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An increase in angiotensin II (ANG II) under conditions of high salt intake can result in renal damage. The extent to which ANG II does this directly or by way of stimulating aldosterone (Aldo) secretion is a subject of some debate. In the present study, we sought to determine the separate effects of Aldo and ANG II on the expression of plasminogen activator inhibitor-1 (PAI-1) and other factors related to renal fibrosis in the stroke-prone spontaneously hypertensive rat (SHRSP). Saline-drinking male SHRSPs underwent adrenalectomy (ADX) or sham operation (Sham). Treatment groups consisted of ADX + ANG II (25 ng/min sc) and ADX + Aldo (40 microg.kg(-1).day(-1) sc). After 2 wk of treatment, circulating Aldo levels were reduced to the limit of detection, renal PAI-1, transforming growth factor-beta1 (TGF-beta1), and osteopontin expression, and phospho-Smad2 (p-Smad2) level were decreased severalfold, and Smad7 (an inhibitory regulator of TGF-beta1 action) expression was increased in ADX compared with Sham rats. Infusion of Aldo into ADX SHRSPs restored the renal mRNA expression of PAI-1, TGF-beta1 (along with restored p-Smad2 level), and osteopontin and reduced that of Smad7, whereas ANG II had no or a lesser effect. The findings were confirmed by histological examination of renal tissue. In summary, in the saline-drinking SHRSP, Aldo increased renal profibrotic factors and produced renal injury whereas ANG II in the absence of the adrenals had no effect.

Aldosterone, but not angiotensin II, increases profibrotic factors in kidney of adrenalectomized stroke-prone spontaneously hypertensive rats