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 effect of drastic sodium chloride changes (performed by using low-Na diet + furanthril and high-Na diet) on renin-angiotensin-aldosterone system, vasopressin and renal prostaglandins was studied in normal subjects after inhibition of prostaglandin synthesis by indomethacin (0.35 mg/kg three times daily for 13 days). The purpose of the investigation was to evaluate the mechanism of prostaglandin-vasopressin interrelationship. Indomethacin inhibition of PG-synthesis was performed, and after high-Na provocation, an increase of vasopressin and cyclic AMP excretion by 15% and 376% more than that without indomethacin was found. Indomethacin by itself caused sodium retention and antidiuretic effect. The results confirmed the assumption that renal prostaglandins are modulators of renin release from the kidney and that they alternate vasopressin effect on urine concentration, most probably through adenylate cyclase-cAMP system.
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PMID:Humoral factors involved in the regulation of sodium-fluid balance in normal man. II. Effect of indomethacin on sodium concentration, renal prostaglandins, vasopressin and renin-angiotensin-aldosterone system. 609 12

This study was performed to examine an involvement of adenohypophysial arachidonic acid metabolites in the local mechanisms controlling the release of peptide hormones from the corticotrope cells of the anterior pituitary gland. Therefore, we investigated the effect of blockers of the lipoxygenase (nordihydroguaiaretic acid, NDGA), cyclooxygenase (indomethacin) or both of these enzyme systems (BW755C; eicosatetraynoic acid, ETYA) on the release of beta-endorphin-like (beta-E-IR) and adrenocorticotropin-like immunoreactivity (ACTH-IR) from rat anterior pituitary quarters incubated in vitro. NDGA and ETYA did not influence the basal release of beta-E- and ACTH-IR. However, upon stimulation by arginine-vasopressin (AVP) or synthetic ovine corticotropin-releasing factor (CRF(1-41], NDGA inhibited beta-E-IR release by 40%. ETYA inhibited AVP-induced release of beta-E- and ACTH-IR by 75%. Indomethacin and BW755C (lower concentration) enhanced beta-E-IR release, induced by AVP, by about 100%, whereas BW755C (higher concentration) had no effect. When indomethacin was present, NDGA, ETYA and BW755C (higher concentration) inhibited AVP-induced release of beta-E- and ACTH-IR. Prostaglandin E2 (PGE2) inhibited beta-E-IR release in response to AVP but failed to do so in the presence of NDGA. 12-OH-5,8,10,14-eicosatetraenoic acid (12-HETE) had no effect. When anterior pituitary quarters were incubated with 3H-arachidonic acid (3H-AA), NDGA and BW755C (higher concentration) but not indomethacin and BW755C (lower concentration) blocked the formation of a metabolite which co-migrated with 12-HETE on thin-layer chromatography.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin and adrenocorticotropin release from rat adenohypophysis in vitro: evidence for local modulation by arachidonic acid metabolites of the cyclooxygenase and lipoxygenase pathway. 609 88

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

Vasopressin causes relaxations of isolated basilar and left circumflex coronary arteries of the dog. After removal of the endothelium the inhibitory effect of vasopressin is abolished in the basilar and reduced in the coronary arteries. By contrast, vasopressin causes contractions of femoral arteries, which are not affected by the removal of endothelium. Indomethacin, nordihydroguaiaretic acid, atropine, propranolol and cimetidine do not reduce the inhibitory effect of vasopressin in basilar arteries. However, the V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP blocks the vasopressin-induced relaxations, indicating that the effect of the hormone on the endothelium is mediated by activation of specific V1-vasopressinergic receptors.
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PMID:Vasopressin induces endothelium-dependent relaxations of cerebral and coronary, but not of systemic arteries. 624 63

The role of prostaglandins in the regulation of renal function was studied in seven healthy female volunteers taking a constant metabolic diet containing 59 meq of sodium and about 50 meq of potassium daily. Each subject underwent two renal clearance studies, during which vasopressin (priming dose, 200 mU; "sustainer," 200 mU/hour at 1 ml/min) was infused intravenously. The first clearance study served as the control; indomethacin (2 mg/kg/day) was given for seven days before the second clearance study to inhibit prostaglandin synthesis. Food and fluid were withheld for 12 hours before the studies. Urine was collected through an indwelling bladder catheter at 30 minute intervals. Glomerular filtration rate was estimated from inulin clearance and renal blood flow from para-aminohippurate (PAH) clearance. Indomethacin was associated with a significant increase in maximal urinary osmolality from 826 +/- 47 mosmol/kg H2) to 920 +/- 32 mosmol/kg H2O (P < 0.01). Minimal "free water" clearance was -1.40 +/- 0.02 ml/min before and -1.63 +/- 0.04 ml/min (P < 0.01) after the administration of indomethacin. Indomethacin did not affect urine flow, urinary sodium or potassium excretion, glomerular filtration rate or renal plasma flow. In addition, indomethacin did not affect the urinary excretion of cyclic adenosine monophosphate (AMP). Plasma arginine-vasopressin, measured in two subjects by radioimmunoassay, did not change with blockade of prostaglandin synthesis. It appears that prostaglandins antagonize the hydro-osmotic effect of antidiuretic hormone by an intrarenal mechanism, independent of changes in renal hemodynamics or cation excretion. This mechanism is probably mediated by an alteration in the water permeability of the collecting ducts. Since urinary cyclic AMP did not change during blockade of prostaglandin synthesis, whereas urinary osmolality increased, a change of vasopressin-dependent cyclic AMP production in the kidney was probably not reflected in urinary cyclic AMP.
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PMID:The role of the prostaglandin system in the regulation of renal function in normal women. 625 59

The relationship of the vascular effect of captopril to angiotensin converting enzyme activity and prostaglandin-dependent mechanism was studied in rat isolated kidneys, perfused with Krebs-Henseleit at 20 ml/min per 2 kidneys, with basal perfusion pressures of 78 +/- 1 mm Hg (Mean +/- S.E.M.). Two doses of captopril were used; both low (0.05 microgram/ml) and high doses (5 microgram/ml) inhibited maximally the vasoconstrictor responses to 100 and 200 ng of angiotensin I. Captopril at the low dose did not affect the renal vasoconstrictor responses to norepinephrine (NE) (25-400 ng), whereas high-dose reduced the vasoconstriction to all doses of NE. Treatment with captopril tended to diminish dose-related release of prostaglandins in response to NE. Indomethacin (1 microgram/ml) prevented NE-induced release of bioassayable and radioimmunoassayable prostaglandins but did not affect the ability of captopril to reduce NE-induced vasoconstriction. High-dose captopril also decreased the vascular reactivity to angiotensin II (5 ng) and lysine vasopressin (10 mU); however, the renal vasoconstriction caused by PGE2 (80 ng) was unaffected by captopril. We conclude that high-dose captopril decreased vascular reactivity by a mechanism independent of converting enzyme inhibition and unrelated to a prostaglandin-dependent vascular mechanism.
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PMID:Captopril decreases vascular reactivity independently of changes in converting enzyme activity and prostaglandin release in the rat isolated kidney. 629 42

The calcium ionophore A23187 (IP) inhibited the antidiuretic hormone (ADH)-stimulated hydro-osmotic response in toad urinary bladder but had no effect on the osmotic transfer of water in the absence of hormone. Extracellular calcium was necessary for this effect at lower but not at higher IP concentrations. The hydro-osmotic response to exogenous cyclic AMP was unaltered by IP, but the same response produced by inhibition of phosphodiesterase was reduced significantly. Cyclic AMP concentrations in isolated toad bladder epithelial cells were reduced by 50% with IP or exogenous prostaglandin E2 (PGE2). Indomethacin, a prostaglandin synthesis inhibitor, prevented the inhibitory actions of the IP on the ADH-mediated response. Collectively, these observations suggest a key role for cellular calcium in modulating the actions of antidiuretic hormone and are consistent with the hypothesis that the ionophore, through increasing intracellular calcium, stimulates the synthesis of prostaglandins which have a negative feedback on adenylcyclase. This effect would terminate the action of the hormone.
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PMID:Role of calcium and prostaglandins in the antidiuretic hormone response. Effect of ionophore A23187. 630 7

Renal cortical prostaglandin synthesis, particularly by arterioles and glomeruli, is important to preserve renal blood flow (RBF) and glomerular filtration rate (GFR). Glomeruli and arterioles synthesize not only the vasodilatory prostaglandins PGE2 and PGI2, but also the vasoconstrictor, thromboxane A2. The primary renal cortical actions of these prostaglandins are renal vasodilatation and maintenance of GFR (PGE2 and PGI2) or renal vasoconstriction and reduction of GFR (thromboxane A2). Vasodilatory renal prostaglandins are relatively unimportant under normal circumstances but play a modulatory role after ischemia or in the presence of increased concentrations of vasoconstrictor substances such as angiotensin II (ANG II), vasopressin or norepinephrine. ANG II and vasopressin stimulate the synthesis of PGE2 in rat glomerular epithelial and mesangial cells maintained in cell culture. These stimulatory actions of constrictor peptides are dependent upon calcium entry into the cells since removal of extracellular calcium or co-incubation with verapamil or nifedipine block the prostaglandin stimulatory capacity of ANG II or vasopressin. In vivo indomethacin potentiates the actions of ANG II on the kidney, particularly the reduction of RBF and GFR. Isolated rat glomeruli contract in response to ANG II and this contractile effect, which reflects reduction in glomerular filtration surface area, can be potentiated by cyclooxygenase blockade. Conversely, arachidonic acid reduces the glomerular contractile effect of ANG II. The importance of renal prostaglandins in support of RBF and GFR has been studied in dogs after chronic bile duct ligation (CBDL). CBDL dogs have significant increase in renal PGE2 and PGI2 which maintain RBF and GFR since cyclo-oxygenase inhibition resulted in a 50% decrease in both RBF and GFR. Indomethacin, ibuprofen, naproxen, and sulindac sulfide had comparable effects. The pro-drug, sulindac sulfoxide, was tested in normal volunteers and found to spare renal prostaglandin synthesis whereas indomethacin reduced renal synthesis of PGE2 and PGF2 alpha by more than 50%. In vitro, sulindac sulfide is a potent inhibitor of renal prostaglandin synthesis by kidney cells in culture. It is, therefore, concluded that renal prostaglandins play an important vasoregulatory role. Furthermore, sulindac sulfoxide may spare renal cyclo-oxygenase and thereby preserve renal function.
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PMID:Mechanisms of the nephrotoxicity of non-steroidal anti-inflammatory drugs. 659 99

The increased renal sodium and water excretion after an intravenous infusion of Ringer solution has been investigated in anaesthetized dogs. The response of the kidneys has been examined in four combinations. The functional parameters of renal function have been compared during volume expansion by 1.5-2.0% body weight Ringer solution and overhydration by 2.5% Ringer solution for 60 min. In the control animals, volume expansion by 2% body weight Ringer solution resulted in a significant increase in sodium excretion and urine flow. When these animals were infused with 2.5% body weight Ringer solution a marked increase in water excretion was observed with a smaller increment in sodium excretion, and the urine became hypo-osmotic as compared to the plasma. No difference was found in glomerular filtration rate and PAH clearance. In the group No. 2, the effect of 4 mg/kg indomethacin infusion was studied. The inhibition of prostaglandin synthesis considerably reduced the diuretic effect of Ringer infusion and did not affect sodium excretion. In the group No. 3, the animals received lysine-8-vasopressin i.v. in a preliminary dose of 10 mU/kg during 10 min and then 50 mU/kg over 60 min in infusion. Volume expansion with 2.5% body weight of Ringer solution resulted in a marked increase in sodium and water excretion but no difference was found in glomerular filtration rate and PAH clearance. Dilution of the urine i.e. a decrease of urinary osmolarity, in spite of the vasopressin infusion, was significantly higher in this group than in the control animals (group No. 1). In the fourth series, after 4 mg/kg of indomethacin the same dose of vasopressin was administered as in group No. 3. Indomethacin was observed to inhibit the diuretic effect of vasopressin and did not affect the saluretic effect. From these data it was concluded that medullary tonicity affected renal water handling during extracellular isosmotic hypervolaemia induced by Ringer infusion. This mechanism depends on medullary prostaglandin synthesis and is independent from the plasma vasopressin concentration. Our findings clearly indicate that extracellular hypervolaemia increases renal sodium excretion and lysine-8-vasopressin was found to potentiate this effect. This sodium excretion increasing mechanism does not depend on renal prostaglandin secretion, nor were glomerular factors responsible for the increase of sodium and water excretion.
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PMID:Inhibition of prostaglandin synthesis and the action of vasopressin during extracellular volume expansion in the dog. 665 Jan 87

1. The renal vascular responses to the peptide hormones angiotensin II (ANG II), arginine-vasopressin (AVP) and bradykinin (BK) were studied in anaesthetized rats with flow-meter techniques. The contribution of prostaglandins (PG) to their renal vascular effects was assessed with the aid of the PG-synthesis inhibitor indomethacin. 2. ANG II and AVP induced a dose-dependent increase in renal vascular resistance (RVR). The renal vasoconstrictor effects of both peptides were significantly augmented in rats pretreated with indomethacin. Indomethacin alone induced an increase in RVR, but not in mesenteric vascular resistance (MVR). 3. BK in low doses (1 micrograms/kg . min) tended to decrease RVR but increased RVR in high doses (20 micrograms/kg . min). MVR was reduced after all doses. The renal vasoconstrictor effect of BK was not affected by the ANG II-antagonist saralasin but almost completely blocked by indomethacin. 4. These results suggest that in the rat, as in other animal species and in man, renal PG's attenuate the renal effects of vasoconstrictor hormones such as ANG II and AVP. Although it has no such effect in other species. BK in high doses induces renal vasoconstriction in the rat, which appears also to be mediated by PG's. This response might be peculiar to the rat, since PG's act as renal vasodilators in other species.
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PMID:Renal vascular effects of angiotensin II, arginine-vasopressin and bradykinin in rats: interactions with prostaglandins. 682 26

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