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)

We have examined the actions and interactions of arginine vasopressin (AVP), angiotensin-II (AII), and oxytocin (OT) on the ACTH secretory response of dispersed rat anterior pituitary cells in a microperifusion system. There was a dose-dependent ACTH secretory response to a 3-min perifusion of AII which reached its maximum 10 sec after the cells were exposed to AII and fell rapidly to baseline within 2 min, despite continued infusion of AII. This brief spike type of pattern is similar to that produced by AVP, but different from the sustained plateau response induced by CRF. The threshold stimulating concentration of AII was about 10(-9) M; the maximally stimulating concentration was not defined, but was 10(-6) M or more. The initial ACTH response to OT was similar, but fell to a plateau 2 min after the cells were exposed to OT and remained constant until perifusion with OT was stopped, after which it fell rapidly to baseline. The threshold stimulating concentration of OT was 10(-8) M; the maximally stimulating concentration was not defined, but was 10(-6) M or more. The ACTH secretory response to 10(-8) M AII was greatly diminished when cells were exposed to 10(-6) AVP or 10(-6) M OT before AII infusion. However, prior exposure to AII had no effect on the magnitude of the ACTH secretory response to either AVP or OT. The effects of simultaneous perifusion of AII and AVP and of AII and OT were additive. When AVP and OT were perifused sequentially, the ACTH secretory response to the peptide that was infused second was completely abolished. Furthermore, the combination of AVP and OT stimulated no greater response than either agent alone. When cells were perifused with the combination of 10(-7) M OT and 10(-7)- to 10(-5)-M concentrations of two potent AVP V1 receptor antagonists, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]-Arg8-vasopressin and [1-deaminopenicillamine-2-(O-methyl)tyrosine]-Arg8-vasopressin, both phases of the response to OT were progressively and almost completely inhibited. The initial spike phase was inhibited at lower antagonist concentrations than the sustained plateau phase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Kinetic actions and interactions of arginine vasopressin, angiotensin-II, and oxytocin on adrenocorticotropin secretion by rat anterior pituitary cells in the microperifusion system. 255 32

Plasma concentrations of adrenocorticotrophin (ACTH) and cortisol were measured during insulin-induced hypoglycemia and lysin-8-vasopressin (LVP) test in 60 healthy subjects, non-smokers and habitually smokers of 10 or more cigarettes/24 hours. A marked and statistically significant rise of both hormones was found in non-smoker subjects, whereas smokers showed poor and not significant modifications. These results suggest that continuous chronic inhalation of nicotine may act as a powerful stimulus on the hypothalamo-hypophyseal structures that control the hypothalamic CRF and/or ACTH production and release. Central nervous mechanisms of hormonal regulation may become less sensitive and efficient when an acute rise of ACTH is required, as during stimulating tests. Our investigation confirms that cigarette smoking is heavily responsible of endocrine disorders, in particular of hypophyseal-adrenal axis.
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PMID:[Effect of smoking on the hypophyseo-adrenal axis]. 255 87

The role of protein kinase C (PKC) on vasopressin (VP) action was investigated by inhibition of endogenous PKC using prolonged incubation of the cells with phorbol ester, and by direct measurement of PKC activity in pituitary cells. Preincubation of the cells for 6 h with 100 nM TPA at 37 C resulted in a 90% decrease in total PKC activity. In the PKC-depleted cells, cAMP responses to stimulation with 100 nM CRF for 30 min were normal, but the potentiating effects of VP and PMA on CRF-stimulated cAMP production were abolished. The stimulation of ACTH secretion by VP and PMA alone was also abolished in PKC- depleted cells. PKC activity in cytosolic and detergent-solubilized membrane fractions from enriched pituitary corticotrophs obtained by centrifugal elutriation, was directly measured by enzymatic assays and by immunoblotting techniques. Basal PKC activity was higher in the cytosol than in the membranes (8.43 +/- 0.47 and 1.93 +/- 0.11 pmol 32P incorporated/10 min, respectively). After incubation of the cells with VP for 15 min or [3H] phorbol-12-myristate-13-acetate (PMA) for 30 min, PKC activity in cytosol was decreased by 40% and 89%, respectively, while the activity in the membrane was increased by 138% and 405%, respectively. Such VP- and PMA-induced translocation of PKC was also observed when the enzyme content in the cytosol and the membranes was measured by immunoblotting using a specific anti-PKC antibody and [125I]protein A. Autoradiographic analysis of immunoblots revealed an 80 kilodalton band characteristic of PKC, with OD higher in the cytosolic than in the membrane fractions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protein kinase C mediates the effect of vasopressin in pituitary corticotrophs. 256 Aug 4

The cytoarchitecture and immunocytochemical distribution of neuropeptides (corticotropin-releasing factor, CRF; neuropeptide Y, NPY; oxytocin, OXY; vasopressin, VP; and vasoactive intestinal polypeptide, VIP) were studied in the hypothalamic suprachiasmatic nuclei (SCN) in male and female ground squirrels of two species (Spermophilus tridecemlineatus and S. richardsonii). Immunoreactive (IR) perikarya were found in sections incubated with VP or VIP antisera. VP-IR cell bodies were seen in the dorsal and medial parts of the nucleus in colchicine-treated animals. IR fibers were distributed throughout the SCN. In the ventral part of the nucleus, VIP-IR cells were seen in untreated animals and were more pronounced in colchicine-treated animals. VIP-IR fibers and terminals form a dense plexus throughout the nucleus. Furthermore, NPY-IR terminals and fibers with multiple varicosities, but no IR perikarya, were present in the suprachiasmatic nuclei. Within the borders of the SCN, no cell bodies or fibers were stained with CRF or OXY antisera in any animal.
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PMID:Immunohistochemical evidence for the presence of neuropeptides in the hypothalamic suprachiasmatic nucleus of ground squirrels. 258 47

Luteinizing hormone is the major regulator of Leydig cell differentiation and steroidogenic function. A number of hormones produced by the Leydig cell (e.g. estrogen, angiotensin, CRF, vasopressin) and the tubular compartment (inhibin, TGF beta), can influence both acute and long-term actions of LH. Conversely, hormones produced in the Leydig cells modulate tubular function (e.g. androgen, beta-endorphin, oxytocin). The LH stimulatory event can be negatively influenced by the action of angiotensin II through the guanyl nucleotide inhibitory unit of adenylate cyclase. We have recently discovered an action of corticotrophin releasing hormone through specific high-affinity low-capacity receptors in the Leydig cells which involves a pertussis toxin insensitive guanyl nucleotide regulatory unit with interaction between signalling pathways and resulting inhibition of LH induced cAMP generation and consequently of steroidogenesis. In contrast to other tissues the CRF receptor in the Leydig cells did not couple to Gs. CRF action is exerted through direct or indirect action of protein kinase C, at the level of the catalytic subunit of adenylate cyclase. Physiological increases in endogenous LH cause positive regulation of membrane receptors and steroidogenesis, while major elevations in circulating gonadotropin can induce down-regulation of LH receptors and desensitization of steroid responses in the adult cell. Gonadotropin-induced desensitization in adult rat tests include an estrogen mediated steroidogenic lesion of the microsomal enzymes 17 alpha-hydroxylase/17,20-desmolase. For further understanding of the regulation of this key enzyme of the androgen pathway the rat P450(17) alpha cDNA was cloned and sequenced. This cDNA expressed in COS-1 cells 17 alpha-hydroxylase/17,20-desmolase activities. From the deduced amino acid sequence, two transmembrane regions were identified, a signal peptide for insertion in the ER, and a 2nd transmembrane region separated from the first by 122 amino acids. The carboxy terminal non-transmembrane region possesses 4 hydrophobic clefts, of which cleft II would contain the putative steroid binding site for both hydroxylase and lyase activities. The rat cDNA was employed to evaluate the hormonal regulation of mRNA levels in adult and fetal Leydig cells. Low dose hCG treatment caused an early increase in mRNA levels followed by a return to control values at later times, while with higher desensitizing doses the initial increase in mRNA was followed by a marked reduction in mRNA at 24 h and a small recovery at 48 h. Fetal rat Leydig cells treated with E2 showed a 70% decrease in P450 mRNA levels, and testosterone production closely followed the changes in mRNA.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:LH action in the Leydig cell: modulation by angiotensin II and corticotropin releasing hormone, and regulation of P450(17) alpha mRNA. 269 45

The effect of lactation on stress-induced hormone responses and changes in hypothalamic mRNA was assessed in female rats. In control animals the stimulus of ip hypertonic saline resulted in increased plasma levels of corticosterone, oxytocin, and vasopressin and hypothalamic content of CRF and enkephalin mRNA. In lactating females, however, the corticosterone response to this stress failed to reach significance, the plasma oxytocin response was markedly reduced, and the vasopressin response was unaffected. Lactation also resulted in an abolition of the CRF and enkephalin mRNA responses to stress. In contrast, the hypothalamic CRF response to adrenalectomy was unaffected by lactation status. Removal of the pups from their mothers resulted in a return of CRF and enkephalin mRNA responses to stress within 2 days. Lactation is associated with a selective inhibition of normal hypothalamic stress responses.
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PMID:Lactation inhibits stress-mediated secretion of corticosterone and oxytocin and hypothalamic accumulation of corticotropin-releasing factor and enkephalin messenger ribonucleic acids. 278 27

We examined the effect of neurohypophysectomy with and without vasopressin replacement on the ACTH response to hypotension and ovine CRF infusion and on the adrenocortical response to ACTH and angiotensin II infusion in conscious dogs. Nitroprusside hypotension (decrease in mean arterial pressure of 25 mm Hg) in the intact state resulted in large increases in plasma arginine vasopressin (pAVP; from 2.6 +/- 0.3 to 296 +/- 63 pg/ml) and ACTH (from 35 +/- 6 to 395 +/- 92 pg/ml). Neurohypophysectomy resulted in greatly attenuated pAVP (8.4 +/- 1.6 pg/ml) and ACTH (80 +/- 10 pg/ml) responses to hypotension which were not normalized by physiological low dose vasopressin replacement (6-18 pg/kg.min continuously, iv, for 2 weeks). However, acute administration of vasopressin (4-6 ng/kg.min) simultaneously with hypotension in the neurohypophysectomized (neurohypox) dog, which produced pAVP levels equivalent to the hypotensive response to intact dogs, almost completely normalized the ACTH response to hypotension (to 248 +/- 74 pg/ml). The ACTH response to 20 ng/kg.min ovine CRF, iv (from 43 +/- 8 to 268 +/- 77 pg/ml), was not attenuated by neurohypophysectomy. The cortisol responses to infusion of 0.5 and 2 ng/kg.min ACTH-(1-24), iv, were essentially normal in neurohypox dogs. However, the ACTH and aldosterone responses to 5 ng/kg.min angiotensin II infusion iv were attenuated in neurohypox dogs off AVP replacement. Histological examination revealed normal adrenal glands and anterior pituitaries in neurohypox dogs. Immunocytochemical staining for vasopressin and neurophysin revealed normal cell bodies in the paraventricular and supraoptic nuclei of the hypothalami from neurohypox dogs. However, median eminence staining for AVP and neurophysin was greatly diminished in neurohypox dogs. In summary, neurohypophysectomy 1) attenuated the ACTH response to hypotension and angiotensin II, but not to CRF, and 2) attenuated the aldosterone response to high dose angiotensin II. Furthermore, the deficit in ACTH secretion was almost completely normalized by increasing plasma AVP levels to those observed in the intact dogs. We conclude that an action of circulating pAVP increases ACTH secretion by a direct effect at the pituitary and by activating afferent input to the hypothalamus.
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PMID:Control of adrenocorticotropin secretion and adrenocortical sensitivity in neurohypophysectomized conscious dogs: effects of acute and chronic vasopressin replacement. 283 Oct 29

Control of ACTH secretion in the pituitary in the absence of target cells for CRF, the most potent ACTH secretagogue, was studied in dissociated bovine anterior pituitary cells treated with a potent selective cytotoxin. The cytotoxin is a conjugate of the CRF analog [Nle21,38, Arg36]rat (r) CRF and the plant toxin gelonin. Dissociated bovine anterior pituitary cells were pretreated with vehicle, 2 nM ovine CRF, 2 nM cytotoxic conjugate, or unconjugated [Nle21,38,Arg36]rCRF and gelonin in amounts equivalent to that of 2 nM cytotoxic conjugate for 12 h, then extensively washed and cultured for 3 days before acute secretion experiments. Unstimulated ACTH secretion was similar in all groups. ACTH secretion in response to CRF was attenuated by pretreatment with the cytotoxic conjugate; CRF (2.5 nM)-stimulated secretion was 7.0, 6.3, and 2.8 times the unstimulated rate in cells pretreated with vehicle, 2 nM CRF, or 2 nM cytotoxic conjugate, respectively. Likewise, the ACTH secretory response to a cAMP analog was attenuated by pretreatment with the conjugate; 8-bromo-cAMP (10 mM)-stimulated secretion was 6.8, 7.1, and 3.3 times the unstimulated rate in cells pretreated with vehicle, CRF, or conjugate, respectively. In contrast, the ACTH responses to vasopressin (VP) or oxytocin (OR) remained intact. VP stimulated the ACTH secretion rate by 4.2, 4.0, and 3.5 times, respectively, in the three groups. OT stimulated the ACTH secretion rate by 2.7, 2.6, and 2.3 times in the three groups. Pretreatment with the conjugate attenuated the response to CRF and VP in combination by the same amount as it attenuated the response to CRF alone. The ACTH secretory responses in cells pretreated with unconjugated [Nle21,38,Arg36]rCRF and gelonin were not different from responses in cells pretreated with vehicle. These results suggest that there is a separate mechanism or cell type for OT- and VP-stimulated ACTH secretion distinct from that responsible for the action of CRF on pituitary cells.
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PMID:Dissociation of the adrenocorticotropin secretory responses to corticotropin-releasing factor (CRF) and vasopressin or oxytocin by using a specific cytotoxic analog of CRF. 283 Oct 39

The hypothalamo-pituitary-adrenal axis is controlled by complex regulatory mechanisms. Numerous factors such as CRF, vasopressin, oxytocin, angiotensin II and conceivably other hormones--all controlled by various substances acting on central locations--stimulate the release of the stress hormone ACTH. On the other hand, glucocorticoids inhibit the secretion of ACTH by acting at the hypothalamic and/or pituitary level. The release of ACTH is therefore the final outcome of the interactions between the hypothalamus, the adrenal gland and possibly other organs. The multimolecular nature of the factors responsible for the control of the pituitary-adrenal axis is an attractive hypothesis because of the great variety of stress stimuli. The various factors could have specific roles in various stress situations. They provide a highly sensitive mechanism regulating very finely the stress hormone in response to a whole variety of endogenous and exogenous stimuli. Depending on the type of stress, they may therefore singly or in combination affect the amount and duration of ACTH and steroid secretion. The released glucocorticoids may then produce their numerous effects on inflammatory and immunological processes, carbohydrate metabolism, shock and water balance. It has been postulated that these effects may be important in order to prevent host responses from over-reacting to stress and threatening homeostasis. However, proof of the necessity of the glucocorticoid hypersecretion in response to stress remains elusive.
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PMID:Stress and the pituitary-adrenal axis. 283 73

A 71-year-old man was referred to Tokai University Hospital because of cold intolerance, slow speech and slowing down of his intellectual and motor activities. Free thyroxine index, and free T-4 and T-3 levels were low (1.4, 0.7 ng/dl and 0.4 ng/ml, respectively) with normal TSH (2.5 microIU/ml). A skull X-ray showed enlargement of the sella turcica and his CT scan revealed an intrasellar mass. LH, FSH, ACTH and PRL did not rise in response to the intravenous administration of LH-RH and insulin. A diagnosis of pan-hypopituitarism due to a pituitary tumor was established. The release of ACTH and cortisol was restored under stimulation of CRF or lysine vasopressin. TSH responded to TRH in a delayed manner. The pituitary tumor was removed by a transsphenoidal operation and diagnosed histologically as craniopharyngioma. Our hospital has experienced nine cases of craniopharyngioma in the last 10 years but the present case was the only intrasellar craniopharyngioma.
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PMID:A case of intrasellar craniopharyngioma. 283 33


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