URN zum Zitieren dieses Dokuments: urn:nbn:de:bvb:355-epub-269699
Scholz, H. und Kurtz, Armin
(1990)
Role of protein kinase C in renal vasoconstriction caused by angiotensin II.
The American journal of physiology. Cell physiology 259 (3 Pt 1), C421-C426.
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Zusammenfassung
In this study we have examined the subcellar pathways along which angiotensin II (ANG II) causes renal vasoconstriction. Using the isolated perfused rat kidney model, we found that renal vasoconstriction produced by ANG II (100 pM) was not altered by the calmodulin antagonists calmidazolium (1 microM) and N-(6-aminohexyl)-5-chloro-1-naphthalensulfonamide (W-7, 10 microM) but was blunted by ...
Zusammenfassung
In this study we have examined the subcellar pathways along which angiotensin II (ANG II) causes renal vasoconstriction. Using the isolated perfused rat kidney model, we found that renal vasoconstriction produced by ANG II (100 pM) was not altered by the calmodulin antagonists calmidazolium (1 microM) and N-(6-aminohexyl)-5-chloro-1-naphthalensulfonamide (W-7, 10 microM) but was blunted by staurosporine (100 nM) and 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine (H-7, 50 microM), two structurally distinct putative protein kinase C inhibitors. The phorbol ester 4 alpha-phorbol 12,13-didecanoate (1-100 nM) did not alter renal vascular resistance, whereas phorbol 12-myristate 13-acetate (PMA, 1-100 nM) caused potent and dose-dependent vasoconstriction that was prevented by staurosporine (100 nM) and H-7 (50 microM). The vasoconstrictory effects of ANG II and PMA were attenuated by the calcium channel blockers verapamil (5 microM) and nifedipine (5 microM) and were reversibly inhibited when cobaltous chloride (2 mM) was added to the perfusate. Taken together, our findings support the concept that the renal vasoconstrictory effect of ANG II is essentially mediated by protein kinase C activation, which either requires or enhances the entrance of extracellular calcium.
Bibliographische Daten exportieren
| Dokumentenart: | Artikel |
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| Datum: | 1990 |
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| Institutionen: | Biologie und Vorklinische Medizin > Institut für Physiologie > Prof. Dr. Armin Kurtz |
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| Identifikationsnummer: | |
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| Klassifikation: | | Notation | Art |
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| 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine | MESH | | Alkaloids/pharmacology | MESH | | Angiotensin II/pharmacology | MESH | | Animals | MESH | | Cobalt/pharmacology | MESH | | Enzyme Inhibitors/pharmacology | MESH | | Imidazoles/pharmacology | MESH | | Isoquinolines/pharmacology | MESH | | Male | MESH | | Nifedipine/pharmacology | MESH | | Piperazines/pharmacology | MESH | | Protein Kinase C/metabolism | MESH | | Rats | MESH | | Rats, Inbred Strains | MESH | | Regional Blood Flow/drug effects | MESH | | Renal Circulation/drug effects | MESH | | Staurosporine | MESH | | Tetradecanoylphorbol Acetate/pharmacology | MESH | | Vasoconstriction/drug effects | MESH | | Verapamil/pharmacology | MESH |
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| Dewey-Dezimal-Klassifikation: | 500 Naturwissenschaften und Mathematik > 570 Biowissenschaften, Biologie
600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin |
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| Status: | Veröffentlicht |
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| Begutachtet: | Ja, diese Version wurde begutachtet |
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| An der Universität Regensburg entstanden: | Unbekannt / Keine Angabe |
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| Eingebracht am: | 04 Dez 2012 14:41 |
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| Zuletzt geändert: | 02 Jun 2018 19:26 |
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| Dokumenten-ID: | 26969 |
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