Supersensitivity of vascular smooth muscle to catecholamines in aldosterone-salt hypertensive rats appears to reside beyond the α<sub>1</sub>-adrenoceptor. The objective of this study was to assess the norepinephrine-stimulated production of arachidonic acid metabolites by aorta from control-salt rats (CSR) and aldosterone-salt hypertensive rats (AHR) to determine whether these metabolites might contribute to the altered sensitivity. Norepinephrine increased in a time-dependent manner the production of 6-keto-prostaglandin F α<sub>1</sub> (6-keto-PGF α<sub>1</sub>), thromboxane B<sub>2</sub> (TXB<sub>2</sub>) and prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) by the aortae of CSR. Production was an α<sub>1</sub>-adrenoceptor-mediated event since it was inhibited greatly by prazosin but not by yohimbine. Basal values of the metabolites did not differ for 6-keto-PGF α<sub>1</sub> and TXB<sub>2</sub>, but were higher in AHR compared with CSR for PGE<sub>2</sub>. The norepinephrine concentration-response curve for 6-keto-PGF α<sub>1</sub> was shifted significantly to the right for the AHR group compared with CSR (EC<sub>50</sub> = 2.30 + 0.55 and 0.29 ± 0.07 µ M, respectively) indicating decreased production of norepinephrine-stimulated prostaglandin I<sub>2</sub> in AHR. The norepinephrine-stimulated TXB<sub>2</sub> concentration-response curves for AHR and CSR were similar. Indomethacin was an effective inhibitor of TXB<sub>2 </sub>and 6-keto-PGF <sub>1</sub>α production in both. Norepinephrine-stimulated contraction was significantly affected by indomethacin in CSR but not in AHR. Whereas we observed an attenuation of a norepinephrine-stimulated vasodilatory substance in aortae of AHR compared with CSR, the effect of attenuation on vascular activity is presently unclear.