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)

Preeclampsia is characterized by increased vascular sensitivity to Angiotensin II, endothelial damage, and arteriolar spasm. We hypothesize that these events may be initiated by stimulation of V1 receptors. V1 receptors are normally activated by vasopressin. However, V1 receptors may be activated by the nonapeptide formed when vasopressin is metabolized by the placental enzyme--vasopressinase. This enzyme, found only in humans, cleaves the ring structure of vasopressin, but leaves the N-terminal end, the locus of pressor activity, intact. The resulting molecule, vasopressinase altered vasopressin (VAV), may be present in greater concentration in preeclamptic women and over the months of the second trimester initiate the cascade of pathophysiologic changes resulting in toxemia.
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PMID:A proposed relationship between vasopressinase altered vasopressin and preeclampsia. 219 37

The concentrations of vasopressin in the amniotic fluid were measured in 40 patients. The pregnancies were complicated by diabetes, toxemia or imminent premature delivery and in one case by polyhydramnion. The gestation time varied from 33 to 41 weeks. In addition, we measured vasopressin concentrations after transabdominal drainage of fetal bladder in three cases with urethral obstruction. Detectable concentrations of vasopressin in the amniotic fluid were found in all but four of the 40 cases observed. The vasopressin concentrations varied from 0.21 to 1.81 pg/ml. There were no systematic differences in the values in relation to duration of gestation or disease present. The highest vasopressin concentration was observed in the patient with polyhydramnion. No detectable amount of vasopressin was found in the urine of the three fetuses examined. The results suggest that, in contrast to earlier studies, the placenta may be permeable to small amounts of vasopressin or may itself be an origin of this hormone. The maternal complications present seem to have no effect of the vasopressin concentrations in the amniotic fluid.
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PMID:Fetal vasopressin in late pregnancy. Levels in amniotic fluid and in fetal urine. 347 81

A 29-year-old nullipara was admitted at 31 weeks' gestation because of toxemia. She noted gradually polyuria, severe thirst, malaise, nausea and anorexia. A water-deprivation test and administration of aqueous vasopressin confirmed the diagnosis of nephrogenic diabetes insipidus. At 33 weeks' gestation, blood chemistry studies revealed moderately elevated transaminase levels and hyperuricemia. Male twins were delivered by vacuum extraction at 35 weeks' gestation. After delivery, she became drousy and icterus appeared. Acute hepatic failure with marked hyperuricemia was diagnosed. She was treated with glucose solution with glucagon and soluble insulin, branched chain amino acids, gabexate mesilate, lactulose and famotidine. Her consciousness cleared rapidly and all laboratory data became normal by 15 days postpartum. The urine volume was about 5 liters per day from the first to sixth postpartum day. The diuresis decreased after the eighth postpartum day. Rare pregnancy complicated by transient nephrogenic diabetes insipidus and acute hepatic failure is discussed.
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PMID:Transient nephrogenic diabetes insipidus associated with acute hepatic failure in pregnancy. 365 42

The 24-hour urinary excretion of kallikrein (K) and prostaglandin E2 (PGE2), which reflects their intrarenal synthesis, was measured in 7 normal women (NW), 10 women with essential hypertension (EH), 26 normal pregnant women (NP), 12 women with hypertension in pregnancy (HP), and 4 women with toxemia. All pregnant women were in the last trimester of their pregnancy (week 24-40). K was raised in NP (99.6 +/- 8.1 KU/24 h) and HP (106.5 +/- 8 KU/24 h) compared to NW (57 +/- 8.23 KU/24 h) (p less than 0.05). PGE2 excretion was decreased in EH (403.25 +/- 90.6 ng/24 h) compared to NW (508.6 +/- 80.26 ng/24 h). During pregnancy PGE2 was increased to 1,088 +/- 93.2 ng/24 h in NP and significantly more in HP, 1,885 +/- 40 ng/24 h (p less than 0.002). In this regard it differed from K. These data may suggest that, in addition to K, other factors (as angiotensin II and/or antidiuretic hormone) possibly activate renal PGE2 production in HP. In toxemia, K (23 +/- 6.1 KU/24 h) and PGE2 (583 +/- 172.83 ng/24 h) were markedly decreased. The above results suggest that the renal kallikrein-kinin and prostaglandin systems may play a role in sodium homeostasis during pregnancy. Their exact influence on the pathogenesis of hypertension in nonpregnant, pregnant, and toxemic subjects awaits further investigation.
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PMID:Urinary kallikrein in normal pregnancy, pregnancy with hypertension, and toxemia. 385