Changes in internal vascular diameter and thus local peripheral resistance contribute to the regulation of arterial blood pressure and the distribution of blood flow to distal tissues. In renal arterioles, depolarization-elicited vasoconstriction is counter-regulated by a secondary, nitric oxide (NO)-mediated dilatation termed recovery. This phenomenon is associated with transfer of a calcium signal from the smooth muscle cells to the endothelial cells. Another type of rapid interference with vasoconstrictor responses occurs after 5 min of exposure to aldosterone, which inhibits depolarization-induced constriction in the afferent arteriole also in a NO-dependent manner. Longer (50 min) exposure of renal arterioles to aldosterone significantly inhibits recovery. The mechanism underlying the blunting by aldosterone of vasodilatation recovery is not clear. The present study was designed to test the hypothesis that the procontractile effect of long-term treatment with aldosterone observed in renal arterioles of the rabbit is a more general phenomenon in blood vessels and can be evoked in mouse arteries and that it involves suppression of NO release combined with local production of vasoconstrictor mediators.
