Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of Na-Li countertransport (CT), a marker of the risk of essential hypertension, was determined in 55 primigravid women during pregnancy, together with urinary 11-dehydro-thromboxane B2 (11-dehydro-TXB2) as a marker of thromboxane A2 synthesis. The mean Na-Li CT (mean +/- SEM) value was increased significantly at 20 weeks gestation and thereafter, and reached higher levels in late pregnancy than in non-pregnant controls (0.31 +/- 0.02 vs. 0.21 +/- 0.01mmol per hr per liter RBC, p less than 0.05). Fifty five primigravid women could be divided into two groups, depending upon Na-Li CT activity either higher or lower than the value of 0.25mmol per hr per liter RBC at any time in the pregnancy up to term. At 20 weeks gestation all but one of 13 women in the lower-activity group had Na-Li CT activity less than 0.20 mmol per hr per liter RBC, and none developed PIH, whereas out of 42 women in the higher-activity group, all but one had Na-Li CT activity more than this value, and 8 developed PIH. Urinary 11-dehydro-TXB2 increased as pregnancy progressed, maximum levels being attained in women at term, about 3 times higher than in controls (4.19 +/- 0.35 vs. 1.36 +/- 0.10 ng per mg creatinine, p less than 0.05). Although the formation of thromboxane A2 was reported to be higher in pregnancy complicated by hypertension, no significant difference existed in the levels of 11-dehydro-TXB2 between women with PIH and women with uncomplicated pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Increased red-cell sodium-lithium countertransport activity and urinary 11-dehydrothromboxane B2 during pregnancy]. 154 69

A simple non-invasive continuous-wave Doppler ultrasound system was used to record the flow velocity wave forms of the maternal uterine artery and the fetal umbilical artery in 113 normal pregnancies and 39 cases of PIH or essential hypertension complicating pregnancy. The systolic/diastolic (S/D) ratio of flow velocities was measured as an index of peripheral resistance. In normal pregnancy the umbilical artery velocity wave S/D ratio declined from 3.9 to 2.1 during the 20th to 40th week while the uterine artery S/D ratio remained constant between 1.8 to 1.9. After the 30th week, either an umbilical artery S/D ratio greater than or equal to 3, or uterine artery S/D ratio greater than 2.6 was defined as abnormal. In 32 PIH cases there were 9 with abnormal umbilical artery S/D ratio and 4 with abnormal uterine artery S/D ratio and the umbilical arterial change seemed to precede the uterine arterial. The rate of abnormal velocity wave forms in PIH was significantly higher than that in normal pregnancy. If both uterine and umbilical artery wave forms were abnormal the fetal outcome was usually poor. The results showed that the method is good for predicting the fetal outcome and once again supported the hypothesis that spasm of arterioles and venules in the placenta leading to high peripheral resistance especially in the fetal side may play an important role in the pathogenesis of PIH.
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PMID:[Doppler flow velocity wave forms of the maternal uterine artery and fetal umbilical artery in normal pregnancy and pregnancy induced hypertension]. 269 3

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.
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PMID:Renin and aldosterone concentrations in pregnant essential hypertensives - a prospective study. 634 44

PIH, the most common complication of pregnancy, remains a major source of maternal-child morbidity and mortality. Yet the etiology of this disorder is still little understood. There is now a growing body of evidence linking PIH and insulin resistance. Both proteinuric and non-proteinuric PIH predict future essential hypertension, and to a lesser extent, diabetes, disorders strongly related to glucose intolerance and insulin resistance. PIH is associated with diabetes, occurring in up to 50% of diabetic pregnancies. PIH is characterized by the same features that define IRS, including hypertension, dyslipidemia, disruption of endothelial and platelet function and related disturbances of prostanoid synthesis, coagulation and fibrinolytic abnormalities, hyperuricemia, atherosclerotic changes, and obesity. During the last decade, controlled studies by at least 11 different research groups in nine countries have established significant positive associations between both proteinuric and nonproteinuric PIH and various measures of insulin resistance. In particular, prospective investigations by at least five groups of investigators have indicated that relative hyperinsulinemia, glucose intolerance, and insulin insensitivity predict the subsequent development of PIH. These and other studies suggest that insulin resistance may play a causal role in the pathogenesis of PIH, and that some aspects of PIH may represent an early manifestation of IRS, precipitated by the profound metabolic and hemostatic challenges of gestation.
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PMID:Pregnancy-induced hypertension and insulin resistance: evidence for a connection. 1020 92