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 role of calcium in the stimulation of ACTH secretion by CRF and other regulators was studied in rat anterior pituitary cells. Incubation of cultured pituitary cells in normal calcium with CRF, vasopressin, angiotensin II, or norepinephrine increased the rate of ACTH release for up to 45 min and then became constant for up to 3 h. In the absence of extracellular calcium, the initial rate of stimulated secretion was unaffected, but after 45 min the secretion rate decreased by 40% for CRF and to a greater extent for the other stimuli. Addition of calcium after 90 min in calcium-free medium restored the CRF-stimulated ACTH release rate to the control value. The absence of extracellular calcium had no effect on CRF-stimulated cAMP accumulation, but intracellular calcium depletion by preincubation of the cells with EGTA completely inhibited CRF-stimulated cAMP production and ACTH release. The voltage-dependent calcium channel antagonist nitrendipine and the calcium channel agonist BK 8644 had little effect on the CRF-stimulated ACTH release rate, while they, respectively, inhibited and enhanced the stimulation by vasopressin and high potassium. In calcium-depleted cells incubated with the calcium ionophore A23187, CRF stimulation of cAMP production and ACTH release were dependent upon extracellular calcium concentrations from 0.1-100 microM. These findings have defined two phases in the stimulation of ACTH release by CRF and cAMP-independent stimuli in cultured pituitary cells: an early phase with a rapid increase in the ACTH release rate which is independent of extracellular calcium, and a late phase of constant secretion rate, with partial extracellular calcium dependence for the stimulation by CRF and complete calcium dependence for the stimulation by non-cAMP-mediated stimuli.
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PMID:Calcium-dependent control of corticotropin release in rat anterior pituitary cell cultures. 244 83

Atrial natriuretic factor (ANF) is a humoral agent isolated in recent years from cardiac atrial tissue, and produced by atrial cardiocytes as a peptide precursor containing 152 amino acids. In secretory atrial granules, it is stored in reserve form as a prohormone and released into circulation as a 28-amino acid peptide from the C-terminal portion of the peptide precursor representing the active circulating hormone. ANF possesses potent natriuretic, myorelaxant, vasodilatory and blood pressure-lowering properties. Besides, it inhibits renin, aldosterone and vasopressin secretion. It is present also in the CNS and its function is closely related to the sympathetics nerves. By its direct renal and vascular effect, renin-angiotensin-aldosterone system and vasopressin inhibition and, by its neuromodulatory action on the central and sympathetic nerves, ANF plays an important role in electrolyte, volume and pressure homeostasis. The development of a radioimmunoassay for ANF determination in the plasma of rats and man enabled us to follow up its changes under various experimental conditions (water deprivation, increased or decreased salt intake, effect of anaesthetics, ontogenetic changes in ANF concentration during development of hypertension in the spontaneously hypertensive rat) and in clinical studies (effect of ECV expansion in controls, arterial hypertension, liver cirrhosis as well as ANF changes in congestive heart failure or chronic renal failure). These findings of ours have supported the concept that ANF represents an important adaptive and corrective mechanism mobilized during intravascular volume and blood pressure changes in an effort to normalize these. ANF is expected to find use also in the treatment of oedema, arterial hypertension and acute renal failure.
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PMID:Atrial natriuretic factor and its role in the regulation of electrolyte, volume and pressure homeostasis. 252 70

Water immersion (WI)-induced alterations of circulating plasma volume (PV), plasma renin activity (PRA), plasma levels of aldosterone (Ald), vasopressin (AVP) and atrial natriuretic peptide (ANP) were examined in 12 patients with noninflammatory acute renal failure (ARF) at the anuric/oliguric phase, in 20 hemodialyzed patients with chronic renal failure and in 15 healthy subjects. Patients with acute and chronic renal failure showed significantly elevated basal ANP concentrations (138.67 +/- 12.88 and 295.8 +/- 21.87 pg/ml, respectively) as compared with normals (74.54 +/- 4.1 pg/ml) and significantly elevated PRA (20.85 +/- 3.24 and 6.60 +/- 0.94 ng/ml/h, respectively versus 2.33 +/- 0.31 ng/ml/h), plasma levels of Ald (16.11 +/- 1.26 and 18.11 +/- 1.58 ng/dl, respectively versus 12.71 +/- 1.03 ng/dl) and AVP (6.95 +/- 0.62 and 6.08 +/- 0.54 pg/ml, respectively versus 2.68 +/- 0.48 pg/ml). After 2 hrs of WI a significant decline of PRA, Ald and AVP but an increase of ANP was noted in all examined groups. The absolute WI-induced increase in plasma ANP was significantly less marked in uremic patients than in normals. The endocrine profile of patients with ARF differed only quantitatively from that of patients with CRF both under basal and WI conditions. WI was followed by a significant increase of PV which was significantly more marked in patients with ARF (+ 16.42 +/- 1.73%) than in CRF (10.57 +/- 0.37%) and in normals (+11.3 +/- 1.6%). Only in healthy subjects a significant correlation was found between WI-induced changes of PV and ANP, PRA and Ald, and between PRA and AVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Water immersion-induced alterations of plasma atrial natriuretic peptide level and its relationship to the renin-angiotensin-aldosterone system and vasopressin secretion in acute and chronic renal failure. 252 41

The vasopressin binding to intact platelet from patients with chronic renal failure (CRF) was investigated in relation to the abnormalities in platelet aggregation. The immunoreactive arginine vasopressin (AVP) in platelet-free plasma (PFP) but not in platelets was significantly higher in non-dialyzed patients with CRF than in normal subjects. Binding studies using [3H]AVP demonstrated a decreased number of binding sites (Bmax) on platelets from patients with CRF compared to normal controls with no significant difference in affinity (Ka). A significant diminution of the maximal percentage aggregation with AVP was found in patients with CRF. An inverse relation between Bmax and the PFP AVP levels and a highly significant relation between Bmax and the maximal percentage aggregation with AVP in patients with CRF and normal controls were observed. At 4 weeks after the introduction of hemodialysis in patients with CRF, the PFP AVP levels decreased and Bmax increased significantly, and the maximal percentage aggregation tended to increase. The present findings suggest that a reduced number of AVP receptors on platelets might account for decreased platelet aggregation with AVP, and the elevated plasma AVP levels might induce a down-regulation of the AVP receptor number on platelets in patients with CRF.
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PMID:Platelet vasopressin receptor in patients with chronic renal failure. 253 88

Insulin administration to overnight fasted rats causes a dose-dependent decline in plasma glucose concentrations and a dose-dependent increase in plasma ACTH concentrations. The ACTH response, but not the glucose response, was blocked by treatment with chlorpromazine-morphine-pentobarbital, indicating that the main factors triggering the ACTH response are of central, rather than peripheral, origin. To study whether insulin affected the turnover of CRF and vasopressin (AVP) in the zona externa of the median eminence (ZEME), we determined the rate of decline of both hypophysiotropic factors in rats with or without blockade of axonal transport by colchicine. In the ZEME, the concentrations of CRF and AVP were assessed by quantitative immunocytochemistry (QICC) in tissue sections or by RIA in median eminence extracts. QICC allows selective quantification of AVP and other peptides within the ZEME. The changes in the CRF content, as measured by QICC and RIA, were linearly correlated (r = 0.99), demonstrating that changes in peptide-staining intensity reflect changes in peptide content. Colchicine, when given intracisternally in a nontoxic dose of 5 micrograms, had no marked effect on resting plasma levels of ACTH and only slightly reduced the ACTH response to insulin-induced hypoglycemia. In the ZEME, CRF and AVP concentrations at rest were not affected by colchicine. In colchicine-treated rats insulin-induced hypoglycemia resulted in a prominent decline in CRF and AVP concentrations in the ZEME. The CRF concentration declined at a rate of 23%/h over a period of 3 h. The AVP concentration declined to a similar extent as CRF over the first hour, but tended to fall at the later time points. We conclude that hypoglycemia increases turnover of both CRF and AVP in the ZEME. However, the turnover rates of both hypophysiotropic peptides do not appear to be quantitatively coupled.
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PMID:Hypoglycemia enhances turnover of corticotropin-releasing factor and of vasopressin in the zona externa of the rat median eminence. 254 3

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


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