It has been recognized that Ang- may exert cellular actions by stimulation of a specific receptor, the mas receptor, that are antagonistic to those of Ang-II, including a vasodilatory, natriuretic, antiproliferative and antifibrotic effect. Those observations led others to postulate that Ang- could be a protective peptide in glomerular diseases. Indeed, chronic subcutaneous administration of Ang- was shown to be protective in rodent models of diabetic glomerulopathy and anti-Thy1.1 nephritis. In contrast, others have found that Ang- is not protective in models of progressive glomerulosclerosis and FSGS, and is detrimental in models of diabetic glomerulopathy. Of note, most laboratories studied early stages of the disease and administered the heptapeptide for only 1–6 weeks. Therefore, we opted to expand the investigation of the effect of Ang- to advanced stages of glomerular disease and during longer duration of treatment. Previous work demonstrated that rat glomeruli primarily convert Ang-I to Ang- and Ang-. Studies from a single laboratory suggested that Ang may modulate the pressor actions of Ang-II. However, the effects of chronic systemic administration of Ang have not been studied to date. In addition, Ang could be converted to Ang-III by ACE, and Ang-III has been proposed to promote natriuresis by virtue of being the predominant agonist of tubular Ang-II type 2 receptors. Therefore, we also evaluated the effect of chronically infused Ang- on kidney damage in a model of glomerular disease. Thus, we hypothesized that Ang- and/or Ang- may ameliorate glomerular damage in a rat model of FSGS by diminishing the degree of Ang-II-mediated injury. To test our hypothesis, we selected the fawn-hooded hypertensive rat, a well characterized model of spontaneous hypertension and proteinuria associated with a histological lesion of FSGS. In addition, because stimulation of the Ang-II type 2 Pazopanib receptor has been reported to counteract some of the detrimental effects of Ang-II via the AT1 receptor, we assessed the ability of Ang to bind to Ang receptors. Our study demonstrates that chronic intravenous administration of Ang does not ameliorate glomerulosclerosis in a spontaneous rat model of FSGS. The lack of benefit of these alternative Ang peptides was observed regardless of the delivered dose or the stage of the disease studied. We opted to infuse the peptides longer that previously done by others in order to allow more time for the peptide to elicit a measurable effect. Those studies demonstrated that Ang- can elicit biological actions that are antagonistic to those of Ang-II. Stimulated by those observations, many laboratories have searched for a renoprotective effect of Ang- in various rodent models of human glomerular disease.