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)

Epidemiological information on calcium oxalate urolithiasis is reviewed and interpreted according to a proposed stress-related mechanism. This mechanism involves hypothalamo-hypophyseal secretion firstly of vasopressin which acts directly to produce hypertonic urine and secondly of adrenocorticotropin which acts via a secondary hyperparathyroid mechanism to raise serum calcium levels.
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PMID:Stress as a principal cause of calcium oxalate urolithiasis. 302 44

A rapid method for isolating highly purified rat liver plasma membrane vesicles using isotonic medium and Percoll self-forming gradient centrifugation is described. The vesicles were characterized by enzyme markers and electron microscopy. The method also yielded a fraction rich in nuclei. The vesicles transported Ca2+ in an ATP-dependent manner and this was enhanced by oxalate. The Vmax for Ca2+ uptake was 0.65 +/- 0.08 nmol/mg X min, which was approximately 18-fold higher than for other liver plasma membrane preparations, and the Km for Ca2+ was 5.2 +/- 0.4 nM. Calcium uptake was inhibited by 40-50% in vesicles isolated from rat livers perfused for 3 min with 10(-7)M vasopressin. The half-maximally effective concentration of vasopressin was 5 X 10(-10)M which correlates with that for raising cytosolic Ca2+ and phosphorylase a. Inhibition was not significant in vesicles from livers perfused with vasopressin for only 1 min, indicating that inhibition of the Ca2+ pump may not be involved in the rise in cytosolic Ca2+ observed at 1-2 s with this hormone. Epinephrine (10(-5)M) and angiotensin II (10(-7)M) inhibited Ca2+ uptake by 31 +/- 10 and 26 +/- 5%, respectively, at 3 min. Glucagon (10(-7)M) had no effect. It is proposed that the inhibitory action of the Ca2+-dependent hormones on the plasma membrane Ca2+ pump plays an important role in the actions of these hormones by prolonging the elevation in cytosolic Ca2+.
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PMID:Vasopressin-, angiotensin II-, and alpha 1-adrenergic-induced inhibition of Ca2+ transport by rat liver plasma membrane vesicles. 669 8

Oxalate was shown to enter isolated rat hepatocytes and to inhibit gluconeogenesis from lactate, pyruvate, and alanine, but not from glutamine, proline, propionate or dihydroxyacetone. Oxalate apparently acts by inhibiting pyruvate carboxylase (EC 6.4.1.1.). It is known to inhibit the isolated enzyme, and inhibition of gluconeogenesis was much greater in a bicarbonate-deficient medium where pyruvate carboxylase activity limits the overall rate of the pathway. A slight inhibition of gluconeogenesis from asparagine was observed, suggesting that oxalate may also inhibit gluconeogenesis at another site. Chelation of extracellular Ca2+ does not contribute to the inhibition of gluconeogenesis. Compared to oxalate, other Ca2+ chelators have little effect upon gluconeogenesis. Also, oxalate inhibits gluconeogenesis effectively both in low Ca2+ medium and in medium containing 2.6 mM Ca2+. Chelation of intracellular Ca2+ also appears to be of little importance, since oxalate does not block the glycogenolytic effects of epinephrine, vasopressin, and angiotensin which are thought to act via Ca2+ as the second messenger. The inhibition of gluconeogenesis could conceivably contribute to the toxic actions of oxalate and to the hypoglycemic action of dichloroacetate, a compound that is metabolized to oxalate. However, oxalate did not cause hypoglycemia in the suckling rat, a model in vivo system very dependent upon gluconeogenesis for maintenance of normal blood glucose levels. Thus, inhibition of gluconeogenesis is probably of little importance in oxalate toxicity and the hypoglycemic effects of dichloroacetate.
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PMID:Studies on the inhibition of gluconeogenesis by oxalate. 677 9

The pathogenesis of active renal stone disease (ARSD) is still not fully elucidated. In the present study the role of atrial natriuretic peptide (ANP) and arginine-vasopressin (AVP) as potential pathogenetic factors in ARSD were examined. Thirty patients with ARSD and 21 healthy subjects (HS) were examined both under bed rest (BR) and head-out water immersion (WI) conditions. Serum concentrations of electrolytes (Na, Ca, Mg), ANP and AVP were assessed before (0'), and after 60 and 120 minutes of BR or WI, respectively. Urinary excretions of Na, Ca, Mg, and oxalates were also estimated during BR and WI. Patients with ARSD showed higher basal plasma levels of ANP and a greater response of ANP secretion, but a lower suppression of plasma AVP to WI induced hypervolaemia as compared with the controls. In addition, in patients with ARSD the physiological relationship between plasma AVP concentration and urinary excretion of Ca and Mg (positive correlation), between plasma ANP level and urinary excretion of Ca and Mg (negative correlation), and between plasma ANP and AVP concentration (negative correlation), respectively, were absent. In addition, patients with ARSD showed a positive correlation between plasma ANP and urinary oxalate excretion. From the results obtained in this study we conclude that both AVP and ANP may be involved in the pathogenesis of ARSD.
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PMID:Atrial natriuretic peptide and arginine-vasopressin secretion in patients with active renal stone disease. 969 46