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)

Patients with end stage renal failure have been shown to have higher basal concentrations of plasma arginine vasopressin than subjects with normal renal function. Immunoreactive vasopressin was detected in plasma from patients with severe chronic renal failure and a healthy subject at an elution volume identical to that previously determined with synthetic vasopressin. Assay of all fractions yielded identical chromatograms in the renal failure and healthy control groups. We conclude that the plasma immunoreactive vasopressin in end stage renal failure plasma coelutes with synthetic vasopressin and that the elevated concentrations found in these patients are not due to non-specific depression of binding in the vasopressin radioimmunoassay by circulating substances in renal failure.
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PMID:Immunoreactive vasopressin in end stage renal failure. 225 98

Hemostatic defects resulting in life-threatening hemorrhagic episodes are a common occurrence in the chronic renal failure patient. Hemorrhagic tendencies correlate best with laboratory tests of bleeding times. The identification of a specific hemostatic defect and its role in bleeding dyscrasias has yet to be elucidated. Our studies demonstrate that factor VIII coagulant activity and factor VIII related antigen (vWF:Ag) are normal or greatly elevated in uremic renal failure patients with greatly prolonged bleeding times. The multimeric state of the von Willebrand factor is also normal in these patients. The bleeding times were normalized in all 15 patients, 90 minutes post-infusion with desmopressin (DDAVP). No significant changes in factor VIII/vWF associated properties, blood cell counts, or coagulation factors were observed post-DDAVP treatment. However, a significant increase in platelet serotonin uptake (p less than .025) and ATP release (p less than .025) was detected after DDAVP treatment. These results indicate that DDAVP acts on the platelet membrane. This is further substantiated by the ability of DDAVP to block vasopressin-induced platelet aggregation in a dose- and time-dependent fashion. Perturbations in the movement and storage of serotonin and the release of adenosine 5'-triphosphate (ATP) in the platelets of uremic individuals are proposed to play a critical role in regulating bleeding times.
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PMID:Desmopressin-induced improvement in bleeding times in chronic renal failure patients correlates with platelet serotonin uptake and ATP release. 226 75

Refractory ascites (or diuretic-resistant ascites), i.e. ascites that cannot be mobilized by medical treatment (low sodium diet and high doses of furosemide and spironolactone) is an infrequent phenomenon in cirrhosis. It usually occurs in patients with functional renal failure as a consequence of alteration in both pharmacokinetics and pharmacodynamics of diuretics. Peritoneovenous shunting, a procedure which improves systemic hemodynamics and renal function and suppresses the plasma levels of renin, aldosterone, norepinephrine and antidiuretic hormone in cirrhotics with ascites, has been proposed as the treatment of choice in patients with refractory ascites. Unfortunately it is associated to a high rate of severe complications and does not prolong the survival of these patients. Moreover, in approximately one third of the patients the shunt becomes occluded within the first year after operation. Recent studies have shown that repeated large volume paracentesis (4-64 per day until disappearance of ascites) or total paracentesis (complete mobilization of ascites in only one paracentesis session) associated to i.v. albumin infusion are an effective and safe therapy of ascites. At present, there is only one controlled trial comparing therapeutic paracentesis versus peritoneo-venous shunt in the management of patients with refractory ascites. In this study, there were no significant difference between both therapeutic groups with respect to survival. However, the incidence of readmission to hospital for the treatment of ascites was higher in the paracentesis group. Therefore, both procedures are valid therapeutic alternatives for that type of patients. Future studies are necessary to investigate if there are subsets of cirrhotics with refractory ascites in which one of these two types of treatment is especially indicated.
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PMID:Diuretic-resistant ascites in cirrhosis. Mechanism and treatment. 226 4

ANF is an exciting, newly discovered hormone that has significant potential for furthering our understanding of the complex interactions involved in fluid and electrolyte balance. In addition to effects on water and salt balance, it is a potent vasodilator, as well as inhibitor of renin, angiotensin II, aldosterone, and vasopressin. ANF is primarily produced in the atria, but production in the brain is suggestive of action as a neuropeptide and as a potential regulator of CSF production. Receptors are found throughout the heart, vascular tree, kidney, adrenal gland, and brain. The stimulus for release appears to be atrial stretch, which may be secondary to intravascular fluid changes. It causes hemoconcentration and may be an important regulator of interstitial fluid distribution as well as capillary permeability. Patients with CHF and renal failure have been found to have elevated levels that decrease in response to treatment. Potentially, it may be useful as a therapeutic agent in acute renal failure, CHF and other fluid disturbances. ANF is a testament to the incredible advances in peptide biology. Within 2 years of the discovery, ANF was sequenced and cloned. Since that time, literally thousands of papers describing its actions have been published. Our knowledge about this hormone grows at an exponential rate. It is clear that this hormone is intimately involved in the regulation of fluid and electrolyte balance, vascular tone, and the pathophysiology of CHF but many questions remain unanswered. Continued research will provide many of the missing pieces to this very complex, new hormone system.
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PMID:Atrial natriuretic factor. 252 98

This work was aimed to assess the secretion of volume related hormones in heart transplant patients (HTP) and their relationship to excretory renal function studied under bed rest and water immersion conditions. Fractional sodium (FENa%) and potassium (FEK%) clearance, plasma renin activity (PRA), plasma aldosterone (Ald), vasopressin (AVP) and atrial natriuretic peptide (ANP) were estimated in six HTP with moderate renal failure (C creat = 69 +/- 6.9 ml/min) and in 10 healthy subjects (N) (C creat = 110 +/- 2.0 ml/min). All HTP were treated with cyclosporine A and azathioprine. In HTP basal AVP (6.18 +/- 0.92 pg/ml) and ANP (138.17 +/- 14.69 pg/ml) levels were significantly higher than in normals (2.07 +/- 0.11 pg/ml and 74.10 +/- 7.10 pg/ml, respectively). HTP were also characterized by increased FENa% and FEK% both under bed rest (DI) and water immersion (WI) conditions. As abnormalities of excretory renal function in HTP were not significantly related to the plasma endocrine profiles factors other than PRA, Ald, AVP and ANP seemed to be also involved in their pathogenesis.
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PMID:Renal response to central volume expansion induced by water immersion (WI) in heart transplant patients. 253 69

It has not yet been clarified whether prilocaine-induced methemoglobinemia is a problem in patients with chronic anemia. We therefore performed supraclavicular brachial blockade for upper limb surgery (6 mg/kg prilocaine 2% + 0.1 IU vasopressin/ml) in ten female patients with chronic renal failure (mean Hb 8.19%) requiring hemodialysis. Before the blockade, a catheter was inserted into the opposite internal jugular vein and blood samples were drawn before and 10, 15, 20, 30, 45, 60, 90, 120 and 180 min after injection. Plasma prilocaine concentrations and methemoglobin levels were within the ranges measured by other authors in healthy patients. There was no correlation between plasma prilocaine levels and methemoglobinemia. We therefore consider prilocaine to be a safe local anesthetic in patients with renal failure and chronic anemia.
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PMID:[Supraclavicular plexus blockade using prilocaine in patients with chronic anemia]. 271 Sep 68

Derangements in leukocyte function occur in patients with primary hyperparathyroidism and in those with uremia, which is a state of secondary hyperparathyroidism, suggesting that parathyroid hormone (PTH) may affect leukocyte function. We examined the interaction between PTH and random migration of human polymorphonuclear leukocytes (PMNL) utilizing a modified Boyden chamber. Intact 1-84 PTH but not its amino-terminal (1-34 PTH) or its carboxy-terminal (53-84 PTH) fragments produced marked and significant (p less than 0.01) stimulation of random migration in a dose-dependent manner. Inactivation of 1-84 PTH abolished its effect and other peptide hormones (calcitonin, glucagon, insulin and vasopressin) did not stimulate migration of PMNL. The effect of PTH on migration was not due to action of the hormone on chemotaxis. PTH did not enhance cAMP or cGMP production by PMNL. The stimulation of PMNL motility by PTH was independent of calcium concentration in media, was not mimicked by calcium ionophore and was not blocked by verapamil. Quinidine also produced significant (p less than 0.01) increase in random migration of PMNL and this effect was not additive to that of PTH. Prolonged exposure to PTH (16-20 h) was associated with significant inhibition of random migration of PMNL. The migration of PMNL from patients with advanced renal failure was significantly (p less than 0.01) reduced and there was a significant (p less than 0.01) inverse relationship between random migration of PMNL and serum levels of PTH. Also PTH produced only modest stimulation of random migration of PMNL in most patients with renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of parathyroid hormone on random migration of human polymorphonuclear leukocytes. 285 73

The ability of the kidneys to excrete sodium and free water is often impaired in patients with cirrhosis. Sodium retention is a sine qua non for ascites formation. The impairment of water excretion causes hyponatremia and hypo-osmolality. In addition, these patients frequently have functional renal failure caused by intense renal vasoconstriction. The renin-angiotensin-aldosterone system and the sympathetic nervous system, which are activated in most cirrhotic patients with ascites, and a nonosmotic hypersecretion of antidiuretic hormone are important mechanisms of sodium and water retention. Angiotensin II and sympathetic nervous activity may also be involved in the pathogenesis of functional renal failure. The renal production of prostaglandins is increased in cirrhotic patients with ascites as a homeostatic response to antagonize the vascular effect of endogenous vasoconstrictors and the tubular action of antidiuretic hormone. Nonsteroidal anti-inflammatory drugs should, therefore, be administered with caution in these patients because they may induce acute renal failure and water retention. Although sulindac inhibits the renal synthesis of prostaglandins in cirrhotic patients with ascites, it appears to have less effect on renal function than do other nonsteroidal anti-inflammatory drugs administered to these patients.
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PMID:Renal function abnormalities, prostaglandins, and effects of nonsteroidal anti-inflammatory drugs in cirrhosis with ascites. An overview with emphasis on pathogenesis. 294 81

Atrial natriuretic factor, plasma renin activity, and plasma vasopressin were measured in 38 patients with chronic renal failure prior to and after hemodialysis. The objective of the study was to evaluate the effect of acute volume changes on the level of atrial natriuretic factor. Blood pressure prior to dialysis was 154 +/-/83 +/- mmHg, and 132 +/-/78 +/- mmHg post dialysis (p less than 0.005) while heart rate increased from 82.5 +/- 1.8 beats per minute to 91.2 +/- 2.4 after dialysis (p less than 0.005). The average weight of patients was reduced from 60.2 +/- 2.4 kg to 57.8 +/- 2.4 kg (p less than 0.005). While the plasma levels of atrial natriuretic factor in normal individuals were 65.3 +/- 2.9 pg/ml (n = 59), these levels were 251.4 +/- 28 pg/ml prior to dialysis in the patients with renal failure, and 173.3 +/- 18.0 pg/ml after dialysis (p less than 0.005). Twenty-nine patients had a reduction in the levels of this atrial natriuretic factor, 5 had no change, and 4 had an increase. The atrial factor was not detected in the dialysate fluid of 6 patients in whom it was measured. Peripheral renin values were unchanged from 2.12 +/- 0.68 to 2.07 +/- 0.8 ng/ml/hr. Plasma vasopressin before dialysis was significantly higher than normal, and increased from 7.04 +/- 0.56 to 9.95 +/- 1.55 pg/ml following dialysis (p less than 0.05). The changes in atrial natriuretic factor values correlated most significantly (r = 0.47, p less than 0.005) with the changes in weight, but no single variable could explain the changes in atrial natriuretic factor.
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PMID:Influence of hemodialysis on the plasma levels of the atrial natriuretic factor in chronic renal failure. 295 3

The aim of the study was to investigate the urinary excretion of 6-keto-PGF1 alpha (a stable metabolite of PGI2), thromboxane B2 (TxB2; a stable metabolite of TxA2), and PGE2 in 18 normal subjects, 49 cirrhotics with ascites without renal failure (GFR = 90 +/- 4 ml/min, means +/- S.E.M.) and 20 cirrhotics with functional renal failure (FRF) (GFR = 36 +/- 3). The study was made after 5 days on a 50 mEq sodium diet and without diuretics. Plasma renin activity (PRA), plasma norepinephrine concentration (NE) and plasma antidiuretic hormone concentration (ADH) were also measured. Cirrhotics without FRF showed a significantly higher urinary excretion of 6-keto-PGF1 alpha, TxB2 and PGE, (15.9 +/- 1.7 ng/h, 3.0 +/- 0.3 ng/h, and 6.2 +/- 1.0 ng/h) than did normal subjects (9.2 +/- 0.9, 1.3 +/- 0.1 and 2.3 +/- 0.4). On the contrary, the urinary excretion of these prostaglandins was normal or reduced in patients with FRF (5.3 +/- 0.8, 1.3 +/- 0.2 and 1.9 +/- 0.4). PRA, NE and ADH were significantly increased in cirrhotics with FRF (15.2 +/- 3.9 ng/ml/h, 1026 +/- 149 pg/ml and 4.1 +/- 0.3 pg/ml) and in patients without FRF (8.0 +/- 1.4, 667 +/- 67 and 3.9 +/- 0.3) as compared to normal controls (1.3 +/- 0.2, 275 +/- 46 and 2.4 +/- 0.2). These results suggest that renal hemodynamics in cirrhosis depends upon a critical equilibrium between the activity of endogenous vasoconstrictor systems and the renal production of the vasodilator prostaglandins PGI2 and PGE2. In addition, they do not support FRF in cirrhosis being related to an increased renal production of the vasoconstrictor prostaglandin TxA2.
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PMID:Urinary excretion of 6-keto-prostaglandin F1 alpha, thromboxane B2 and prostaglandin E2 in cirrhosis with ascites. Relationship to functional renal failure (hepatorenal syndrome). 346 43


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