54

A new peptidergic paraventriculo-infundibular system has been revealed using anti-corticoliberin (CRF) antibodies. The localization of its perikarya in the paraventricular nuclei as well as the distribution of its fibres and perivascular nerve-endings within the median eminence are different from those of other systems stained with antibodies directed against gonadoliberin, somatostatin, vasopressin or oxytocin.
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PMID:[Corticoliberin neurons in the rat brain]. 621 70

Electrical stimulation of rat posterior lobes in vitro inhibited bioactive corticotropin (ACTH) release from the intermediate lobe and promoted the release of corticotropin-releasing factor(s) (CRF). Both effects were calcium dependent. Released posterior lobe CRF was inactivated by thioglycolate, and the CRF activity could be accounted for by vasopressin. Results suggest strongly that vasopressin is the predominant CRF released from neurohypophysial axons, and that intermediate lobe ACTH release is submitted to an inhibitory control.
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PMID:Release of corticotropin and corticotropin-releasing factors from rat posterior pituitary in vitro. 624 58

Incubation of anterior pituitary (AP) fragments of rats was used to determine the specific role played by vasopressin (VP) in the overall effect of crude hypothalamic median eminence (HME) extract on ACTH release. Using the property of an AVP antiserum (AS) to completely abolish the CRF-like effect of hypothalamic VP without apparently affecting the effect of CRF, we show that under specific incubation conditions, the effect of the two secretagogues are additive at the pituitary level. ACTH secretion of pituitaries was enhanced when incubation was carried out in the presence of VP together with a maximum effective dose of VP-free HME extract (from Brattleboro rats). These observations favor the hypothesis that VP and CRF have different receptor sites in the anterior pituitary.
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PMID:Involvement of vasopressin in corticotropin-releasing effect of hypothalamic median eminence extract. 624 85

Electrical stimulation of the neural lobe (NL) of the pituitary induces a rise in plasma corticosterone indicating the release of adrenocorticotropin (ACTH) in rats pretreated with dexamethasone, morphine and pentobarbitone. 7-8 days after placing an anterolateral cut around the medial basal hypothalamus (MBH), the rats failed to respond with ACTH release to electrical stimulation of the NL; the number of nerve fibers and terminals in the NL decreased to less than 5% of the normal; and ACTH releasing activity of acid extracts of the NL was undetectable using both in vivo and in vitro tests, which are insensitive to vasopressin. After lesions of the paraventricular nuclei the stimulation of the NL elecited a rise of plasma corticosterone that was significantly less than that in the controls. These results suggest that the NL of the pituitary contains electrically excitable fibers capable of releasing corticotropin-releasing factor (CRF; distinct from vasopressin) and that these fibers probably originate from outside the MBH, with a portion of them coming from or through the paraventricular nuclei or their immediate vincinity.
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PMID:Effect of electrical stimulation of the neurohypophysis on ACTH release in rats with hypothalamic lesions. 625 93

Electrical stimulation of the neural lobe of the pituitary resulted in an increase of corticosterone secretion in both normal and Brattleboro rats. Bioassaying the corticoliberin (CRF) activity of stalk-median eminence and neural lobe extracts obtained from normal and Brattleboro rats revealed that the endogenous vasopressin was not a prerequisite of ACTH-releasing potency. Arginine-8-vasopressin failed to potentiate the CRF activity of the different extracts. These data suggest that a nonvasopressin substance(s) with CRF activity can be released from the neurohypophysis of the rat, and it may contribute to activating the pituitary-adrenal axis under certain experimental conditions.
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PMID:Corticoliberin activity of rat neurohypophysis is distinct from vasopressin. 626 93

Initially the hypothalamic factor responsible for the release of corticotropin (CRF), was thought to be a simple peptide. More recent work has led to the conclusion that CRF is a multifactorial complex. In 1979 we proposed that vasopressin, much disputed as a CRF candidate, was a major constituent of the complex, interacting with a potentiating the CRF activity of the other component(s). The recent characterization of a 41 residue ovine hypothalamic peptide capable of releasing adrenocorticotropic hormone (ACTH) in a dose-related manner has allowed us to compare its CRF bioactivity with that of vasopressin and simple extracts of the hypothalamus, and to investigate any interaction it may have with vasopressin and other hypothalamic factors in the release of ACTH. We report here that the new CRF is more potent than vasopressin in releasing ACTH. When given simultaneously with vasopressin a fourfold potentiation of CRF activity with steep dose-response characteristics were observed. It also potentiated vasopressin-free hypothalamic extracts, suggesting that a new CRF does not account for all the nonvasopressin portion of the CRF complex.
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PMID:Corticotropin releasing activity of the new CRF is potentiated several times by vasopressin. 628 93

Most of the experimental evidence for a role of arginine-vasopressin (AVP) in adrenocorticotropic hormone (ACTH) release comes from in vitro studies. The multimolecular nature of the hypothalamic factor responsible for corticotropin (CRF) release has long been recognized, but the importance of AVP as a cofactor is controversial. The recently characterized 41-residue peptide fulfills the criteria for a physiological role in ACTH release and it is potentiated in vitro by AVP. In vivo, AVP is able to stimulate ACTH secretion, and Brattleboro rats, deficient in AVP, show a reduced activity of the hypothalamo-hypophysial-adrenocortical system (HHCS) (see ref. 13 for references). Direct evidence for involvement of AVP in the physiological release of ACTH is, however, still lacking. The recent development of AVP receptor antagonists provides the opportunity to test this hypothesis directly. I report here that pretreatment by 1-deaminopenicillamine, 2-(O-methyl)tyrosine arginine-vasopressin (dPTyr(Me)AVP), a potent antagonist of the vasopressor, behavioural and ACTH-releasing properties of AVP, does not modify the ACTH and corticosterone secretion induced by exposure to a novel environment, but totally inhibits the increase of ACTH and corticosterone levels induced by AVP. The results do not support the hypothesis for a physiological involvement of AVP in ACTH release.
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PMID:The vasopressin receptor antagonist dPTyr (Me) AVP does not prevent stress-induced ACTH and corticosterone release. 630 Jun 79


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