The relative contributions of vasoconstrictor and dilator systems are balanced in health. The balance is reset in disease, often favoring a predominant role of vasoconstrictors, perhaps due to positive interactions between constrictor systems. For example, in hypertension, chronic high levels of Ang II stimulate the production TxA₂/PGH₂ and/or isoprostane that activate constrictor TP receptors in the vasculature. The present study evaluated a modest concentration of Ang II administered acutely into the renal artery on urinary excretion of TxB₂ and isoprostane and possible renal TP receptor activation that might amplify Ang II-induced renal vasoconstriction. TP receptors were blocked with SQ29548 co-infused with Ang II. Results were compared with a time-control group of continuous Ang II infusion (40 ng/min/kg body wt) over 90 min. TP receptor antagonism during 30-60 min had no effect on the reduction in RBF produced by Ang II (15.8 ± 2.8 vs. 13.2 ± 4.9% (p>0.6). Likewise, there was no difference between groups during Ang II-induced renal vasoconstriction between 60-90 min in presence or absence of TP receptor antagonist (RBF -8.6 % ± 4.0 vs. -9.6 ± 4.5 % (p>0.8). Systemic AP was stable throughout, so RBF changes reflected localized changes in renal vascular resistance. Urinary excretion of TxB₂ and isoprostane were nearly doubled by Ang II. The present data indicate that short-term intrarenal infusion of Ang II rapidly increases renal production of TxA₂ but that the Ang II-induced renal vasoconstriction is independent of TP receptor activation during the initial 90 min of local challenge with Ang II.