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)

Platelet behaviour was studied in groups of women suffering from mild and severe pre-eclampsia, and compared with normal pregnant and non-pregnant controls. Platelets from women with severe pre-eclampsia were less responsive than normal to a variety of aggregating agents, and this impairment was significant in response to collagen and vasopressin. Women with severe pre-eclampsia had raised plasma adenine nucleotide levels and lowered platelet 5-hydroxytryptamine levels compared with the controls. Platelets from women with mild pre-eclampsia showed only a slight difference from normal. These findings may be the result of platelets having undergone aggregation and disaggregation within the circulation, and suggest that platelets may be involved in the pathogenesis of pre-eclampsia.
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PMID:Abnormal platelet function in pre-eclampsia. 62 22

Primary peripheral arterial vasodilation with relative underfilling of the arterial circulation occurs in early pregnancy and leads to several consequences, including decreased systolic and diastolic blood pressures, enhanced cardiac output secondary to afterload reduction, stimulation of the renin-angiotensin-aldosterone axis, nonosmotic stimulation of thirst and vasopressin release, and renal sodium and water retention with expansion of the extracellular fluid and plasma volume compartments. These are events known to occur in all states of arterial vasodilation. Pregnancy has, however, several unique features. Primary arterial vasodilation generally is associated with no change or a decrease in renal blood flow and glomerular filtration rate and failure to escape from the sodium-retaining effects of aldosterone. In early pregnancy, renal blood flow and glomerular filtration rate increase by 30-50% in parallel with the peripheral arterial vasodilation but before plasma volume expansion. No known vasodilator exhibits such a profound effect on renal hemodynamics. Vasodilating prostaglandins may contribute to, but cannot explain, this remarkable enhancement of renal hemodynamics in early pregnancy. Therefore, a highly potent, as yet undefined, systemic and renal vasodilator must be unique to pregnancy. The increased glomerular filtration rate and filtered sodium load with enhanced distal tubular sodium delivery allows escape from aldosterone, an effect not observed in other states of arterial underfilling. This vasodilator may also account, at least in part, for the vascular resistance to angiotensin known to occur in normal pregnancy. This hypothesis for the normal physiology of pregnancy sets the stage for understanding the pathogenesis of preeclampsia-eclampsia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peripheral arterial vasodilation hypothesis of sodium and water retention in pregnancy: implications for pathogenesis of preeclampsia-eclampsia. 206 82

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 contractile responses to various endogenous vasoactive agents were investigated in isolated human uteroplacental arteries from normotensive (NT) patients and patients with pre-eclampsia (PE) undergoing caesarian section. Tissue samples were obtained from the uterine incision and from macroscopically normal cotyledons. Vascular ring preparations of intramyometrial and stem villous arteries (length 1.0-1.3 mm, outer diameter 400-600 microns) were dissected and mounted in organ baths and isometric tension was recorded. Concentration-response relationships for vasopressin (VP), oxytocin (OX), angiotensin II (Ang II), noradrenaline (NA), 5-hydroxytryptamine (5-HT), prostaglandin F2 alpha (PGF2 alpha) and prostaglandin E2 (PGE2) were assessed. For each compound, the mean maximum contractile effect (Emax) and the drug concentration producing half-maximal response (EC50) were determined. In intramyometrial arteries from NT and PE patients, VP, Ang II, NA, 5-HT and PGF2 alpha induced contraction while OX and PGE2 produced weak or no responses. Preparations from PE patients showed higher Emax values, while no differences in EC50 were found between the two groups. In fetal stem villous arteries, Ang II, 5-HT, PGF2 alpha and PGE2 induced contractions, while VP, NA and OX produced weak responses. No differences in Emax or EC50 values were found between the fetal vessels of PE and NT patients. No qualitative differences were demonstrated in response to the agents tested between the vessels (fetal and maternal) from NT women at term and PE patients. However, the results may reflect quantitative differences, suggesting increased contractility of maternal uteroplacental arteries from women with PE.
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PMID:Effect of endogenous vasoconstrictors on maternal intramyometrial and fetal stem villous arteries in pre-eclampsia. 276 Apr 57

Decreased free water excretion and the development of interstitial edema are recognized characteristics of preeclampsia. However, the pathophysiology of decreased urine excretion in preeclampsia is presently controversial: diminished glomerular filtration, renal arteriolar spasm, elevated plasma vasopressin levels, and plasma volume contraction have been suggested as etiologies. We studied seven pregnant patients with a diagnosis of mild preeclampsia to assess the role of vasopressin, serum protein, and glomerular function in the renal excretion of water. The ability to excrete a water load was significantly and directly correlated with serum albumin (P less than 0.05) and protein (P less than 0.02) concentrations. Neither plasma vasopressin nor creatinine clearance correlated with water excretion. The similarity of preeclampsia and the nephrotic syndrome with regard to the renal excretion of water is discussed.
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PMID:Water excretion in preeclampsia: behavior as nephrotic syndrome. 405 79

The maternal serum concentration of antidiuretic hormone (ADH) in a pregnancy uncomplicated by preeclampsia is identical to the ADH concentration in the nonpregnant female and normal male. However, elevated maternal ADH secondary to fetal hypothalamic ADH production and a genetic defect in maternal vasopressinase may be a cause of preeclampsia.
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PMID:A hypothesis on the role of antidiuretic hormone in preeclampsia. 664 13

Both fetal and maternal blood pressure is regulated mainly by the humoral factor, vasoactive peptides such as angiotensin II and vasopressin, but not by autoregulation and the autonomic nervous system. It is known that the normal musculoelastic tissue in the vessel wall of the coiled artery, which supplies blood to the uteroplacental blood pool, is replaced by fibrinous tissue with advancing gestation. Therefore uteroplacental circulation is similar to arterio-venous shunt; it is possibly important for the homeostasis of maternal blood pressure. It is known that hypoxemia results in both the redistribution of feto-placental blood flow, the increase of blood flow in the placenta, and the increase of fetal vasoactive peptides. Since placental proteases (vasopressinase and angiotensinase) degrade vasoactive peptides, placental proteases protect the placental vessels from the vasoconstriction by vasoactive peptides and might contribute to the redistribution of feto-placental blood flow. Therefore placental proteases effect on fetal blood pressure via regulation of fetal vasoactive peptides, which regulate placental blood flow. Although human and animal pregnancy is normally associated with a refractory response to the pressor effect of exogenously infused angiotensin II, patients with pre-eclampsia as well as nonpregnant women are sensitive to angiotensin II; thin phenomenon has been studied as one of the causes of pre-eclampsia. Since the administration of placental angiotensinase was effective in lowering blood pressure in rats with hypertension induced by the infusion of angiotensin II, placental proteases are possibly involved in the refractory response to exogenously infused angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Possible role of placental proteases via degradation of vasoactive peptides in the maternal and fetal blood pressure]. 808 9

Oxytocinase (EC 3.4.11.3) activity was determined in 80 amniotic fluid samples obtained from 40 normotensive primigravidas (median age 27 years) and 40 primigravidas (median age 29 years) with pregnancies complicated by preeclampsia between 32 and 39 weeks of gestation. The enzyme activity was significantly lower in preeclampsia than in normal pregnancy with matched gestations (p < 0.01). Considering the possible involvement of vasopressin and angiotensin II in preeclampsia, it is suggested that the enzyme which degrades these pressor hormones may play a role in the pathogenesis of hypertensive pregnancy.
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PMID:Decreased levels of amniotic fluid oxytocinase activity in preeclampsia. 850 9

Although many protease exist in human placenta, their physiologic roles are still unknown. Our study showed that placenta proteases metabolize vasoactive peptides possibly derived from the fetus. Because vasopressin and angiotensin are known to play an important role in normal and aberrant (preeclampsia) fetal-placental circulation, the clearance of these peptides in the placenta is important in controlling fetal blood pressure. Vasopressin and angiotensin act as a fetal-placental vasoconstrictor; therefore, placental proteases in human placenta are likely to work as a clearance factor for these peptides. Although human and animal pregnancy is normally associated with a refractory response to the pressor effect of exogenously infused angiotensin II, patients with preeclampsia, as well as nonpregnant women, are sensitive to the pressor effect of angiotensin II. Our study suggested that the decreased pressor responsiveness to angiotensin II in pregnancy is caused by increased inactivation of angiotensin II by angiotensinase in pregnant serum and the placenta. Although vasopressinase and angiotensinase activities increase with advancing gestation in normal pregnant sera, the activities of both enzymes in severe preeclampsia sera were clearly lower than those in normal pregnancy. Therefore, it is reasonable to speculate that the increased sensitivity to angiotensin II of preeclampsia is attributable to the decreased degradation of angiotensin II by placental angiotensinase. The negative correlations between the systolic to diastolic ratio obtained from pulsed Doppler measurement techniques and the activities of both enzymes in preeclampsia sera suggested that the systolic to diastolic ration, which reflected constriction of placental vessels, is influenced by the concentration of vasoactive peptides in the fetal-placental circulation due to changes in the activities of placental proteases. Placental proteases play important roles in controlling fetal and maternal blood pressure through regulation of the concentration of vasoactive peptides in the interface (placenta) between fetus and mother.
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PMID:Effects of placental proteases on maternal and fetal blood pressure in normal pregnancy and preeclampsia. 878 84

Synthetic 1-deamino-8-D-arginine-vasopressin (DDAVP) is used in the management of diabetes insipidus (DI). We conducted a systematic literature review of DDAVP use during pregnancy, with particular attention to its safety for both mother and infant. Studies were identified through Ovid MEDLINE from 1976 to July 1997 using the combined terms "desmopressin," "DDAVP," and "pregnancy". Review articles and published letters were also explored. One hundred one articles were retrieved, of which 20 met all the inclusion criteria. Included in the 20 articles were 53 cases with the use of DDAVP for the management of DI. The therapeutic daily dose of DDAVP was approximately 29 micrograms intranasally (range 7.5-100 micrograms), with adequate DI control observed. Three of 14 women with sufficient information developed preeclampsia, a nonsignificant difference from the expected rate of 5 percent (the Fisher exact test, 2-P = .08). The mode of delivery was defined for 22 cases, with 16 uneventful vaginal births, and six cesarean delivery. There was no evidence of a drug interaction among the five women who received both DDAVP and intravenous oxytocin. Information was available on 49 live births born to DI mothers on DDAVP. The mean gestational age at delivery was 37.4 weeks (SD 1.3 weeks), with an estimated mean birth weight of 2963.8 gm (range 2000-4420 gm). Forty-three offspring were reported as healthy (event rate 87.8 percent; 95 percent CI 77.2-95.3 percent). Of the remaining six infants, one developed DI at 18 months of age; a second was under 2500 gm at birth, but survived; the third developed hypotonia and failure to thrive at 21 months, two others had Down syndrome; and the sixth died of severe cardiac anomalies. Similar data were seen among the 41 infants whose mothers had used DDAVP throughout pregnancy. In conclusion, DDAVP use during pregnancy seems to be safe for both mother and child. Delivery does not seem to be augmented by its use, nor are there likely any associated adverse neonatal effects. A large database of DDAVP use during pregnancy is needed to confirm these findings.
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PMID:DDAVP use during pregnancy: an analysis of its safety for mother and child. 966 31


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