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Erniedrigte renale Prostaglandin E2-Ausscheidung und verminderte Stimulierbarkeit der Plasmareninaktivität bei Patienten mit essentieller Hypertonie

Reduced urinary prostaglandin E2-excretion and diminished responsiveness of plasma renin activity in patients with essential hypertension

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Summary

Under basal conditions prostaglandin (PG) E2-excretion was significantly lower in 35 patients with essential hypertension studied than in 22 age-and sex-matched controls (p<0.02). PGF-excretion was similar in both groups. Within the first 15 minutes after furosemide i.v., PGE2-excretion rose substantially less in the patients than in the controls (p<0.001), while the increase in PGF-excretion was not different for both groups. The coincident rise of plasma renin activity was significantly lower in the hypertensive (167%±11, SEM) than in the normotensive (386%±46) group (p<0.001). Our results support the assumption that a decrease in renal cortical (vascular?) synthesis of vasodilatating PG's may be the cause for both, the diminished secretion of renin and the increase of vascular resistance in the kidney, which are often associated in essential hypertension.

Zusammenfassung

Die renale Prostaglandin (PG)-Ausscheidung und die Stimulierbarkeit der Reninsekretion wurde bei Patienten mit essentieller Hypertonie (n=35) und bei altersgleichen normotensiven Kontrollpersonen (n=22) vergleichend untersucht. Bei den Patienten mit essentieller Hypertonie wurde eine erniedrigte basale Ausscheidung des vasodilatierenden PGE2 (p<0,02) bei im Normbereich liegender Ausscheidung des vasokonstriktorischen PGF im Urin festgestellt. Darüber hinaus stieg innerhalb der ersten 15 min nach i.v.-Gabe von 40 mg Furosemid die PGE2-Ausscheidung bei Patienten mit essentieller Hypertonie signifikant geringer an als bei den Kontrollpersonen (p<0,001), während der Anstieg der PGF-Ausscheidung in beiden Gruppen gleich war. Zum gleichen Zeitpunkt lag der prozentuale Anstieg der Plasmareninaktivität nach Furosemid bei Hypertonikern (167±11 (SEM)) deutlich unter dem Anstieg der Kontrollgruppe (386±46,p<0,001). Unsere Ergebnisse unterstützen die Annahme, daß eine erniedrigte renal-kortikale, (vaskuläre?) Synthese vasodilatierender Prostaglandine die Ursache sowohl für die verminderte Stimulierbarkeit der Reninsekretion als auch für den gesteigerten renalen Gefäßwiderstand bei essentieller Hypertonie ist.

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Scherer, B., Held, E., Lange, H.H. et al. Erniedrigte renale Prostaglandin E2-Ausscheidung und verminderte Stimulierbarkeit der Plasmareninaktivität bei Patienten mit essentieller Hypertonie. Klin Wochenschr 57, 567–573 (1979). https://doi.org/10.1007/BF01491135

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