Aldosterone Contributes to Sympathoexcitation in Renovascular Hypertension
| Autor: | Gisele S. Lincevicius, Dulce Elena Casarini, Ruy R. Campos, Erika E. Nishi, Caroline Gusson Shimoura, Juliana C. Perry, Guiomar Nascimento Gomes, Cássia T. Bergamaschi |
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| Rok vydání: | 2015 |
| Předmět: |
Male
medicine.medical_specialty Sympathetic Nervous System medicine.drug_class Spironolactone Kidney Plasma renin activity Receptor Angiotensin Type 1 Renovascular hypertension Renin-Angiotensin System chemistry.chemical_compound Heart Rate Internal medicine Renin Renin–angiotensin system Internal Medicine medicine Animals Arterial Pressure Rats Wistar Aldosterone Antihypertensive Agents Mineralocorticoid Receptor Antagonists Medulla Oblongata Angiotensin II receptor type 1 business.industry Baroreflex medicine.disease Angiotensin II Actins Disease Models Animal Hypertension Renovascular medicine.anatomical_structure Endocrinology chemistry Mineralocorticoid business |
| Zdroj: | American Journal of Hypertension. 28:1083-1090 |
| ISSN: | 1941-7225 0895-7061 |
| Popis: | BACKGROUND Although angiotensin II (Ang II) is essential to the development of renovascular hypertension, aldosterone plays a role as well. Recent studies have demonstrated a cross-talk between Ang II type 1 and mineralocorticoid receptors in the brain and kidneys. However, the role of aldosterone in the autonomic and renal dysfunction of renovascular hypertension is not well understood. AIM The current study evaluated whether aldosterone contributes to cardiovascular and renal dysfunction in the 2 kidney-1 clip (2K1C) model. METHODS Mean arterial pressure (MAP) and baroreceptor reflex for control of the heart rate were evaluated in 2K1C treated or not treated with spironolactone (200mg/kg/day, 7 days). Tonic and reflex control of renal sympathetic nerve activity (rSNA) were assessed in urethane-anaesthetized rats. Plasma renin activity (PRA), kidney renin protein expression, renal injury, and central AT1 receptor protein expression were assessed. RESULTS Spiro reduced MAP (198±4 vs. 170±9mm Hg; P < 0.05), normalized rSNA (147±9 vs. 96±10 pps; P < 0.05), and increased renal baroreceptor reflex sensitivity in the 2K1C rats. Spiro reduced α-smooth muscle actin expression in the nonclipped kidney in the 2K1C group (5±0.6 vs. 1.1±0.2%; P < 0.05). There was no change in PRA; however, a decrease in renin protein expression in the nonclipped kidney was found in the 2K1C treated group (217±30 vs. 160±19%; P < 0.05). Spiro treatment decreased AT1 receptor in the central nervous system (CNS) only in 2K1C rats (138±10 vs. 84±12%; P < 0.05). CONCLUSION Aldosterone contributes to autonomic dysfunction and intrarenal injury in 2K1C, these effects are mediated by the CNS. |
| Databáze: | OpenAIRE |
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