Angiotensin IV (Ang IV) has been reported to induce renal vasodilatation in some papers and renal vasoconstriction in others (Coleman et al., 1998; Fitzgerald et al., 1999). In the present study, we investigated the effect of Ang IV on simultaneously measured cortical and total renal blood flow in vivo. Intravenous bolus injection of Ang IV (0.3, 1, 3, 10, 30, 100 nmol/kg) caused dose-dependent increases in mean arterial pressure (MAP), and dose-dependent decreases in renal cortical blood flow (CBF) and total renal blood flow (RBF). The decreases of CBF and RBF highly correlated, which rules out the possibility that former contradicting reports on Ang IV-induced renal hemodynamic changes are due to different methods of measurement of either CBF or RBF. Moreover, the AT₁ receptor antagonist EXP 3174 (1 mg/kg) abolished the observed effect of Ang IV on blood pressure and renal blood flow. Other routes of Ang IV administration, such as intrarenal infusion and intracerebroventricular (ICV) injection were also studied. At a dose of 1 nmol/20ml/min, a 10-min intrarenal infusion of Ang IV also caused a renal vasoconstrictor effect. ICV bolus injection of Ang IV at dose of 10 nmol/2.5ml increased MAP and renal vascular resistance, which could be abolished by pretreatment with an ICV bolus injection of the AT₁ receptor antagonist candesartan. We observed no effects of the more selective AT₄ receptor agonist, LVV-hemorphin-7 (Moeller et al., 1997) on MAP or RBF following intravenous injection, intrarenal infusion or ICV administration. Thepresent results suggest that Ang IV increased MAP and induced renal vasoconstriction through the activation of AT₁ receptors; Ang IV did not appear to have AT₄ receptor-mediated in vivo renal hemodynamic effects.