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 effects of various neurogenic peptides and neurotransmitter substances on the release of ACTH induced by hypothalamic corticotropin releasing factor (HY-CRF) were investigated using monolayer cultured anterior pituitary cells. Test substances were given in combination with 0.05-0.1 hypothalamic extract (HE)/ml, because HE evoked a significant ACTH release and a linear dose response relationship was demonstrated sequentially between 0.0165 HE/ml and 0.5 HE/ml. Relative high doses of lysine-vasopressin showed a slight additive effect on the release of ACTH induced by 0.1 HE/ml. Leu-enkephalin, dopamine, prostaglandin E1 and E2 slightly reduced the release of ACTH induced by HY-CRF, but the inhibitory effect of these substances were not dose-related. Other tested substances including luteinizing hormone releasing hormone, thyrotropin releasing hormone, somatostatin, melanocyte stimulating hormone release inhibiting factor, beta-endorphin, neurotensin, substance P, vasoactive intestinal polypeptide, angiotensin II, norepinephrine, serotonin, acetylcholine, histamine and gamma-amino butyric acid showed neither agonistic nor antagonistic effect on the release of ACTH induced by HY-CRF. These results indicate that the release of ACTH is controlled specifically by HY-CRF and corticosterone, and modified slightly by some other substances such as vasopressin and prostaglandins, and that the effect of most other neurogenic peptides and neurotransmitter substances is negligible or non-physiological at the pituitary level.
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PMID:ACTH release in pituitary cell cultures. Effect of neurogenic peptides and neurotransmitter substances on ACTH release induced by hypothalamic corticotropin releasing factor (CRF). 3 43

Biologically active peptides and neurotransmitter substances were added to anterior pituitary cell cultures to examine the presence of corticotropin releasing factor (CRF)-like activity. Hypothalamic extract (HE) induced significant dose-related increase of ACTH, and the lowest effective dose was 0.01 HE/ml. Other tested substances including luteinizing hormone-releasing hormone, thyrotropin releasing hormone, melanocyte stimulating hormone release inhibiting factor, somatostatin, substance P, neurotensin, beta-endorphin. leu-enkephalin, met-enkephalin, bradykinin, norepinephrine, dopamine, serotonin, acetylcholine, histamine, gamma-amino butyric acid or gamma-hydroxy butyric acid showed no CRF-like activity. Relatively high doses of lysine vasopressin, arginine vasopressin and angiotensin II increased the release of ACTH in pituitary cell cultures, but the maximal ACTH response was markedly less than with HE. These results indicate that cultured anterior pituitary cells are sensitive and fairly specific in detecting CRF(s) comparing with other detecting procedures.
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PMID:Specificity of cultured anterior pituitary cells in detecting corticotropin releasing factor(s): the effect of biologically active peptides and neurotransmitter substances on ACTH release in pituitary cell cultures. 3 34

Obviously, the analysis of dynamic changes in the hypothalamic activity of corticotropin-releasing factor (CRF) is essential for understanding of the central regulatory mechanism of ACTH secretion. However, the significance of the changes in CRF activity will be extremely lessened if the effect of CRF per se be modified at the pituitary level. In fact, Yates et al. (1971) reported that the CRF effect was potentiated by the presence of vasopressin. Therefore, in this study we attempted first to determine if vasopressin does potentiate the CRF action. Next, we analyzed some aspects of CRF dynamics in the rat hypothalamus under prolonged stress. (1) Potentiation of CRF action by vasopressin. This possibility was examined by the following approaches: i) Adrenocortical responses to various mild stressors (exposure to sound, i.p. injection of saline solution, tail cut) were greater in dehydrated rats than in normal controls. ii) Similarly, the adrenocortical response to intravenous injection of stalk-median eminence extract (SME) through the tail vein under Nembutal anesthesia was larger in the dehydrated rat than in control. iii) Prior to SME administration, vasopressin in a subthreshold dose was injected intravenously to assay rats pretreated with chlorpromazine (CPZ)-morphine (M)-Nembutal (Nb). The adrenocortical response to SME, injected into the carotid artery 1 min later, was found significantly to increase due to prior administration of vasopressin. iv) However, no potentiating effect of vasopressin was observed when SME and vasopressin (4 mU) were placed stimultaneously into the anterior pituitary tissue by the intrapituitary injection technique. v) In addition, no potentiating effect was observed in vitro incubation experiments under varying incubation conditions. Thus, it was shown that vasopressin has some potentiating effect on the stress response in vivo, but the effect is not at the pituitary level. (II) Analysis of dynamic changes in hypothalamic CRF activity. CRF activity was estimated by the intrapituitary injection method of Hiroshige, the plasma ACTH and corticosterone levels being followed simultaneously. Plasma ACTH was determined by radioimmunoassay partly with RCC-RIA Kit, and partly with ACTH antisera (kindly supplied by Dr. W.F. Ganong) by the method of Berson and Yalow. i) In intact normal rats, the response pattern of hypothalamic CRF activity under etherlaparotomy stress was characteristically biphasic, i.e., composed of rapid and slow phases, while the plasma ACTH and corticosterone showed a sustained high level over a 2 hr of observation period.
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PMID:[Analysis of dynamics of corticotropin-releasing factor (CRF) activity in the rat hypothalamus under stress]. 18 25

Partial adrenocortical insufficiency as a result of an insufficiency of the hypothalamic corticotropin releasing factor (CRF) was demonstrated in a 53-year-old female patient. Somatotropic, gonadotropic and thyreotropic functions of the pituitary gland were shown to be normal by a simultaneous pituitary stimulation test. This held true especially for the adrenocorticotrophic function: administration of lysine-vasopressin induced a normal rise in immunoreactive plasma-ACTH. Thus, a pituitary defect as a primary cause of the disease could be excluded and evidence was provided that there was a lack in hypothalamic stimulae absence of elevated ACTH levels hyperpigmentation of the skin existed. Possible explanations are discussed.
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PMID:Adrenal insufficiency secondary to hypothalamic corticotropin releasing factor (CRF) insufficiency with hyperpigmentation: a case report. 18 35

The in vitro corticotropic releasing effects of vasopressin (VP) and hypothalamic median eminence (HME) extract were compared as a function of their concentration and preincubation and incubation times. Whereas HME extract augmented the ACTH secretion from non-preincubated adenohypophyses, VP released corticotropin from the pituitaries only after a 2 h preincubation period. The disappearance of endogenous VP during the preincubation time rendered the gland responsive. The maximal stimulation of ACTH secretion by VP was markedly less than that induced by HME extract. The results suggest the presence of VP receptor sites in the anterior pituitary (AP) which are probably different from the receptor sites of the hypothalamic corticotropin releasing factor (CRF).
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PMID:Comparative in vitro studies on corticotropin releasing activity of vasopressin and hypothalamic median eminence extract. 19 42

Features of several assays for corticotropin-releasing factor (CRF) were compared, with reference to sensitivity, precision, specificity and convenience. In general, in vivo assays are less specific, whereas in vitro assays with isolated pituitary cells appear to suffer from vulnerability. Promising approaches for overcoming this difficulty are appearing: one is the cell culture technique and the other is the perfusion of pituitary cell column. However, the findings with vasopressin are again discordant. So far, the in vivo-in vitro assay system appears to be the most satisfactory. In this connection, special emphasis was laid on the CRF assay by out intrapituitary injection technique through the parapharyngeal approach, which has features of both in vivo and in vitro systems. The drawbacks with this assay are its complexity and relatively lower precision. Problems of the use of dexamethasone are discussed from a viewpoint of possible multistage feedback inhibition, as postulated by Yates et al. Several findings on the CRF dynamics were mentioned, in order to exemplify the findings obtained with our assay: it was shown that the two-peaked changes of CRF after ether-laparotomy stress in adult rats were composed of heterogeneous components, as revealed by differential effect of cycloheximide. Pretreatment with cycloheximide similarly abolished the delayed CRF peak that was observed in 2-day-old neonatal rats under stress. These findings suggest an operation of a biochemical denominator in common with both cases.
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PMID:Assays and dynamics of corticotropin-releasing factor activity in rat hypothalamus. 21 12

Hypophysectomized rats bearing three transplanted pituitaries under the kidney capsule responded to synthetic lysine vasopressin or pitressin with a significant elevation of plasma corticosterone, whereas hypophysectomized rats with no grafts did not. This response was completely abolished by pretreatment of animals with dexamethasone but was unaltered by central hypothalamic destruction. Corticotropin-releasing factor content of the hypothalamic median eminence, hypophyseal stal-, or pars nervosa of the posterior pituitary of intact rats was unchanged 5 or 10 min after ip injection of vasopressin compared to the basal level. We conclude that vasopressin and dexamethasone act directly on the adenohypophysis in vivo to exert their stimulatory or inhibitory effect on ACTH secretion.
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PMID:Studies on the site of action of vasopressin in inducing adrenocorticotropin secretion. 21 60

Transverse sections of the median eminence from fetal and neonatal rats were examined by the immunoperoxidase technique to detect the presence of oxytocin, vasopressin and neurophysin. Neurophysin was observed in the 18-day fetus. Vasopressin and oxytocin were not detected until after birth, on the 4th and 8th days respectively. There was an accumulation of material crossreactive with neurophysin and vasopressin antibodies in the palisade layer of the median eminence between the 4th and 9th days after birth. This distribution of immunoreactive material in the palisade layer was suggestive of neurosecretory substances localized in two fibre tracts on either side of the median eminence. The data are consistent with the accumulation of corticotropin releasing factor and an associated neurophysin in this area. It is suggested that the accumulation of material occurs because of the relative immaturity of the capillary loops that constitute the primary plexus of the hypophysial portal system.
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PMID:Maturation of the hypothalamo-neurohypophysial system. II. Neurophysin, vasopressin and oxytocin in the median eminence of the developing rat brain. 31 38

ACTH and cortisol diurnal variations and responses to two types of stress (insulin-induced hypoglycemia and isolation-restraint stress) or to an acute injection of lysine-vasopressin were studied in intact and anti-corticotropin-releasing factor (CRF) actively immunized rams. Immunization was obtained by the injection of synthetic ovine CRF coupled to BSA with carbodiimide. All animals developed antibodies anti-CRF and displayed an alteration of their general condition and a body weight reduction. The mean basal ACTH and cortisol secretion as well as the number and mean amplitude of diurnal pulses of these hormones was significantly reduced in the group of anti-CRF immunized rams. However, the reduction in all three parameters was much more pronounced for cortisol than for ACTH. No ACTH and cortisol response to insulin-induced hypoglycemia and isolation-restraint stress was observed. The stimulating action of lysine-vasopressin on ACTH release was significantly reduced as compared to controls. These results indicate that CRF is a major physiological component of the ovine hypothalamo-hypophysial-adrenal axis and participates in the events that regulate ACTH and cortisol diurnal variations and response to stress.
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PMID:Effect of chronic active immunization anti-corticotropin-releasing factor on the pituitary-adrenal function in the sheep. 131 53

We evaluated whether the brain kallikrein-kinin system plays a role in the regulation of adrenocorticotropin (ACTH) release in rats. Intracerebroventricular (icv) injection of bradykinin (0.24 nmol) increased plasma immunoreactive ACTH (irACTH) levels (from 93 +/- 4 to 200 +/- 12 pg/ml, P less than 0.01). This effect was prevented by icv kinin antagonist at 15.4 nmol/h (from 98 +/- 5 to 108 +/- 6 pg/ml; not significant). The antagonist did not alter the increase in plasma irACTH levels induced by icv corticotropin-releasing factor (CRF), arginine vasopressin, or prostaglandin E2. Melittin (7 nmol/h icv) increased plasma irACTH from 95 +/- 4 to 268 +/- 7 pg/ml (P less than 0.01). This effect was prevented by icv kinin antagonist (15.4 nmol/h), kallikrein antibodies (13 pmol/h), or indomethacin (0.28 mmol/h). ACTH response to melittin was not altered by antagonists of CRF or vasopressin. Intra-arterial injection of insulin (0.3 IU/kg body wt) reduced plasma glucose levels to a similar extent in rats given icv kinin antagonist or vehicle; the ACTH response to insulin-induced hypoglycemia was slightly less in rats given kinin antagonist than in those given vehicle (55 +/- 5 vs. 86 +/- 4 pg/ml, P less than 0.05). The brain kallikrein-kinin system may play a role in the regulation of ACTH secretion in stimulated conditions.
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PMID:Role of brain kallikrein-kinin system in regulation of adrenocorticotropin release. 131 88


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