Aldosterone-induced endothelial dysfunction of rat aorta: role of poly(ADP-ribose) activation
| Autor: | Arda Tasatargil, Bedriniam Dalkiran, Nazli Ece Gungor, Ciler Celik-Ozenci, Merih Tekcan |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Male
Nitroprusside medicine.medical_specialty Medicine (General) Endothelium Poly ADP ribose polymerase Vasodilation Aorta Thoracic Apoptosis Blood Pressure In Vitro Techniques Poly(ADP-ribose) Polymerase Inhibitors chemistry.chemical_compound Endocrinology R5-920 Heart Rate Internal medicine Internal Medicine medicine In Situ Nick-End Labeling Animals Endothelial dysfunction Enzyme Inhibitors Rats Wistar Aldosterone business.industry Isoproterenol Phenanthrenes medicine.disease Immunohistochemistry Acetylcholine Rats Enzyme Activation medicine.anatomical_structure chemistry PARP inhibitor Sodium nitroprusside Endothelium Vascular Poly(ADP-ribose) Polymerases business medicine.drug |
| Zdroj: | Journal of the Renin-Angiotensin-Aldosterone System, Vol 10 (2009) |
| ISSN: | 1470-3203 |
| Popis: | Introduction. The aim of this study was to investigate whether activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) contributes to the development of aldosterone-induced endothelial dysfunction and treatment with the potent PARP inhibitor 1,5-isoquinolinediol (3 mg/kg/day, i.p.) could prevent endothelial dysfunction caused by aldosterone. Methods. Infusion of subpressor doses of aldosterone with subcutaneously implanted mini-osmotic pumps (0.05 mg/kg/day) to rats for 21 days induced the development of endothelial dysfunction. In order to evaluate endothelial function, isometric tension studies were performed in response to acetylcholine and sodium nitroprusside.Additionally, PAR (the end product of activated PARP) and PARP-1 expressions in the endothelium of thoracic aortas were evaluated by immunohistochemistry. Results. There was a significant loss of endothelium-dependent vasodilatation in response to acetylcholine in aldosterone-infused rats. In animals treated with 1,5-isoquinolinediol, the effect of aldosterone on vascular responsiveness was less than the untreated groups. Immunohistochemical studies demonstrated that aldosterone administration increased PAR and PARP-1 expressions in the endothelium of thoracic aortas, whereas PARP inhibition decreased their expressions to control levels. Conclusion. Our results indicate that PARP activation in the vascular system may be a contributory factor to the impaired endothelial function associated with aldosterone administration. |
| Databáze: | OpenAIRE |
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