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

A total of 154 patients with essential hypertension (EH), 24 patients with renovascular hypertension (RVH), and 130 Wistar rats were investigated. PGE2 and PGF2 alpha levels were assayed radioimmunologically in renal venous blood and urine of the patients, and the synthesis of PGE2 and PGF2 alpha in renal tissue, renal PGE-9-ketoreductase activity and urinary PG excretion were measured in rats. It was demonstrated that the PGE2 synthesis was depressed in the vascular channel and the renal uropoietic system, with elevated F/E rations, in patients with arterial hypertension. Clinical and experimental studies showed prolonged and excessive salt consumption to be a cause of these changes, rooted in suppressed renal biosynthesis of both PGs and increased conversion of PGE2 to PGF2 alpha. In addition, renal PGE2 inactivation was increased in EH patients, as compared to those with RVH. PGE2 produced in the kidneys of EH patients is always a depressor natriuretic substance, whereas the role of PGF2 alpha is dependent on the water-salt balance. Furosemide and, to a smaller extent, other diuretics, as well as some hypotensive agents, increase urinary PG excretion and depress the F/E ratio in the urine. Repeated PGE2 infusions are shown to enhance the sensitivity of EH patients to hypotensive drugs, so they can be used for the treatment of refractory EH cases.
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PMID:[Renal prostaglandins and hypertension]. 345 67

The state of the renal prostaglandins (PG) system was assessed in 54 patients with essential hypertension, stage IB-IIA, as compared to that of patients with symptomatic arterial hypertensions. A decrease in renal PGE2 production, noted in all hypertensive patients and determined on the basis of its diurnal excretion, was particularly pronounced in essential hypertension. Diurnal PGE2 excretion decreased as hypertension progressed in patients with essential hypertension, and renal PGF2 alpha production became prevalent. Renal function is dependent on the level of PG production by the kidney. As renal concentration capacity decreases and renographic findings become less satisfactory, PGE2 excretion decreases as well. Salt loads can bring out functional insufficiency of the renal PG system in essential hypertension, as reflected in a much smaller increase in PGE2 excretion, as compared to the control values, at early stages of salt loading and a considerable increase in PGF2 alpha excretion. In essential hypertension, inadequate renal prostaglandin response to salt loading is, to a certain degree, related to changed renal PGE-9-ketoreductase activity.
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PMID:[Status of the humoral system of renal prostaglandins in patients with hypertension]. 658 45

The 24-hour urinary excretion of prostaglandins (PGs) E2 and F2 alpha (which reflects the renal synthesis of these substances) was measured by radioimmunoassay in normal nonpregnant women (NW, n = 23), nonpregnant women suffering from essential hypertension (HW, n = 23), normal pregnant women (NP, n = 24) and women with hypertension in pregnancy (HP, n = 14). All pregnant women were in the third trimester of their pregnancy (week 24-40). The excretion of both PGE2 and PGF2 alpha was increased in NP as compared to NW. PGF2 alpha was relatively more elevated, leading to a decreased PGE2/PGF2 alpha ratio. In HP, PGE2 and PGF2 alpha excretions were even greater, and the PGE2/PGF2 alpha ratio was even lower than in NP. This contrasted with the lowered PGE2 excretion in HW. The increased renal PGs synthesis in normal pregnancy could be related to the effects on the kidney of several hormonal changes peculiar to pregnancy. In addition, the lowered PGE2/PGF2 alpha ratio suggests the possibility of an increased activity of the PGE2-9-ketoreductase, which could be related to the changes in renal sodium handling observed in pregnancy. The pattern of PGE2 excretion in HP is opposite to that observed in HW (i.e. increase rather than decrease). However, both groups share the lowered PGE2/PGF2 alpha ratio with respect to the normotensive counterparts. The causes of altered PG synthesis in pregnant women with hypertension are presently unclear.
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PMID:Increased renal prostaglandins in normal pregnancy and in pregnancy with hypertension. 696 Dec 93