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 major complication of extracorporeal membrane oxygenation (ECMO) for the treatment of neonatal respiratory failure is bleeding related to heparinization. Systolic hypertension has emerged as another serious side effect in our experience. Thirty-eight of the first 41 newborns we treated with ECMO developed a systolic blood pressure greater than 90 mm Hg. The mean hypertension index (HI blood = hours greater than 90/hr on ECMO) was 0.17 +/- 0.16. Possible biochemical mediators were assayed in 17 patients. Plasma renin activity (PRA), aldosterone, epinephrine, norepinephrine, prostaglandin E2, thromboxane, and antidiuretic hormone were elevated. Angiotensin-converting enzyme (ACE) and prostacyclin were not elevated. Eighteen patients (44%) had intracranial hemorrhage (ICH), and 11 patients (27%) had clinically significant ICH. The HI was significantly (p less than 0.005) lower in those patients without ICH (0.11 +/- 0.01) than in those patients with ICH (0.25 +/- 0.04). PRA at hour 12, day 2, and day 3 was significantly higher (p less than 0.05) in patients experiencing ICH (62 +/- 42; 93 +/- 15; 73 +/- 30 ng/ml/hr) than in those without ICH (27 +/- 25; 14 +/- 8; 12 +/- 4 ng/ml/hr). An aggressive approach to medical management evolved that included hydralazine, nitroglycerine, and captopril, which protected against ICH. Two of 23 patients (9%) treated with the protocol sufferred clinically significant ICH, whereas nine of 18 patients (50%) treated before implementation of the protocol experienced ICH. The ACE inhibitor captopril was most effective in the control of hypertension. We conclude that systolic hypertension is common during neonatal ECMO, is associated with ICH, and is related to a high PRA. Aggressive management of hypertension during ECMO can reduce the incidence of ICH, and captopril is an important component of this aggressive medical management.
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PMID:Hypertension during extracorporeal membrane oxygenation: cause, effect, and management. 282 41

Prostaglandin E1 (PGE1) at 1 nM inhibits arginine-vasopressin (AVP)-induced water reabsorption in the rabbit cortical collecting tubule (RCCT), while 100 nM PGE1, by itself, stimulates water reabsorption (Grantham, J. J., and Orloff, J. (1968) J. Clin. Invest. 47, 1154-1161). To investigate the basis for these two responses, we measured the effects of prostaglandins on cAMP metabolism in purified RCCT cells. In freshly isolated cells, PGE2, PGE1, and 16,16-dimethyl-PGE2 acting at high concentrations (0.1-10 microM) stimulated cAMP accumulation; however, one PGE2 analog, sulprostone (16-phenoxy-17,18,19,20-tetranor-PGE2 methylsulfonilamide), failed to stimulate cAMP accumulation or to antagonize PGE2-induced cAMP formation; PGD2, PGF2 alpha, and a PGI2 analog, carbacyclin (6-carbaprostaglandin I2), also failed to stimulate cAMP synthesis. These results suggest that there is a PGE-specific stimulatory receptor in RCCT cells which mediates activation of adenylate cyclase. Occupancy of this receptor would be anticipated to cause water reabsorption by the collecting tubule. At lower concentrations (0.1-100 nM) PGE2, PGE1, 16,16-dimethyl-PGE2, and, in addition, sulprostone inhibited AVP-induced cAMP accumulation by fresh RCCT cells in the presence of cAMP phosphodiesterase inhibitors. Pertussis toxin pretreatment of RCCT cells blocked the ability of both PGE2 and sulprostone to inhibit AVP-induced cAMP accumulation. In membranes prepared from RCCT cells, sulprostone prevented stimulation of adenylate cyclase by AVP. These results suggest that E-series prostaglandins (including sulprostone) can act through an inhibitory PGE receptor(s) coupled to the inhibitory guanine nucleotide regulatory protein, Gi, to block AVP-induced cAMP synthesis by RCCT cells. Occupancy of this receptor would be expected to cause inhibition of AVP-induced water reabsorption in the intact tubule. Curiously, after RCCT cells were cultured for 5-7 days, PGE2 no longer inhibited AVP-induced cAMP accumulation, but PGE2 by itself could still stimulate cAMP accumulation. In contrast to PGE2, epinephrine acting via an alpha 2-adrenergic, Gi-linked mechanism did block AVP-induced cAMP formation by cultured RCCT cells. This implies that some component of the inhibitory PGE response other than Gi is lost when RCCT cells are cultured.
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PMID:Regulation of cyclic AMP metabolism in rabbit cortical collecting tubule cells by prostaglandins. 283 64

The presence of alpha 1-receptors has been demonstrated in numerous venous fragments for various animal models. On the other hand, the presence of alpha 2-receptors in the saphenous of the dog is a matter of debate. Beta 2-receptors are activated by isoproterenol, noradrenaline and adrenaline in precontracted veins (part of the facial vein of the rabbit may be an exception). Preferential blocking by atenolol of beta 1-receptors in the jugular veins of the rat suggests that these receptors may mediate vasodilation. The saphenous veins of the dog provide the only example where specific dopaminergic receptors have been noted following partial antagonism with haloperidol. The vasoconstrictive action of acetylcholine has been seen in venous segments of numerous species and indicates the presence of muscarinic receptors. The existence of angiotensin receptors can be postulated despite the weak and inconstant in vitro and in vivo (the dorsal cerebral sinus in the dog excepted) reactions observed and the use of a non-specific antagonist. The same is true for bradykinin and vasopressin. The marked vasoconstrictive action of serotonin on all veins studied is evidence for the presence of receptors. The nature of the antagonists is subject to some divergence of opinion. Nevertheless, D tryptamine muscular receptors (or 5 HT2) can be identified due to the lack of morphine-mediated response and the efficacy of methysergide. The presence of a third type of serotoninergic receptor has only been reported once, following observations of vasodilation in the sheep. H1 receptors are involved in histamine-mediated vasoconstriction. The presence of H2 receptors which mediate vasodilation in precontracted veins remains hypothetical. Prostaglandins exhibit different efficacies in producing contraction in isolated veins; PGF2 alpha is more efficacious than PGE1 and PGE2. Prostacyclin induces contraction of human saphenous veins in a dose-dependent manner. PGE2 and particularly PGE1 can induce relaxation in precontracted veins, as is also true for prostacyclin. Receptors for these prostaglandins must exist at the post-junctional level. P2-receptors mediate transmission of the vasoconstrictive action of various purine derivatives.
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PMID:[Pharmacology of the venous system]. 288 Oct 27

The effects of human alpha atrial natriuretic factor following bolus injection of increasing doses and during a continuous 30 minute infusion were investigated in 7 patients with severe congestive cardiac failure (NYHA III-IV). The natriuretic factor was measured in plasma before and after the bolus application or infusion. The plasma levels were raised in 6 patients. A significant inverse correlation was observed between the basal levels of the atrial factor and cardiac output. In addition, there was a dose-dependent fall in preload and afterload as well as in the peripheral vascular resistance and there was an improvement in cardiac performance. The alpha atrial natriuretic factor inhibited aldosterone and cortisol secretion and promoted diuresis and the urinary excretion of sodium and potassium. The plasma concentrations of renin, noradrenaline, vasopressin, 6-keto-prostaglandin F1 alpha, the stable metabolite of prostacyclin, and prostaglandin E2 remained unchanged.
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PMID:[The atrial natriuretic factor in severe congestive heart failure. Plasma level, hemodynamic, hormonal and renal effects]. 293 Dec 68

Treatment for 8 days with a new nonsulfhydryl angiotensin-converting enzyme inhibitor, quinapril (CI-906), produced a marked and progressive reduction in the blood pressure of spontaneously hypertensive rats. Quinapril was given p.o. in a dose of 20 or 40 mg/kg once daily. Both doses increased plasma renin activity and decreased the urinary excretion of aldosterone. These results, together with a marked decrease in serum angiotensin-converting enzyme activity, indicate that the drug produced a considerable fall in circulating angiotensin II. The urinary excretion of vasopressin was not altered by the smaller dose of quinapril but was reduced by the larger dose, which increased water intake and urine excretion. Quinapril did not affect plasma kininogen or the urinary excretion of kallikrein. The urinary excretion of neither the prostacyclin metabolite 6-keto-prostaglandin F1 alpha nor the thromboxane metabolite thromboxane B2 were altered by the drug. However, quinapril did produce a temporary decrease in the excretion of prostaglandin E2, the effect passing off with the continuation of the treatment. These data indicate that vasodilatory prostanoids do not contribute to the blood pressure lowering effect of quinapril in spontaneously hypertensive rats. The inhibition of the renin-angiotensin system is probably the principal mechanism of the drug's antihypertensive action, but these results do not rule out the possibility that an increase in vasodilatory kinins may also be involved.
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PMID:Inhibition of angiotensin-converting enzyme with quinapril (CI-906): investigation of antihypertensive mechanisms in spontaneously hypertensive rats. 300 40

We have evaluated the hypothesis that vasoactive hormones increase cellular cyclic AMP (cAMP) levels in cultured vascular smooth muscle cells from rat mesenteric arteries by stimulating endogenous prostaglandin (PG) synthesis. Vasopressin and angiotensin II, which were shown previously to provoke the synthesis of PGs in cultured vascular smooth muscle cells, increased cellular cAMP concentrations by about 2-fold, whereas a peptide analog of vasopressin, 1-desamino-8-D-arginine vasopressin, mostly lacking vasopressin's ability to elicit PG synthesis, was ineffective. Two other chemically dissimilar effectors that provoked the synthesis of PGs in cultured vascular smooth muscle cells, namely arachidonate and ionophore A23187, also increased cellular cAMP levels. The increase of cAMP by vasopressin and angiotensin II was transient, reaching a maximum at 1 to 2 min of incubation, followed by a decline to basal levels. Acetylsalicylic acid, a specific inhibitor of PG synthesis, completely prevented vasopressin- and arachidonate-evoked increases of cAMP but did not affect basal cAMP concentrations. Exogenous prostacyclin and prostaglandin E2 dose-dependently increased cAMP concentrations although prostacyclin was more effective than prostaglandin E2. The ability of exogenous prostacyclin to evoke cAMP increases was not inhibited by acetylsalicylic acid. The results support the hypothesis that the stimulation of endogenous PG synthesis by vasoactive hormones in turn modulates cellular cAMP levels in cultured vascular smooth muscle cells from rat mesenteric arteries.
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PMID:Increase of cyclic AMP concentrations in cultured vascular smooth muscle cells by vasoactive peptide hormones. Role of endogenous prostaglandins. 302 53

Vasopressin-prostaglandin (PG) interaction, especially the role of the inhibitory effects of PGE2 on vasopressin action, was studied using toad urinary bladders. The PGH2, at 1 X 10(-7) M, inhibited vasopressin-stimulated water flow (Marumo, 1982); PGE2 inhibited the water flow at 10(-8) M, but PGD2, PGF2 alpha, and PGI2 did not do so even at 10(-7) M. Thus, PGE2 has a physiological effect in contrast to other PGs converted from PGH2. Indomethacin enhanced both the vasopressin- and cyclic AMP-stimulated water flow across the toad bladder. However, the half maximum activation dose for vasopressin was 2 X 10(-10) M, but for cyclic AMP, as much as 3 X 10(-8) M. The PGE2 inhibited both vasopressin- and cyclic AMP-stimulated water flow. However, PGE2 inhibited vasopressin action in a dose-dependent manner which was not noted as a PGE2 effect on cyclic AMP action. The W-7, which is a specific inhibitor of calmodulin, suppressed cyclic AMP-stimulated water flow in a dose-dependent manner. Thus, PGE2 may suppress vasopressin-stimulated water flow at a site of cyclic AMP generation under physiological conditions. Thromboxane B2 (TXB2) enhanced vasopressin-stimulated water flow but not cyclic AMP-stimulated one. Thus PGE2 and TXB2 may be concluded as negative or positive modulators of vasopressin action in the toad bladder on the step(s) as the site of cyclic AMP generation under physiological conditions.
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PMID:Role of inhibitory and stimulative effects of prostaglandins on vasopressin-stimulated osmotic water flow in the toad bladder. 303 49

Animals and humans undergoing a treatment with cyclosporin (CsA) show a reversible increase in renal vascular resistance and decrease in glomerular filtration rate. The causes of these abnormalities have not yet been established. In animals potential mechanisms for CsA induced renal functional impairment are an increase in urinary thromboxane A2 excretion, plasma renin activity and renal sympathetic nervous system activity and an enhancement of vasopressin stimulated Ca++ mobilisation and cell contraction in vascular smooth muscle cells. In human, the problem is far less clear. CsA induces an inhibition in PRA and urinary prostaglandins excretion. Furthermore CsA does not modify urinary and plasma levels of catecholamines. Whatever the mechanism underlying the vasoconstriction induced by CsA, the inhibition of PGI2 synthesis and angiotensin II formation may participate in the decrease in renal blood flow and glomerular filtration rate which is observed in patients receiving CsA.
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PMID:[Functional renal effects of cyclosporin. Physiopathological mechanisms]. 305 May 79

Synthesis of prostaglandins (PGs) was characterized in the lateral wall (LW) of guinea-pig cochlea. Basal synthesis at 37 degrees C was about 480 pg/LW (12.8 ng X mg-1 protein) for PGI2 and 85 pg/LW (2.3 ng X mg-1 protein) for PGE2, levelling out after 10 min of incubation. Incubation with arachidonic acid (10(-5) M) increased PGI2 and PGE2 synthesis by 44% and 1020%, respectively, showing that arachidonic acid availability is a synthesis-limiting factor. The stimulating effect of the Ca++ ionophore A23187 (5 X 10(-6) M) on PG synthesis was weak (about +50%) but was enhanced (about +140%) by preincubation with arachidonic acid. Angiotensin II (10(-6) M), vasopressin (5 X 10(-7) M), and furosemide (10(-8) to 10(-3) M) did not alter PG secretion. Neither aspirin nor indomethacin prevented the development of furosemide ototoxicity (endocochlear potential) in the rat. Perfusion with PGI2 influenced the furosemide effect in some instances.
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PMID:Strial prostaglandins and leukotrienes. Biochemical characteristics and interrelationship with furosemide. 311 70

Low concentrations of Ca2+-mobilizing agonists such as vasopressin, platelet-activating factor, ADP, the endoperoxide analogue U44069 and the Ca2+ ionophore A23187 enhance the binding of [3H]phorbol 12,13-dibutyrate (PdBu) to intact human platelets. This effect is prevented by preincubation of platelets with prostacyclin (except for A23187). Adrenaline, which does not increase Ca2+ in the platelet cytosol, does not enhance the binding of [3H]PdBu to platelets. In addition, all platelet agonists except adrenaline potentiate the phosphorylation of the substrate of protein kinase C (40 kDa protein) induced by PdBu. Potentiation of protein kinase C activation is associated with increased platelet aggregation and secretion. Stimulus-induced myosin light-chain phosphorylation and shape change are not significantly affected, but formation of phosphatidic acid is decreased in the presence of PdBu. The results may indicate that low concentrations of agonists induce in intact platelets the translocation of protein kinase C to the plasma membrane by eliciting mobilization of Ca2+, and thereby place the enzyme in a strategic position for activation by phorbol ester. Such activation enhances platelet aggregation and secretion, but at the same time suppresses activation of phospholipase C. Therefore, at least part of the synergism evoked by Ca2+ and phorbol ester is mediated through a single pathway which involves protein kinase C. It is likely that the priming of protein kinase C by prior Ca2+ mobilization occurs physiologically in activated platelets.
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PMID:Ca2+ mobilization primes protein kinase C in human platelets. Ca2+ and phorbol esters stimulate platelet aggregation and secretion synergistically through protein kinase C. 314 57


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