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)

Administration of vincristine resulted in a hyponatremic state and concurrent elevation of the plasma immunoreactive arginine8-vasopressin (IR-AVP) level in rats. Development of the vincristine-induced hyponatremia and hypoosmolality was accompanied by a loss in weight, a decreased water intake and a large reduction in the daily urine sodium excretion. The cause of the sodium loss is thought to be the diarrhea observed during vincristine treatment. Hematocrit and serum urea nitrogen levels were increased. It is concluded that the condition differs from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH): the increase in plasma IR-AVP concentration may be associated with dehydration due to vincristine toxicity.
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PMID:Hyponatremia and increased secretion of vasopressin induced by vincristine administration in rat. 342 63

The systemic effects of local anesthetic drugs, especially bupivacaine, on myocardial conduction and the increase of cardiotoxicity by hypoxemia, acidosis, and hyperkalemia has been proven in numerous animal experiments. In our department, supraclavicular brachial block with bupivacaine is the method of choice for patients with chronic renal failure requiring operations of the upper limb. The question may be raised whether or not these patients with their concomitant disease--electrolyte and acid-base imbalances, uremic cardiomyopathy--are especially endangered by the use of this drug. Supraclavicular brachial blockade (3 mg/kg bupivacaine 0.5% + 0.1 IU vasopressin/ml) was performed in 10 patients with chronic renal failure requiring hemodialysis. The control group consisted of 10 healthy patients who were admitted for minor hand surgery. Preoperative blood samples were taken for measurements of blood urea nitrogen, serum creatinine, serum electrolytes, and arterial blood gas analysis. Long-term ECG monitoring begun 20 min before injection of the block and continued over a total of 200 min. Serum concentrations of bupivacaine were determined at 10, 20, 30, 60, 120, and 180 min after injection. Comparing the two groups, no severe changes in electrolytes or acid-base status could be found despite some statistical significances. Even though bupivacaine serum concentrations proved to be 3 times higher in the study group than in the control group, no changes in cardiac conduction could be registered. We conclude that bupivacaine is as safe in dialyzed patients with chronic renal failure with regard to possible changes in circulatory parameters and myocardial conduction as in healthy patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparative study of circulatory and ECG-changes after supraclavicular plexus block with bupivacaine-HCl 0.5 per cent in patients with chronic kidney failure]. 365 36

Arginine vasopressin consists of a 20-membered, disulfide-linked macrocyclic ring system called pressinoic acid to which is attached a COOH-terminal tripeptide. The molecular conformation of pressinoic acid has been determined from single crystal x-ray diffraction data. The 20-membered macrocyclic ring, stabilized by two intramolecular hydrogen bonds, has a type I beta-bend centered on Gln4 and Asn5 and a highly distorted type II' bend centered on Phe3 and Gln4. In vasopressin the Asn5 side chain extends away from the macrocyclic ring system and hydrogen bonds to the terminal tripeptide, but in pressinoic acid the Asn5 side chain lies over the molecule and forms a strong hydrogen bond to the nitrogen of Tyr2. The absence of pressor activity in pressinoic acid may be a result of both the loss of the COOH-terminal tripeptide and the incorrect orientation of the Asn5 side chain. Whether this class of hormones has pressor or oxytocic activity is determined by the orientation of the Tyr2 side chain, that is, whether it is extended away from or over the ring system, respectively. In pressinoic acid, the Tyr2 side chain is in the expected "pressor conformation," that is, extended away from the ring system, and is stabilized through a hydrophobic interaction with the Phe3 side chain. Thus, the conformation of the pressinoic acid molecule partly explains the activity of vasopressin-like hormones.
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PMID:Structure of pressinoic acid: the cyclic moiety of vasopressin. 370 48

The synthetic vasopressin analog 1-deamino-8-D-arginine vasopressin (dDAVP) has been shown to influence a wide range of cell-membrane-related events. Accordingly, the effect of dDAVP on membrane transport of various alkylating agents and amino acids was evaluated in L5178Y lymphoblasts in vitro. dDAVP stimulated melphalan uptake but conversely inhibited uptake of nitrogen mustard, choline (the natural transport substrate for the nitrogen mustard carrier), and leucine. No effect on the uptake of cyclophosphamide or glutamine was observed. Increased melphalan uptake was due to effects on both substrate influx and efflux. The effect of dDAVP on melphalan influx was particularly complex: dDAVP stimulated melphalan influx by amino acid transport system ASC but inhibited influx by system L, resulting in a net increase in unidirectional drug influx. Melphalan efflux was inhibited by dDAVP. Decreased uptake of nitrogen mustard, choline and leucine was due, at least in part, to decreased substrate influx. However, the mechanisms of inhibition were dissimilar: inhibition of substrate influx was non-competitive for choline but competitive for leucine. In conclusion, dDAVP induced diverse but apparently specific effects on membrane transport of several alkylating agents and amino acids. Since the accumulation of alkylating agents such as melphalan within tumor cells is a major determinant of cytotoxicity, dDAVP may have a role as a biological response modifier.
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PMID:Modulation of membrane transport of alkylating agents and amino acids by an analog of vasopressin in murine L5178Y lymphoblasts in vitro. 380 Oct 52

We studied the sodium balance and changes in plasma volume by an isotope dilution technique in the first week after an aneurysmal subarachnoid hemorrhage in 21 patients. In 11 of the patients, the plasma volume decreased by more than 10%. This was accompanied by a negative sodium balance and hyponatremia in 6 patients, a negative sodium balance without hyponatremia in 4 patients, and a positive sodium balance in 1 patient. Together with a decrease in plasma volume, blood urea nitrogen content increased and body weight decreased. Three patients developed hyponatremia without a decrease in plasma volume. Serum vasopressin was measured in 14 of the 21 patients. The values were elevated on admission and declined in the first week, regardless of the presence of hyponatremia. These findings indicate that natriuresis and hyponatremia in aneurysmal subarachnoid hemorrhage reflect salt wasting and not inappropriate secretion of antidiuretic hormone and that these changes should be corrected by fluid replacement rather than by fluid restriction.
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PMID:Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. 403 61

The role of prostaglandins in the development of aminoglycoside-induced acute renal failure was studied in CD-COBS rats (200 to 250 g). The animals were treated with gentamicin (80 mg/kg), acetylsalicylic acid (ASA, 100 or 200 mg/kg), or both drugs or saline for 5 or 10 days. Renal function was studied measuring creatinine clearance, blood urea nitrogen (BUN), and serum electrolytes, urine osmolality, and maximal urinary concentrating capacity after water deprivation and vasopressin administration. Gentamicin toxicity on the proximal tubule was evaluated by measuring urinary excretion of the lysosomal enzyme N-acetylglucosaminidase (NAG). Renal prostaglandin (PG) production was evaluated measuring the concentration of PGE2, PGD2, PGF2 alpha, 6-keto-PGF1 alpha, and thromboxane B2 (TXB2) in whole renal homogenate after a 15-min incubation at 37 degrees C using gas chromatography-mass spectrometry. Gentamicin alone reduced the glomerular filtration rate (GFR) 20 to 30% after 5 and 10 days of treatment. Combination with ASA potentiated the toxic effect of the aminoglycoside after 10 but not after 5 days of treatment. Similarly, gentamicin reduced the urinary concentrating capacity and addition of ASA worsened the effects. Gentamicin markedly increased NAG excretion but this effect was reduced by ASA, probably as a result of lysosomal stabilization. ASA alone inhibited the production of prostaglandins in renal tissue by 70 to 90% after single or multiple doses. The animals treated with gentamicin alone presented a significant, specific increase in PGE2 production after 10 days of treatment but this increase did not occur when the two compounds were given together. Since PGE2 has a vasodilatory effect in the kidney these results suggest that it may play a specific role in maintaining normal renal blood flow and GFR during the development of aminoglycoside nephrotoxicity. The inhibition of prostaglandin production by nonsteroid anti-inflammatory drugs prevents this compensatory mechanism and worsens the renal damage.
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PMID:Prostaglandins and aminoglycoside nephrotoxicity. 404 89

Microorganisms in ruminal ingesta and pure cultures of anaerobic ruminal bacteria of different physiological and morphological groups incorporated (14)C from labeled 2-methylbutyrate during growth. The radioactivity was incorporated mainly into lipid and protein. Isoleucine was the only labeled amino acid found in acid hydrolysates of protein from either pure or mixed cultures. Radioactivity in isoleucine synthesized from 2-methylbutyrate-1-(14)C was entirely in carbon-2. Thus, the carboxylation of 2-methylbutyrate is a pathway for synthesis of isoleucine different from that operative in many aerobic and facultative microorganisms. The specific activity of isoleucine from 2-methylbutyrate by Bacteroides rumminicola 23 increased with higher concentrations of 2-methylbutyrate (2.6 to 44 x 10(-5)m) in the growth medium. At the highest concentration, the specific activity of isoleucine synthesized was 40% of the specific activity of the 2-methylbutyrate in the growth medium. The use of enzymatic casein hydrolysate, oxytocin, or vasopressin rather than ammonia as nitrogen source for growth of strain 23 depressed the incorporation of 2-methylbutyrate into isoleucine. Synthesis of isoleucine from 2-methylbutyrate appears to be an important reaction in the rumen.
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PMID:Isoleucine biosynthesis from 2-methylbutyric acid by anaerobic bacteria from the rumen. 581 42

Injury or stress generates a vigorous metabolic response designed to establish the metabolic priorities required for the repair of injured tissues. In this condition, hormones commonly found to be elevated in the plasma include glucagon, catecholamines, glucocorticoids, growth hormone, aldosterone, and antidiuretic hormone. This hormonal profile results in rapid lysis of body protein, an increased rate of fat oxidation, and water and salt conservation. Rates of gluconeogenesis and ureagenesis are accelerated and may result in significant losses in lean body mass, a process that, if allowed to progress, will adversely affect patient survival. Exogenous nutrients provided to the critically ill patient may be poorly tolerated and may result in complications. Dextrose and intravenous fat emulsions provide the major sources of parenteral, nonprotein energy. These energy sources may not be metabolized efficiently in these patients, even though energy expenditure in this condition is increased significantly. Measurement of urinary nitrogen losses yields evidence useful in assessing the patient's degree of stress. In this manner, the patient's energy and protein requirements may be estimated. Formulations of amino acids, including the branched-chain amino acids, in higher concentrations have been reported to have anticatabolic effects and may improve the maintenance of lean body mass in stressed individuals. The stressed patient is prone to metabolic complications and, therefore, requires more careful monitoring of fluid, electrolyte, and acid-base balance, as well as renal, pulmonary, and liver function. Nutritional status is difficult to assess, since negative nitrogen balance may persist and the visceral proteins such as transferrin become altered in stress and, therefore, may not respond to nutritional intervention alone. The goal of nutritional therapy is the preservation of lean body mass by the safe and efficacious provision of metabolic substrate, thus improving patient survival.
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PMID:Nutritional support of the critically ill patient. 640 74

Continuous peritoneal dialysis has been used to maintain anephric dogs at chronically sustained low, normal, and high volume states in order to study the long-term interaction of volume and osmotic stimuli in the control of plasma vasopressin (PAVP). Bilaterally nephrectomized dogs were maintained for 1-3 mo with normal plasma sodium and potassium levels and blood urea nitrogen of 70.1 +/- 10.8 mg/dl. During the first month, the dogs were dialysized to each of the three volume states. After each volume state had been maintained for 7 days, an osmotic forcing with intravenous distilled H2O and hypertonic NaCl was performed in the conscious state to quantitate the relationship between plasma osmolality (Posm) and PAVP. During the osmotic forcings left atrial pressure (LAP) averaged -2.4 +/- 0.5, 2.6 +/- 0.8, and 11.9 +/- 1.1 cmH2O; mean arterial pressure averaged 113 +/- 11, 125 +/- 10, and 148 +/- 8 mmHg, both respective for the low, normal, and high volume states. The slope of the normovolemic Posm-PAVP relationship was determined to be 0.047 pg X ml-1 X mosmol-1 X kg-1, and neither the hypovolemic or hypervolemic relationships were significantly different. The results demonstrate two additional points that must be considered in the control of PAVP. First, the severely depressed sensitivity of osmotic PAVP control suggests that either the dialysis procedures or the absence of the kidneys suppressed or eliminated some factor normally important to the secretion of vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Osmotic control of vasopressin with chronically altered volume states in anephric dogs. 647 13

Plasma vasopressin, arterial blood gas tensions, pH, arterial blood pressure, heart rate and respiration were monitored in conscious rats breathing room air or exposed to varying degrees of hypoxia. A similar series of observations was made in a group of anaesthetized rats and in rats treated with alpha- and beta-adrenergic and dopaminergic blocking agents. The effect of two opioid antagonists on the vasopressin response was also noted. Hypoxia produced an increase in circulating vasopressin concentrations in both conscious and anaesthetized rats. In the conscious animals the increase reached statistical significance when the animals were exposed to 12% oxygen in nitrogen, which produced a fall in arterial PaO2 of 44.7 +/- 5.0%. Guanethidine, phentolamine and propranolol all produced a significant fall in the basal concentrations of vasopressin, while guanethidine, phenoxybenzamine and propranolol blocked the increase seen on breathing 12% oxygen in nitrogen. Naloxone and levallorphan also reduced the vasopressin response to hypoxia. Thus it appears that aminergic pathways play a role in the maintenance of circulating concentrations of vasopressin and in the response to hypoxia. Endogenous opioids also appear to be involved in the hypoxic response.
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PMID:Release of vasopressin in response to hypoxia and the effect of aminergic and opioid antagonists. 663 8


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