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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxytocinase and human placental lactogen (hPL) were measured in 705 serial maternal plasma samples collected from 74 patients whose pregnancies were complicated by hypertension. The trend and absolute levels of each substance were evaluated in a search for reliable antepartum indicators of intrauterine growth retardation (IUGR). There were 21 patients who were delivered of growth-retarded infants and the oxytocinase values were abnormal in 16 cases (75 per cent), while hPL levels were abnormal in 15 cases (71 per cent). There were 24 patients with subnormal placental weights. Abnormal oxytocinase values were observed in 17 (71 per cent) and abnormal hPL in 19 cases (79 per cent). The remaining 37 patients had "normal" fetal and placental weights. Abnormal oxytocinase values were observed in 15 patients (41 per cent) and abnormal hPL in 19 (52 per cent). In this group of pregnant mothers thought to be at risk for IUGR due to pregnancy hypertension, either test alone predicted subnormal neonatal or placental weight in about three fourths of cases. However, in the mothers with hypertension, who had no evidence of IUGR, false abnormal values of oxytocinase and hPL were found in nearly half the patients. No advantage was gained in the predictive accuracy when both tests were used.
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PMID:Oxytocinase and human placental lactogen for the prediction of intrauterine growth retardation. 92 Jul 68

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

To elucidate the involvement of angiotensin in puerperal hypertension with and without preeclampsia in the course of prior pregnancy, we measured plasma angiotensin I levels and serum placental leucine aminopeptidase (P-LAP) activities in several puerperal hypertensive patients. Placental leucine aminopeptidase (P-LAP) activities of puerperal hypertensive patients with severe preeclampsia during prior pregnancy were equal to or somewhat lower levels than those in normal puerperal women after a normal pregnancy. However, their angiotensin I levels were higher than those in normal puerperal women after a normal pregnancy. In puerperal hypertensive patients with and without preeclampsia during prior pregnancy, P-LAP activities tended to show much lower levels that those in normal puerperal women, while angiotensin I levels tended to show much higher levels than those in normal puerperal women, respectively. Since serum placental leucine aminopeptidase acts as an angiotensinase via degradation of angiotensin III (A-III), our present data suggest the involvement of angiotensin in puerperal hypertension.
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PMID:Plasma angiotensin I concentration and serum placental leucine aminopeptidase (P-LAP) activities in puerperal hypertension. 823 62

Transient diabetes insipidus of pregnancy (TDIP) is associated with elevated activity of vasopressinase, a plasma enzyme that opens the vasopressin (AVP) ring to produce a linear peptide that we have named vasopressinase-altered vasopressin (VAV). VAV may play a role in the pathogenesis of the arterial hypertension associated with TDIP. We sought to determine if VAV elevates arterial pressure, the potency of VAV relative to that of AVP, and whether the peptide binds to the vascular AVP receptor. AVP was incubated with vasopressinase and VAV was separated from residual AVP by high-pressure liquid chromatography. Intravenous bolus administration of VAV or AVP to ganglionic blocked rats produced dose-dependent increases in arterial pressure, with VAV demonstrating approximately 6000-fold lower potency than AVP. Vasopressin receptor blockade abolished the response to both AVP and VAV. These results suggests that high levels of VAV may contribute to the hypertension seen in TDIP.
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PMID:Vasopressinase-altered vasopressin elevates arterial pressure in anesthetized rats. 847 82

Pituitary adenomas are the most common pituitary disorder affecting pregnancy, and prolactinomas are the most common of the hormone-secreting pituitary adenomas. Hyperprolactinemia must be corrected to allow ovulation and fertility. Bromocriptine has been shown to be safe for use during early gestation. There is less than a 2% risk of microprolactinoma enlargement during pregnancy but a greater than 15% risk of symptomatic enlargement of a macroprolactinoma. Treatment options for patients with macroadenomas include stopping bromocriptine when pregnancy is diagnosed and reinstituting with tumor enlargement, continuous bromocriptine throughout pregnancy, and prepregnancy tumor debulking by surgery. The diagnosis of acromegaly may be difficult to make during pregnancy and relies, in part, on the persistence of the normal pulsatile secretion of growth hormone and loss of this secretory characteristic with a tumor. The growth hormone oversecretion may exacerbate tendencies to gestational diabetes, fluid retention, and hypertension. Treatment for acromegaly and other tumors generally may be deferred until after delivery. There are rare reports of enlargement of clinically nonfunctioning and growth hormone secreting tumors during pregnancy, and surveillance is needed. Tumors may need to be differentiated from lymphocytic hypophysitis. Patients with chronic hypopituitarism usually will need treatment with gonadotropins or pulsatile GnRH to become pregnant and may need increased steroid coverage during labor and delivery. Hypopituitarism developing during pregnancy is usually caused by lymphocytic hypophysitis and usually also will require steroid replacement therapy. Hypopituitarism arising postpartum may be caused by either lymphocytic hypophysitis or Sheehan's syndrome, and the latter may present as an acute or chronic syndrome. Borderline diabetes insipidus may manifest during pregnancy because of increased vasopressin degradation caused by markedly increased levels of placental vasopressinase. Treatment with desmopressin usually is satisfactory. Patients presenting with either anterior or posterior pituitary insufficiency in the peripartum period should always be evaluated for function of the other portion of the pituitary.
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PMID:Pituitary diseases in pregnancy. 988 Jan 16

From ethical and moral reasons, the progress in neonatology and anesthesiology must not obscure the iatrogenic labors, which begin at the time improper for individual child, especially after induction and - because of that - very often instrumental. Enzymatic monitoring has enabled reduction of the number of preterm and instrumental deliveries, and--more importantly--the elimination of statistical (so-called post-datism) indications for terminating pregnancies instead of natural their individual occurrence in the entire range of physiological norm of human labors from 37 0/7 to 43 2/7 weeks. During pregnancy the mothers organism has to secure a proper environment for the growth and development of the child, which is accompanied by the constant increase in oxytocinase and isoxytocinase. These enzymes are closely connected even with the regulation of ovulation as well as with the embryo nidation and development of early pregnancy. Both enzymes are very important indicator of the threatened life and health of the fetus. It is important since these changes precede clinical symptoms by several weeks. On the other hand, they enable monitoring of the efficiency of ACTH depot therapy as well as pregnancy complicated by diabetes, hypertension and endocrinopathies. The values of prenatal oxytocinasaemia make possible prediction the date and course of delivery. Also, they are highly positively correlated with the weight, length and maturity of the newborn, as well as the size of the placenta. In multifetal pregnancies, levels of both enzymes are higher than in single ones.
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PMID:Enzymes: the most important markers of pregnancy development. 1174 17

Although angiotensin II has long been considered to represent the end product of the renin-angiotensin system (RAS), there is accumulating evidence that it encompasses additional effector peptides with diverse functions. In this respect, angiotensin IV (Ang IV) formed by deletion of the two N terminal amino acids, has sparked great interest because of its wide range of physiological effects. Among those, its facilitatory role in memory acquisition and retrieval is of special therapeutic relevance. High affinity binding sites for this peptide have been denoted as AT(4)- receptors and, very recently, they have been proposed to correspond to the membrane-associated OTase/ IRAP aminopeptidase. This offers new opportunities for examining physiological roles of Ang IV in the fields of cognition, cardiovascular and renal metabolism and pathophysiological conditions like diabetes and hypertension. Still new recognition sites may be unveiled for this and other angiotensin fragments. Recognition sites for Ang-(1-7) (deletion of the C terminal amino acid) are still elusive and some of the actions of angiotensin III (deletion of the N terminal amino acid) in the CNS are hard to explain on the basis of their interaction with AT(1)-receptors only. A more thorough cross-talk between in vitro investigations on native and transfected cell lines and in vivo investigations on healthy, diseased and transgenic animals may prove to be essential to further unravel the molecular basis of the physiological actions of these small endogenous angiotensin fragments.
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PMID:Cellular targets for angiotensin II fragments: pharmacological and molecular evidence. 1258 63

In addition to the neural and autoregulatory factors, blood pressure (BP) is regulated by humoral factors including vasoactive peptides. When evaluating the peptide actions, degradation by proteases should be also considered in addition to the generation of peptides and their receptors. This review describes the roles of aminopeptidase A, placental leucine aminopeptidase and kininase I, which are enzymes responsible for hydrolyzing angiotensin II (AngII), vasopressin (AVP) and bradykinin (BK), respectively, in BP regulation. Especially, we focus on the association of the proteases with preeclampsia, hypertensive disorder peculiar to pregnancy, since one of the representative organs that are rich in theses proteases is placenta. Although the physiological roles of the placental proteases have not been fully understood, several lines of evidence suggest that the proteases are involved in the maintenance of pregnancy homeostasis including fetal and maternal BP regulation through the metabolism of bioactive peptides at the interface between mother and fetus.
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PMID:Role of aminopeptidases in the blood pressure regulation. 1518 14

Pregnancy is marked by the placental production of vasopressinase, an enzyme which accelerates the metabolic clearance of arginine vasopressin (AVP), and serum vasopressinase is reported to be abnormally elevated in hypertensive pregnancy. Since platelet AVP binding capacity is influenced by the plasma AVP concentration, we sought to determine whether alterations in vasopressinase and AVP concentrations affect platelet responsiveness to AVP in normotensive and hypertensive pregnancy. Four groups of 10 women were studied: non-pregnant subjects, normotensive pregnancy, hypertensive pregnancy, and pre-eclampsia (PE). AVP-induced platelet aggregation was measured turbidometrically, serum vasopressinase by chromogenic assay and plasma AVP by radioimmunoassay. Platelet responses to AVP were similar in all groups, as were plasma concentrations of AVP. Vasopressinase was raised in all pregnant patients compared with non-pregnant subjects, and levels were significantly higher in pregnancy-induced hypertension than in either the normotensive or PE groups (p<0.05). No significant correlation was observed between platelet responsiveness to AVP and circulating concentrations of either AVP or vasopressinase. Thus circulating vasopressinase is increased in pregnancy and abnormally so in hypertensive pregnancy. This does not, however, appear to influence ex vivo platelet responsiveness to AVP.
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PMID:Serum Vasopressinase and Platelet Responses to Arginine Vasopressin in Normal Pregnancy, Pregnancy-induced Hypertension and Pre-eclampsia. 2104 9

Reducing angiotensin II (Ang II) production via angiotensin-converting enzyme (ACE) inhibitors is a key approach for the treatment of hypertension. However, these inhibitors may also affect other enzymes, such as angiotensinases and vasopressinase, responsible for the metabolism of other peptides also involved in blood pressure control, such as Ang 2-10, Ang III, Ang IV, and vasopressin. We analyzed the activity of these enzymes in the hypothalamus, plasma, and kidney of normotensive adult male rats after inhibition of ACE with captopril. Aspartyl- (AspAP), glutamyl- (GluAP), alanyl- (AlaAP) and cystinyl-aminopeptidase (CysAP) activities were measured fluorimetrically using arylamides as substrates. Systolic blood pressure (SBP), water intake, and urine flow were also measured. Captopril reduced SBP and increased urine flow. In the hypothalamus, GluAP and AspAP increased, without significant changes in either AlaAP or CysAP. In contrast with effects in plasma, GluAP was unaffected, AspAP decreased, while AlaAP and CysAP increased. In the kidney, enzymatic activities did not change in the cortex, but decreased in the medulla. These data suggest that after ACE inhibition, the metabolism of Ang I in hypothalamus may lead mainly to Ang 2-10 formation. In plasma, the results suggest an increased formation of Ang IV together with increased vasopressinase activity. In the kidney, there is a reduction of vasopressinase activity in the medulla, suggesting a functional reduction of vasopressin in this location. The present data suggest the existence of alternative pathways in addition to ACE inhibition that might be involved in reducing BP after captopril treatment.
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PMID:Angiotensinase and vasopressinase activities in hypothalamus, plasma, and kidney after inhibition of angiotensin-converting enzyme: basis for a new working hypothesis. 2220 40


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