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Renal prostaglandins

Renale Prostaglandine

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Summary

This brief review summarizes the important modulatory effects of endogenous renal prostaglandins (PGs) on renal function. A brief survey of current knowledge of renal PG synthesis reveals the shortcomings of biochemical in vitro studies and points out the necessity to improve methods of in vivo assessment. The problem of measuring circulating levels of PGs and the question of the importance of these PGs for renal function are discussed. Renal blood flow is shown to depend on renal PG's in situations of stress but not under basal conditions. However, in this respect the definition of stress has to include even the mild condition of sodium deprivation. An increasing number of disease states is emerging where renal blood flow is shown to depend on cyclooxygenase activity. Angiotensin II infused or synthesized endogenously seems to be the most likely stress mediator causing enhanced renal PG synthesis which opposes its vasoconstrictor activity. The role of PGs in sodium excretion is not well defined and controversial. In man, most available evidence supports a natriuretic role of renal PGs. However, this role can only be demonstrated under well defined conditions. Inhibitors of PG biosynthesis will cause sodium retention. However, following administration of these drugs a new steady state is reached rapidly characterized by suppressed plasma renin activity and aldosterone. Renal PGs alternate vasopressin effect on urine concentration. The mechanism for this is poorly understood and the role of cAMP in this interaction controversial. Recent evidence showing stimulation of renal PG synthesis by vasopressin independent of its pressor effect is presented. While the stimulatory role of kininogen and kinins on renal PG synthesis has been shown the functional consequences have not been sufficiently defined. Moreover, assessment of the activity of the renal kallikrein-kinin system is at present not possible and no physiological role in renal function has as yet been delineated. Regulation of renal renin release involves PGs. Evidence is presented in support of a role of prostacyclin in baroreceptor and macula densa mediated renin release.

Zusammenfassung

Die folgende Übersicht beleuchtet die für die Nierenfunktion wichtigen Aspekte der in der Niere synthetisierten Prostaglandine (PG). Die Analyse des derzeitigen Wissenstandes über die renale PG-Synthese zeigt die Grenzen der biochemischen in vitro Methoden und die Notwendigkeit der Verbesserung der in vivo Analyse auf. Die Problematik der Messung zirkulierender-PG und die Frage ihrer Bedeutung für die Nierenfunktion wird diskutiert. Der renale Blutfluß hängt unter Streß-Bedingungen von den renalen PG ab, nicht jedoch unter Basalbedingungen. In diesem Zusammenhang beinhaltet die Definition des Streß allerdings auch bereits Natriumarme Ernährung. Bei einer zunehmenden Anzahl von Erkrankungen wird entdeckt, daß PG für die Aufrechterhaltung der Nierendurchblutung von Bedeutung sind. Angiotensin II ist wahrscheinlich der Streß-Faktor, welcher für die erhöhte PG-Synthese verantwortlich ist, welche die Vasokonstriktion partiell antagonisiert. — Die Rolle der PG bei der Natriumexkretion ist nicht exakt definiert und es liegen widersprüchliche Ergebnisse vor. Beim Menschen ist eine natriuretische Wirkung endogener PG wahrscheinlich, kann jedoch nur unter genau definierten Bedingungen nachgewiesen werden. Blocker der PG-Synthese bewirken meist eine Natriumretention. Jedoch kommt es nach Gabe dieser Pharmaka rasch zu einem neuen Fließgleichgewicht für Natrium mit charakteristisch supprimierten Werten für die Plasmareninaktivität und Plasma-Aldosteron.

Die renalen PG reduzieren die hydroosmotische Wirkung von Vasopressin (VP). Der Mechanismus dieser Wirkung ist nicht bekannt und die Rolle des cAMP ungewiß. Neuere Befunde zeigen eine starke Stimulation der renalen PG-Synthese durch VP unabhängig von seiner pressorischen Wirkung.

Stimulation der renalen PG-Synthese durch Kininogen und Kinine ist bekannt, jedoch die funktionelle Bedeutung ist unklar, insbesondere da dem renalen Kallikrein-Kinin-System noch keine physiologische Funktion zugeordnet werden kann. Renale Reninabgabe erfolgt teilweise über PG-abhängige Mechanismen. Die Bedeutung von Prostazyklin für die durch den Barorezeptor und die Macula densa vermittelte Reninabgabe wird dargestellt.

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  1. Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart

    J. C. Frölich & G. Fejes-Toth

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  1. J. C. Frölich
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  2. G. Fejes-Toth
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Frölich, J.C., Fejes-Toth, G. Renal prostaglandins. Klin Wochenschr 60, 1155–1164 (1982). https://doi.org/10.1007/BF01715845

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  • DOI: https://doi.org/10.1007/BF01715845

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