| Dokumentenart: | Artikel | ||||
|---|---|---|---|---|---|
| Titel eines Journals oder einer Zeitschrift: | Pfl�gers Archiv European Journal of Physiology | ||||
| Verlag: | SPRINGER HEIDELBERG | ||||
| Ort der Veröffentlichung: | HEIDELBERG | ||||
| Band: | 442 | ||||
| Nummer des Zeitschriftenheftes oder des Kapitels: | 6 | ||||
| Seitenbereich: | S. 821-827 | ||||
| Datum: | 2001 | ||||
| Institutionen: | Medizin > Lehrstuhl für Innere Medizin II Biologie und Vorklinische Medizin > Institut für Physiologie > Prof. Dr. Armin Kurtz Chemie und Pharmazie > Institut für Pharmazie > Entpflichtete oder im Ruhestand befindliche Professoren > Prof. Wiegrebe | ||||
| Identifikationsnummer: |
| ||||
| Stichwörter / Keywords: | NITRIC-OXIDE-SYNTHASE; MESSENGER-RNA; RENOVASCULAR HYPERTENSION; GENE-EXPRESSION; MACULA DENSA; RAT-KIDNEY; INHIBITION; SPIRONOLACTONE; IDENTIFICATION; STIMULATION; angiotensin II; cyclooxygenase-2; kidney; prostaglandins; renin; spontaneously hypertensive rats (SHR) | ||||
| Dewey-Dezimal-Klassifikation: | 500 Naturwissenschaften und Mathematik > 570 Biowissenschaften, Biologie 600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin 600 Technik, Medizin, angewandte Wissenschaften > 615 Pharmazie | ||||
| Status: | Veröffentlicht | ||||
| Begutachtet: | Ja, diese Version wurde begutachtet | ||||
| An der Universität Regensburg entstanden: | Ja | ||||
| Dokumenten-ID: | 73487 |
Web of ScienceZusammenfassung
Based on recent evidence that renin gene and cyclooxygenase-2 (COX-2) expression in the rat kidney cortex increase in parallel under a variety of conditions, this study aimed to characterize the causal linkage between COX-2 and renin expression. Therefore, we semi-quantitated renocortical renin and COX-2 gene expression when the renin-angiotensin system (RAS) was inhibited by the angiotensin II ...
Zusammenfassung
Based on recent evidence that renin gene and cyclooxygenase-2 (COX-2) expression in the rat kidney cortex increase in parallel under a variety of conditions, this study aimed to characterize the causal linkage between COX-2 and renin expression. Therefore, we semi-quantitated renocortical renin and COX-2 gene expression when the renin-angiotensin system (RAS) was inhibited by the angiotensin II (Ang II) AT1 receptor antagonist candesartan (15 mg/kg per day) and when COX-2 activity was blocked by celecoxib (20 mg/kg twice a day) in three rat strains (Sprague-Dawley, WKY and SHR) at ages of 5, 9 and 15 weeks. We observed that candesartan increased renin mRNA in all rats at all ages, the amplitude of stimulation being inversely related to age. Candesartan increased COX-2 mRNA in all three strains at 5 weeks, and in SID and WKY rats also at 9 weeks. In 9-week-old SUR and in 15-week-old rats of all three strains candesartan did not influence COX-2 mRNA levels. For all rat strains, strain-specific strong linear correlations existed between renocortical COX-2 and renin mRNA levels, both with and without candesartan treatment. The additional feeding of candesartan-treated rats with celecoxib did not change renin mRNA or COX-2 mRNA levels, whilst the renal excretion of sodium and renal cortical prostaglandin E-2 concentration decreased by 26% and 60%, respectively. In summary, these findings, obtained when the renin system was activated by AT(1) receptor blockade, indicate that Ang II is not required to stimulate COX-2 expression and that COX-2 activity is not required to stimulate renin expression. However, the renocortical expression of renin and of COX-2 appear to be highly coordinated under basal conditions and during inhibition of RAS, suggesting the existence of a common denominator for renin and COX-2 expression that remains to be elucidated.
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