Metabolites of arachidonic acid are possible mediators of local renal vasoconstriction in burn shock. The prostanoid precursor arachidonic acid (AA) therefore was infused in the control period and at 1 and 2 h after scalding in anaesthetized rats. To avoid systemic effects, AA was infused at low doses directly into the renal artery through a thin cannula introduced through the aortic wall. After control observations 40% of the body surface was scalded in 80 °C water. Renal arterial blood flow (RBF), measured by an electromagnetic probe, fell to 70% and 58% of the control level at 1 h and 2 h after scalding respectively. Arterial blood pressure was almost maintained. Infusion of AA (5, 15 and 25 nmol) in the renal artery over 15 s caused no effects in the control period, whereas a dose‐dependent decrease in RBF was observed after scalding, and was most pronounced 2 h post‐burn. The highest dose of AA reduced RBF by 37% at I h and by 80% of preinfusion flow at 2 h after scalding. The AA‐induced decrease in RBF was abolished by blocking the thromboxane A2receptors with AH23848. In contrast, inhibition of prostacyclin synthesis or blocking of serotonin S2receptors did not significantly influence the response to AA during shock. Thus, infusion of AA into the renal artery caused a marked reduction of RBF after scalding, at doses that did not induce a change during the control period. The augmented effect of AA infusion maybe due to an increased capacity for synthesis of thromboxane A2(TxA2), and possibly PGH2and PGF2α, after s