Rapid non-genomic vasoconstrictor actions of aldosterone in the renal microcirculation.

There is increasing evidence for the pathophysiological importance of aldosterone in renal diseases. Studies have so far demonstrated that aldosterone exerts deleterious renal effects by inducing oxidative stress, endothelial dysfunction, inflammation and fibrosis through a mineralocorticoid receptor (MR)-dependent genomic mechanisms. On the other hand, a number of recent studies provided evidence that aldosterone can act through a rapid non-genomic mechanism in cardiovascular tissues including the kidney, though the relative importance of such actions in renal diseases remains to be determined. We have recently found that physiological concentrations of aldosterone cause rapid vasoconstriction in the renal microcirculation. The vasoconstrictor actions were compatible with non-genomic; the major characteristics was its relatively early onset (apparent within 5min), which was not affected by either actinomycin D or cycloheximide (inhibitors of transcription or protein synthesis). Thus, in addition to genomic actions, such non-genomic vasoconstrictor actions in the renal microcirculation may contribute to the deleterious renal effects of aldosterone in renal diseases.