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(Hypertension. 2008;52:e134.)
© 2008 American Heart Association, Inc.
Letters to the Editor |
Instituto de Ciencias Biomédicas, Centro Estudios Moleculares de la Célula and, Millenium Nucleus on Immunology and Immunotherapy, Facultad de Medicina, Universidad de Chile, Santiago, Chile
Laboratorio de Fisiología Integrativa y Molecular, Facultad de Medicina, Universidad Los Andes, Santiago, Chile
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
We thank Renke et al1 for their interest in our recent article.2 The clinical study by Renke et al1 indicates that spironolactone, combined with angiotensin-converting enzyme inhibitor and angiotensin II type 1 receptor blocker, may act as an antioxidant, as measured by the urinary excretion of 15-F2t-isoprostane, without producing changes in systemic blood pressure. The results of our experimental chronic renal failure model showed that treatment with spironolactone has antioxidant effects in the heart. In addition, we observed that spironolactone was protective against heart hypertrophy without a significant antihypertensive effect. Several experimental and clinical studies have shown that combined double or triple renin-angiotensin-aldosterone blocking therapy can markedly attenuate the progression of renal injury, without significant hemodynamic effects. Furumatsu et al3 also demonstrated, in a 1-year randomized prospective study, that the triple combined therapy decreased proteinuria and urinary type IV collagen without reducing blood pressure. Although low doses of mineralocorticoid receptor antagonists had been used in several clinical studies, the emergence of hyperkalemia has been associated with the combined therapy, especially when kidney function is reduced.4
The therapeutic benefits of mineralocorticoid receptor blockers may result from a number of mechanisms, including suppression of proinflammatory molecules, inhibition of collagen synthesis, and reduction of oxidative stress.5 Therefore, and considering that blood pressure may not be the unique target to consider for the administration of mineralocorticoid receptor blockers, further studies are needed to clarify the roles of oxidative stress, proteinuria, and/or other markers of tissue damage that may be useful in monitoring the
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