We investigated the in vivo pressor effects of the potent vasoconstrictor Urotensin II (UII). We randomized normotensive Sprague-Dawley rats into 4 groups that received a 7-day UII infusion (cases) or vehicle (controls). Group 1 received normal sodium intake; Group 2 underwent unilateral nephrectomy and salt loading; Group 3 received spironolactone, besides unilateral nephrectomy and salt loading; Group 4 only received spironolactone. UII raised BP transiently after a lag phase of 12-36 hours in Group 1, and progressively over the week in Group 2. Spironolactone did not affect blood pressure, but abolished both pressor effects of UII in Group 3, and left blood pressure unaffected in Group 4. UII increased by 7-fold the renal expression of renin in Group 2, increased aldosterone synthase expression in the adrenocortical zona glomerulosa, and prevented the blunting of renin expression induced by high salt. UII raises BP transiently when sodium intake and renal function are normal, but progressively in salt-loaded uninephrectomized rats. Moreover, it increases aldosterone synthase and counteracts the suppression of renin induced by salt loading. This novel action of UII in the regulation of renin and aldosterone synthesis could play a role in several clinical conditions where UII levels are up-regulated.