Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma renin activity and aldosterone concentrations were measured simultaneously with urinary excretion of kallikrein and four prostaglandins (PGE2, PGF2 alpha, 6 keto PFG1 alpha and TXB2) in 23 patients with pregnancy induced hypertension (17 with permanent PIH and six with labile PIH, since in these latter their hypertension was controlled only by home bed rest) and in 16 normotensive pregnant women at the same stage of gestation (31 +/- 3 weeks). PRA was lower in permanent PIH than in controls and in labile PIH. No difference between the three groups was observed for plasma aldosterone and the urinary excretion of kallikrein and of the prostaglandins except that TXB2 was higher in labile PIH than in permanent PIH. Correlation studies of kallikrein disclosed correlations with most prostaglandin excretions, explained by the physiological stimulation of phospholipase A2 by kallidin. Correlation studies of PRA disclosed unexpected negative correlation with PGE2 and 6 keto PGF1 alpha in the permanent PIH group. In conclusion, labile PIH has a different biological profile than permanent PIH since they have higher PRA and higher TXB2 excretion, an association which suggests a more pronounced ureteral compression by the gravid uterus in this group. Permanent PIH has a disregulation of the renin angiotensin-prostacyclin loop since PRA and 6 keto PGF1 are negatively correlated. This suggests the role of an independent vasopressive substance which would stimulate PGI2 and suppress renin secretion.
 ...
PMID:Renin angiotensin aldosterone system, urinary prostaglandins and kallikrein in pregnancy induced hypertension. Evidence for a disregulation of the renin-angiotensin-prostacyclin loop. 384 87

Serial blood samples were obtained throughout pregnancy from 11 women with essential hypertension (EHT). Seven were treated with labetalol (Trandate) and 4 with alpha -methyl dopa (Aldomet). Nine patients were well-controlled throughout pregnancy. Their mean plasma renin concentrations (PRC) followed the profile determined in 18 normal patients studied serially. They remained in the upper normal range until the last month, when both treatment groups showed a fall in PRC. Mean plasma aldosterone (ALD) also followed a normal profile until late gestation when it too showed a sharp fall. Of the two patients who developed superimposed PIH, one, who received labetalol, developed severe hypertension at 35 weeks, requiring delivery. Although PRC increased early in this pregnancy, ALD did not, remaining low throughout. Serum potassium [K+] measurements were also very low in this patient. The second patient only became hypertensive at 40 weeks and had PRC and ALD profiles resembling those in the successfully treated EHTs. There was a strong positive correlation throughout between serum potassium and ALD measurements (p less than 0.001) but none between PRC and ALD. This latter agrees with the known lack of correlation between PRC and ALD in normal pregnancy and may suggest that changes in electrolyte balance are more important stimuli to ALD secretion during pregnancy.
 ...
PMID:Renin and aldosterone concentrations in pregnant essential hypertensives - a prospective study. 634 44

We have measured simultaneously plasma renin activity (PRA), aldosterone and catecholamines in the plasma of 3 groups of pregnant women after the 20th week: group 1 of 16 normotensive controls, group II of 17 women with rest responding hypertension (RRH), group III of 18 women with permanent hypertension (PIH). All the patients were ambulatory on a normal salt diet. PRA was significantly higher in the RRH than in the control and PIH groups (15,8 +/- 2,3ng/ml/l versus 6,7 +/- 0,5 and 8,9 +/- 0,9 respectively). Plasma epinephrine (PE) and norepinephrine (PNE) were significantly higher in the PIH than in the control and RRH groups (respectively 135 +/- 28 pg/ml versus 56 +/- 13 and 63 +/- 17 for PE and 387 +/- 91 versus 206 +/- 32 and 200 +/- 47 pg/ml for PNE). In the PIH group there was a negative correlation between PRA and blood uric acid. It is concluded that the adrenic system is activated in PIH whereas the renin angiotensin system is activated in RRH of pregnancy.
 ...
PMID:Renin angiotensin aldosterone system and adrenergic system in normotensive and hypertensive pregnancy. 676 65

Serum concentrations and urinary output of calcium, magnesium, sodium and potassium were analysed in normotensive pregnant women and in women with pregnancy-induced hypertension during the third trimester. In addition, plasma renin activity (PRA) was also determined. Significantly lower serum total calcium, urinary calcium and magnesium excretions and plasma renin activity were evident in women with PIH. Urine output and creatinine clearance were not significantly different between the two groups. No significant correlation was evident between serum calcium, magnesium and PRA. The relationship between these parameters and high blood pressure is not immediately apparent. They nevertheless suggest of a disturbance in electrolyte metabolism in women with PIH, that may underly the pathogenesis of this disorder.
 ...
PMID:Serum and urinary divalent cations and plasma renin activity in women with mild pregnancy-induced hypertension. 775 84

The placental lesions of the very low birthweight (VLBW) infant were investigated in relation to clinical complications leading to preterm birth and evidence of growth impairment. The 249 singleton gestations yielding infants less than 1500 g were grouped according to the clinical complications leading to preterm birth as premature membrane rupture (116/249, 47%) preterm labor (55/249, 22%), pregnancy-induced hypertension (PIH, 54/249, 22%), and normotensive abruption (ABR, 24/249, 10%). Specifically excluded from this data set were cases with greater than 2 weeks discordance, fetal congenital anomalies, placenta previa, and maternal medical or gestational diseases such as chronic hypertension and diabetes mellitus, and intrauterine growth retardation (IUGR) as a primary indication for delivery. Placental weight and lesions including decidual vasculopathy and related villous lesions, chronic villitis/intervillositis, and decidual plasmacytosis were considered as variables in analyses in which raw birthweight was the dependent variable and gestational age a confounder. Of the 195 VLBW, 79 (41%) infants from normotensive mothers had lesions of decidual vasculopathy or chronic inflammation. In the VLBW infants from hypertensive mothers, growth restriction was related to markers of decidual vasculopathy. In the absence of maternal hypertension the growth restriction was independently associated with chronic villitis. Decidual vasculopathy (characteristic of PIH) and chronic intrauterine inflammation underlie the complications of many normotensive VLBW infants. The placental lesions in VLBW-IUGR depend on the presence or absence of maternal hypertension. In the absence of maternal hypertension, VLBW-IUGR is associated with chronic inflammation and is independent of decidual vasculopathy. In the presence of maternal hypertension, VLBW-IUGR is directly related to decidual vasculopathy.
 ...
PMID:The very low birthweight infant: maternal complications leading to preterm birth, placental lesions, and intrauterine growth. 777 89

The aim of the present study was to assess whether changes in prostacyclin (PGI2) and thromboxane (TXA2) generation precede the manifestation of pregnancy-induced hypertension (PH). The metabolites 6-oxo-PGF1 alpha and TXB2 were measured in the urine of 69 randomly selected pregnant women from 16-20 weeks of gestation (wg) until delivery and more than 6 weeks postpartum. Between 16-20 and 21-24 wg 6-oxo-PGF1 alpha excretion did not change in patients who later developed PIH (n = 6) but increased significantly in the control group (n = 63). In contrast, a marked rise in TXB2 excretion was found in the PIH group but not in controls. Thereafter significant differences between both groups persisted from 25 wg until delivery. The 6-oxo-PGF1 alpha/TXB2 ratio was below the 10th percentile from 21-24 wg until delivery in patients with developing PIH. The excretion of both metabolites was substantially lower in the non-pregnant state without any difference between patient groups. These results show an altered urinary excretion of both 6-oxo-PGF1 alpha and TXB2 preceding the onset of the disease. A pathophysiological role of PGI2 deficiency and increased TXA2 formation in PIH appears substantiated.
 ...
PMID:Excretion of prostacyclin and thromboxane metabolites before, during, and after pregnancy-induced hypertension. 782 3

Platelet functions are becoming the useful tool for delineating the etiology of pregnancy induced hypertension. Electronmicroscopic studies, efflux and content of 5-HT in platelets and platelet aggregation responses towards various aggregating agents have been measured in 25 normotensive pregnant subjects and 31 PIH subjects. Marked decrease changes have been noted in aggregation parameters with transformation from discoid to "spiny sphere" of platelets with long pseudopods along with prolonged time for spontaneous aggregation by platelets in PIH. Serotonin release from platelets was decreased and reserpine-induced release-reaction showed enhanced kinetics in PIH. Platelet serotonin content was raised and was inversely related to platelet count with severity of syndrome. Hence, a check and balance for platelet activation and aggregation in PIH might be crucial in the development of PIH.
 ...
PMID:Relevance of platelet serotonergic mechanisms in pregnancy induced hypertension. 802 50

The aim of the present study was to investigate the occurrence of changes in the plasma levels of vasoactive prostanoids and inhibitors of blood coagulation in normal pregnancy and in cases of pregnancy induced hypertension. Levels of the coagulation inhibitors antithrombin III, protein C, Protein S as well as the prostaglandin metabolites thromboxane B2 and 6-oxo-prostaglandin F1 alpha were measured between 13 and 37 weeks gestation in 36 primigravidae. In 8 of the examined patients persistently raised blood pressure values of 140/90 and above were measured after 20 weeks of gestation. Our results indicated that an imbalance of vasoactive prostanoids may precede the appearance of clinical symptoms of PIH. The determination of coagulation factors before blood pressure is elevated has no predictive value regarding the later development of PIH. The reduced levels of protein C associated with our PIH group are considered to be the result of an activated coagulation followed by consumption of clotting factors. Reduced measured levels of protein S in normotensive as well as hypertensive pregnancies offer an explanation for the increased risk of thromboembolic disease. This increased susceptibility to thromboembolic disorders is further enhanced by the altered balance between the platelet aggregator and vasoconstrictor thromboxane A2 and its antagonist prostacyclin.
 ...
PMID:[Vasoactive prostanoids and inhibitors of blood coagulation in pregnancy-induced hypertension]. 804 87

Hypertensive diseases represent the most frequent disorders among medical complications of pregnancy. Numerous studies have proven the central role of prostaglandins in these complex diseases. Thus, determination of urinary prostaglandins may lead to a better understanding of the pathomechanismus and may be a basis for therapeutic approaches. Our study included 59 patients with pregnancy-induced hypertension. From these 18 women had a proteinuria > 300 mg/l and were classified as pre-eclamptic. As controls 53 normotensive pregnancies were investigated. Quantification of 6-keto-PGF1 alpha, 2,3-dinor-6-keto-PGF1 alpha, TxB2, 11-Dehydro-TxB2 and PGE2 was performed with radio or enzyme immunoassays after purification with solid phase extraction and partly HPLC. In the third trimester of pregnancy following alterations were found in urine concentrations of prostaglandins in preeclamptic women compared to controls: 6-keto-PGF1 alpha - 54%, 2,3-dinor-6-keto-PGF1 alpha - 29%, PGE beta 2-41%, TxB2-29% and 11-Dehydro-TxB2 + 21%. Thus, our results show a disturbed balance between vasodilatory and vasoconstrictive prostaglandins in PIH patients. This imbalance correlated to the severity of the disease and was more pronounced in preeclamptic patients. The decrease of PGI2- and PGE2-production was more distinct than the increase of thromboxane production. We conclude that the endothelial damage, rather than an overproduction of TxA2 predominantly is responsible for some pathophysiological events in PIH.
 ...
PMID:[Prostaglandins in the urine of hypertensive pregnant patients]. 804 88

The changes of erythrocyte deformability measured by the laser diffractometer in 25 cases of normal pregnancy and 37 cases of pregnancy induced hypertension (PTH) were studied. The results indicated that the erythrocyte deformability remained relatively stable over the course of normal gestation. There was no difference between controls and mild PIH cases (P > 0.05). However, in the moderate and severe PIH cases a significantly lower erythrocyte deformability (P < 0.01) was demonstrated. The relationship of low erythrocyte deformability with PIH needs further investigation.
 ...
PMID:[Changes in erythrocyte deformability in patients with pregnancy induced hypertension and its significance]. 831 33


<< Previous 1 2 3 4 5 6 Next >>