The renin-angiotensin-aldosterone system (RAAS) regulates Na+ balance and blood pressure. Angiotensin II (Ang II) infusion induces hypertension and increases aldosterone (aldo), which should increase Na+ and water retention and exacerbate the hypertension. Elevated aldo has also been associated with fibrosis and tissue damage. Therefore, blockade of RAAS components should attenuate Ang II-induced hypertension. However, the contribution of aldo in renal Na+ and water handling during Ang II hypertension remains inconclusive. This study will test the hypothesis that aldo receptor blockade decreases Na+ and water retention and attenuates blood pressure in Ang II-induced hypertension. Specifically, the aims are 1) to determine the contribution of aldo to Na+ and water retention in Ang II-induced hypertensive rats treated with placebo or mineralocorticoid antagonists maintained, and 2) to determine the contribution of aldo to Na+ and water retention during Ang II-induced hypertension independent of elevated blood pressure and in the presence of reduced renal perfusion pressure. Unlike previous studies, the present study will provide a more comprehensive examination of the renal effects induced by aldo antagonism.
| Ortiz, Rudy M; Kobori, Hiroyuki; Conte, Debra et al. (2010) Angiotensin II-induced reduction in body mass is Ang II receptor mediated in association with elevated corticosterone. Growth Horm IGF Res 20:282-8 |
| Ortiz, Rudy M; Mamalis, Andrew; Navar, L Gabriel (2009) Aldosterone Receptor Antagonism Reduces Urinary C-Reactive Protein Excretion in Angiotensin II-Infused, Hypertensive Rats. J Am Soc Hypertens 3:184-91 |
| Ortiz, Rudy M; Graciano, Miguel L; Seth, Dale et al. (2007) Aldosterone receptor antagonism exacerbates intrarenal angiotensin II augmentation in ANG II-dependent hypertension. Am J Physiol Renal Physiol 293:F139-47 |
| Ortiz, Rudy M; Graciano, Miguel L; Mullins, John J et al. (2007) Aldosterone receptor antagonism alleviates proteinuria, but not malignant hypertension, in Cyp1a1-Ren2 transgenic rats. Am J Physiol Renal Physiol 293:F1584-91 |
