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)

Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the enzyme cyclooxygenase and thereby block the prostaglandin (PG) synthesis in the kidneys. In animals, PG interferes with the formation of aquaporin 2 in the distal renal tubules. The purpose was to measure the effect of ibuprofen on urinary excretion of aquaporin-2 (u-AQP2), urinary output, urinary osmolality (u-osm) and plasma concentration of vasopressin (AVP) in a dose-response study using placebo and ibuprofen 600mg and 1200mg. In 12 healthy subjects, urine was collected in 6 periods between 07.00 h and 13.00 h, and blood samples were drawn at 60-min intervals. The study medication was given 10 h and 1 h before the study. U-AQP2 and AVP were determined by radioimmunoassays. U-AQP2 decreased 33% in the placebo group and increased 47% in the ibuprofen groups. There was a highly significant difference between the placebo group, on the one hand, and the ibuprofen groups, on the other. There was a small but significant increase in AVP in the placebo group and the 600 mg ibuprofen group, but not in the 1200 mg ibuprofen group. Urinary output was at maximum after 2 h, with a 394%, 1020% and 714% increase for placebo, 600 mg ibuprofen and 1200 mg ibuprofen, respectively. U-osm decreased during the experiment in all three groups. Inhibition of renal prostaglandin synthesis by ibuprofen affects the distal part of the nephron by increasing u-AQP2. This increase was not related to changes in AVP, urinary output or urinary osmolality. We suggest that the increased excretion of AQP2 can be explained by an increase in the ratio of AQP2 that is shed into the urine because the endocytic retrieval of AQP2 from the apical membrane is impaired. This could not be revealed by changes in the osmoregulatory system by the low doses of ibuprofen used in the present study.
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PMID:Effect of an acute oral ibuprofen intake on urinary aquaporin-2 excretion in healthy humans. 1176 23

Vasopressin is a potent renal vasoconstrictor in vitro which elicits relatively minor renal vascular effects in vivo. Efficient modulation might occur through shear stress-elicited release of vasodilator compounds from endothelial cells. The aim of this study was to evaluate in vitro, in the isolated perfused kidney, the influence of shear stress and related nitric oxide (NO) release on basal renal vascular tone and on vasopressin-induced renal vasoconstriction. Rat kidneys were perfused at a constant flow rate of 8 ml/min with Tyrode's solution (relative viscosity eta=1) or, in order to increase shear stress, with Tyrode's solution supplemented with 4.7% Ficoll 400 (Ficoll 400; eta=2.3), which is representative of the relative viscosity found in small vessels. Renal shear stress was further elevated during vasoconstriction elicited by vasopressin. Basal renal true vascular conductance, which reflects mean blood vessel radius, was 2.5-fold higher and overall wall shear stress doubled in Ficoll 400 - as compared to Tyrode-perfused kidneys. The decrease in vascular conductance elicited by NO synthase inhibition with N(omega)-nitro-L-arginine (L-NNA) increased with the viscosity of the perfusate. Shear stress was elevated during vasopressin-induced renal vasoconstriction, all the more kidneys were Ficoll 400-perfused. In these kidneys, the concentration-response curve to vasopressin was shifted to the right, giving evidence of hyporeactivity to the peptide. L-NNA potentiated vasoconstriction to vasopressin particularly in Ficoll 400-perfused kidneys, although additional inhibition of cyclooxygenase and/or cytochrome P(450) was without effect. These results provide in vitro evidence that shear stress enhanced by perfusate viscosity increases basal renal vascular conductance by an NO-dependent mechanism. Together with shear stress enhanced during vasoconstriction, it blunts vasopressin-induced renal vasoconstriction.
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PMID:Shear stress modulates vasopressin-induced renal vasoconstriction in rats. 1244 97

The present study was designed to characterize the vasopressin receptor subtype involved in the vasopressin-induced activation of the central sympatho-adrenomedullary outflow using urethane-anesthetized rats. Intracerebroventricularly (i.c.v.) administered vasopressin (0.1, 0.2 and 0.5 nmol/animal) dose-dependently elevated plasma levels of adrenaline and noradrenaline (adrenaline>noradrenaline). The vasopressin (0.2 nmol/animal)-induced elevation of both catecholamines was significantly attenuated by [d(CH(2))(5)(1),Tyr(Me)(2),Arg(8)]-vasopressin, a selective vasopressin V(1) receptor antagonist, in a dose-dependent manner (0.1 and 0.2 nmol/animal, i.c.v.). The same doses (0.1 and 0.2 nmol/animal, i.c.v.) of [1-adamantaneacetyl(1),D-Tyr(Et)(2),Val(4),Abu(6), Arg(8,9)]-vasopressin, a potent vasopressin V(2) receptor antagonist, had no effect; however, a large dose of this antagonist (1.6 nmol/animal, i.c.v.) effectively reduced the vasopressin-induced elevation of catecholamines. On the other hand, [5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tetrahydro-1H-benzazepine], a selective vasopressin V(2) receptor antagonist (5 and 10 nmol/animal, i.c.v.), had no effect on the vasopressin-induced elevation of catecholamines. The vasopressin-induced elevation of catecholamines was abolished by indomethacin, an inhibitor of cyclooxygenase (1.2 micromol/animal, i.c.v.). These results suggest that the vasopressin activates the central sympatho-adrenomedullary outflow by brain vasopressin V(1) receptor- and cyclooxygenase-dependent mechanisms in rats.
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PMID:Vasopressin V(1) receptor-mediated activation of central sympatho-adrenomedullary outflow in rats. 1246 Jun 40

The isometric response to vasopressin of 2-mm-long segments of basilar, coronary, renal and tail arteries from male and female, control (normoglycemic) and streptozotocin-induced diabetic rats was studied. Vasopressin (10(-12)-3 x 10(-8) M) produced arterial concentration-dependent contraction, with a lower potency in coronary arteries from female than from male rats, and was similar for both genders in basilar, renal and tail arteries. This contraction was reduced by diabetes in basilar and coronary arteries, increased in renal arteries, and not modified in tail arteries, in both genders. Inhibition of nitric oxide synthesis with N(W)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) increased the contraction to vasopressin in coronary arteries from control female and diabetic female rats; as well as in renal arteries from control male and control female rats, but not in any other experimental group. Inhibition of cyclooxygenase with meclofenamate (10(-5) M) reduced the contraction to vasopressin in basilar arteries from diabetic female rats and in renal arteries from diabetic male rats, but not in any other experimental group. These results suggest that the response to vasopressin (a) has lower potency in female coronary arteries due to higher nitric oxide production; (b) is reduced by diabetes in basilar and coronary arteries from both genders, by mechanisms independent of nitric oxide and prostanoids; and (c) is increased by diabetes in renal arteries due to reduced production of nitric oxide in females, and to both reduced production of nitric oxide and increased production of prostanoids in males. Therefore, the effects of diabetes on vascular reactivity to vasopressin may differ between vascular beds, and the mechanisms underlay these effects may be distinct between genders.
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PMID:Vascular reactivity to vasopressin during diabetes: gender and regional differences. 1252 53

The aim of the present study was to determine the effect of social stress and significance of prostaglandins (PG) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by corticotropin releasing hormone (CRH) under basal and social crowding stress conditions. The stressed rats were crowded in groups of 24 to a cage for 3 or 7 days, whereas the control animals were haused in groups of 7 to a cage of the same size. The activity of HPA axis was determined by measuring plasma ACTH and serum corticosterone levels 1 h after i.p. CRH administration. Inhibitors of COX-1, piroxicam (0.2, 2.0, and 5.0 mg/kg), and COX-2, compound NS-398 (0.2 and 2.0 mg/kg), were administered i.p. 15 min prior to CRH (0.1 microg/kg i.p.) to control or crowded rats. The obtained results indicate that social stress for 3 and 7 days markedly intensifies the stimulatory action of CRH on ACTH secretion. Neither piroxicam nor NS-398 induce any significant effect on the CRH-elicited ACTH and corticosterone secretion in non-stressed or crowded rats. Therefore, PG generated by COX-1 or COX-2 do not participate to a significant extent in the stimulation of HPA axis by CRH under either basal conditions or during crowding stress. These results also indicate that the stimulatory action of CRH on ACTH secretion is not only completely resistant to desensitization but is sensitized during social crowding stress. The results contrast with a significant involvement of PG in the vasopressin-induced stimulation of HPA response during crowding stress.
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PMID:Effect of cyclooxygenase inhibitors on the CRH-induced pituitary-adrenocortical activity during crowding stress. 1267 22

Plasma noradrenaline reflects the release from adrenal medulla and sympathetic nerves; however, the exact mechanisms of adrenal noradrenaline release remain to be elucidated. The present study was designed to characterize the source of plasma noradrenaline induced by centrally administered vasopressin and corticotropin-releasing hormone (CRH) in urethane-anesthetized rats. Intracerebroventricularly administered vasopressin (0.2 nmol/animal) and CRH (1.5 nmol/animal) elevated plasma levels of noradrenaline and adrenaline. Intracerebroventricularly administered indomethacin [1.2 micromol (500 microg)/animal] (an inhibitor of cyclooxygenase) abolished the elevations of both noradrenaline and adrenaline induced by vasopressin and CRH. Intracerebroventricularly administered furegrelate [1.8 micromol (500 microg)/animal] (an inhibitor of thromboxane A(2) synthase) abolished the elevations of both noradrenaline and adrenaline induced by vasopressin, while the reagent only attenuated the elevation of plasma adrenaline evoked by CRH. Acute bilateral adrenalectomy abolished the elevation of both noradrenaline and adrenaline induced by vasopressin, while the procedure reduced only the elevation of adrenaline induced by CRH. These results suggest that the release of noradrenaline from adrenal medulla and sympathetic nerves is mediated by different central mechanisms. The vasopressin-induced noradrenaline release from adrenal medulla is mediated by brain thromboxane A(2)-mediated mechanisms, while the CRH-induced noradrenaline release from sympathetic nerves is mediated by brain prostanoid (other than thromboxane A(2))-mediated mechanisms. The vasopressin- and CRH-induced adrenaline release from adrenal medulla is also mediated by brain thromboxane A(2)-mediated mechanisms in rats.
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PMID:Role of brain thromboxane A2 in the release of noradrenaline and adrenaline from adrenal medulla in rats. 1270 65

The antagonism between prostaglandin and vasopressin represents a classic negative feedback loop. It is not clear whether cyclooxygenase (COX)-2 and/or COX-1 expression is involved in elevated prostaglandin production stimulated by vasopressin in vivo. In the present study, we explored vasopressin regulation of medullary COX-2 and COX-1 expression acutely and chronically in rats. Medullary COX-1 expression was moderately lower and COX-2 expression was significantly lower in adult male Brattleboro rats than age-matched Long-Evans controls. Chronic treatment of Brattleboro rats with vasopressin for 1 wk led to a decrease in urine volume and a moderate increase in medullary COX-1; in contrast, medullary COX-2 expression was almost undetectable in untreated rats but was dramatically up-regulated with vasopressin treatment and was accompanied by increased urinary prostaglandin E(2) excretion. Further investigation revealed that both V1 and V2 receptors were involved in chronic medullary COX-1 and COX-2 up-regulation. Acute treatment with specific V1 or V2 receptor agonists resulted in specific increases in medullary COX-2, which was prevented by furosemide. Vasopressin did not affect COX-2 expression in cultured renomedullary interstitial cells. These data demonstrate that vasopressin stimulates medullary COX-2 expression through activation of both V1 and V2 receptors, and this stimulation is indirect and probably involves increased medullary electrolyte tonicity.
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PMID:Regulation of cyclooxygenase expression by vasopressin in rat renal medulla. 1468 11

Mesangial cells play an important role in glomerular function. They are an important source of cyclooxygenase (COX)-derived arachidonic acid metabolites, including prostaglandin E(2) and prostacyclin. Prostacyclin receptor (IP) mRNA was amplified from cultured mesangial cell total RNA by RT-PCR. While the prostaglandin E(2) receptor subtype EP(2) was not detected, EP(1,3,4) mRNA was amplified. Also, IP protein was noted in mesangial cells, proximal tubules, inner medullary collecting ducts, and the inner and outer medulla. But no protein was detected in whole cortex preparations. Prostacyclin analogues: cicaprost and iloprost, increased cAMP levels in mesangial cells. On the other hand, arginine-vasopressin and angiotensin II increased intracellular calcium in mesangial cells, but cicaprost, iloprost and prostaglandin E(2) had no effect. Moreover, a 50% inhibition of cicaprost- and iloprost-cAMP stimulation was observed upon mesangial cell exposure to 25 and 35 mM glucose for 5 days. But no change in IP mRNA was observed at any glucose concentration or time exposure. Although 25 mM glucose had no effect on COX-1 protein levels, COX-2 was increased up to 50%. In contrast, PGIS levels were reduced by 50%. Thus, we conclude that the prostacyclin/IP system is present in cultured rat mesangial cells, coupling to a cAMP stimulatory pathway. High glucose altered both enzymes in the PGI(2) synthesis pathway, increasing COX-2 but reducing PGIS. In addition, glucose diminished the cAMP response to prostacyclin analogues. Therefore, glucose attenuates the PGI(2)/IP system in cultured rat mesangial cells.
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PMID:Characterization of the PGI2/IP system in cultured rat mesangial cells. 1506 48

To examine the coronary effects of arginine-vasopressin during reperfusion after a short ischemia, left circumflex coronary artery flow was electromagnetically measured, and 15 min total occlusion of this artery followed by reperfusion was induced in anesthetized goats (five nontreated, five treated with the inhibitor of nitric oxide synthesis Nomega-nitro-L-arginine methyl ester (L-NAME) and five treated with the inhibitor of cyclooxygenase meclofenamate). The vasoactive drugs and L-NAME were intracoronarily injected, and meclofenamate by i.v. route. At 60 min of reperfusion, coronary vascular conductance was not changed significantly in nontreated and was decreased by 35% (P<0.01) in L-NAME-treated and by 30% (P<0.01) in meclofenamate-treated animals. During reperfusion, the coronary vasodilatation with acetylcholine (3-100 ng) and sodium nitroprusside (1-10 microg) was not altered in nontreated animals, and the vasodilatation with acetylcholine but not with sodium nitroprusside was partially decreased in L-NAME--but not in meclofenamate-treated animals. The vasoconstriction in response to arginine-vasopressin (0.03-0.3 microg) was increased during reperfusion in nontreated, was not changed in L-NAME-treated and was decreased in meclofenamate-treated animals. Therefore, it is suggested that during reperfusion after a short ischemia: (1) the coronary vasodilator reserve is preserved; (2) the coronary vasodilatation with acetylcholine is also preserved, but in this vasodilatation, the role of nitric oxide may be attenuated and prostanoids may be not involved; and (3) the coronary vasoconstriction with arginine-vasopressin is increased, probably due to both attenuation of the modulatory role of nitric oxide and the release of vasoconstrictor prostanoids.
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PMID:Vasopressin effects on the coronary circulation after a short ischemia in anesthetized goats: role of nitric oxide and prostanoids. 1524 67

To compare the coronary effects of endothelin-1 and vasopressin, as well as the role of nitric oxide (NO) and prostanoids in these effects, blood flow in the left circumflex (73 animals) or left anterior descending (19 animals) coronary artery (coronary flow) was electromagnetically measured, and both peptides were intracoronarily injected in anesthetized goats under control conditions and after intravenous administration of the inhibitor of NO synthesis NW-nitro-L-arginine methyl ester (L-NAME, 47 mg/kg, nine animals) or the inhibitor of cyclooxygenase meclofenamate (6-8 mg/kg, seven animals). In every animal, both endothelin-1 and vasopressin reduced coronary flow in a dose-dependent way, but these reductions by 0.03, 0.1 and 0.3 nmol of endothelin-1 (16%, 33% and 66%, respectively) were significantly higher than those by the equimolar doses of vasopressin (11%, 22% and 35%, respectively). After L-NAME treatment, the reductions of coronary flow by both peptides were augmented, and this augmentation was about two times higher for endothelin-1 than for vasopressin. Meclofenamate treatment did not affect the reductions of coronary flow caused by both peptides. Therefore, we suggest that endothelin-1 is more effective than vasopressin for producing coronary vasoconstriction, but vasopressin also produces remarkable coronary vasoconstriction. Also, it is suggested that NO may play a more relevant role for modulating the coronary vasoconstriction by endothelin-1 than by vasopressin, and that cyclooxygenase products may not be involved in the coronary effects of these two peptides.
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PMID:Comparison of the in vivo coronary action of endothelin-1 and vasopressin role of nitric oxide and prostanoids. 1525 91


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