Key result
Patients with essential hypertension (n=35) had lower urinary PGE2 and kallikrein excretion and blunted rises in PGE2, kallikrein, and PRA 15 min after 40 mg IV frusemide vs 22 normotensive controls.
Case-Control (n=57)
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Urinary prostaglandins (PG), kallikrein and plasma renin activity (PRA) were measured in 35 patients with essential hypertension and 22 normotensive controls before and 15 min after frusemide (40 mg intravenously). 2. PGE2 and kallikrein excretion rates were lower in hypertensive subjects, and failed to rise to the same extent after frusemide. PGF2 alpha excretion was not significantly different in the two groups of patients either before or after frusemide. PRA rose less in the hypertensive subjects after frusemide. 3. These findings support the view that there is an abnormality of renal vasodilator systems (PGE2 and kallikrein) in essential hypertension.
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Weber et al. (1979) conducted a case-control in Essential hypertension (n=57). Essential hypertension (evaluated before and after intravenous frusemide 40 mg) vs. Normotensive controls was evaluated on Urinary prostaglandins (PGE2, PGF2 alpha), kallikrein excretion rates, and plasma renin activity (PRA). Patients with essential hypertension (n=35) had lower urinary PGE2 and kallikrein excretion and blunted rises in PGE2, kallikrein, and PRA 15 min after 40 mg IV frusemide vs 22 normotensive controls.
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