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)

Prostaglandins PGE2, PGD2, PGI2, and PGF2 alpha, as well as thromboxanes and leukotrienes, are synthesized by the fetal and neonatal kidney. The major prostaglandin, PGE2, PGD2, and PGI2, increase RBF, free water clearance, urine flow, and natriuresis. Alterations in the synthetic and catabolic activity of renal prostaglandins with advancing gestational and postnatal age occur along with concomitant alterations in RBF, GFR, and water and electrolyte excretion, suggesting that the prostaglandins play an important role in renal functional development. Indomethacin treatment may affect both fetal and neonatal renal function. Long-term maternal indomethacin treatment may decrease fetal urine output enough to alter amniotic fluid volume. Neonatal indomethacin therapy may cause transient dose-related renal dysfunction characterized by a decrease in urine output, but this renal dysfunction also depends in part on dosage, timing of therapy, and the cardiovascular and renal status of the infant prior to treatment. New areas of research interest include urinary prostaglandins as a marker for development of essential hypertension, and the possible interaction between antenatal steroids and renal function in the newborn.
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PMID:Prostaglandins and the developing kidney. 310 70

Recent publications have described increased vascular prostacyclin synthesis in vascular tissue from both spontaneous and experimental hypertensive animals and hypertensive humans. The only paper dealing with the platelet sensitivity reported that the cells are not abnormally sensitive to PGI2 in spontaneously hypertensive rats. In 22 patients with essential hypertension the platelet sensitivity to the antiaggregatory prostaglandins PGI2, PGE1, and PGD2 was studied on admission and two weeks after successful treatment with a beta-blocking agent. In all the age groups and in both sexes no differences in platelet sensitivity could be detected. These findings suggest that increased vascular PGI-2 synthesis is not counterbalanced by a change in platelet sensitivity in men.
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PMID:Hypertension and beneficial treatment with beta-blocking agents does not change the platelet sensitivity to the antiaggregatory prostaglandins. 675 58