We measured the release of PGE2, 6kPGF1 alpha, PGF2 alpha, and TXB2 into urine (U) and renal hilar lymph (L) to assess the possible roles of intrarenal prostaglandins (PGs) in arachidonic acid (AA)-induced renal vasodilation and Cl-induced renal vasoconstriction, (a model of tubuloglomerular feedback, TG). AA caused an ipsilateral fall in renal vascular resistance (RVR) and diuresis and increased release of all PGs into U; release of 6kPGF1 alpha into L increased ninefold. Hypertonic NaCl infusion caused ipsilateral vasoconstriction and decreased GFR; the release of TXB2 into U and L increased, but other PGs were not altered consistently. During a background infusion of AA, hypertonic NaCl infusion again evoked TXB2 release into U and L without significant changes in other PGs. AA attenuated the NaCl-induced renal vasoconstriction in dogs with the highest rates of PGE2 release into L. Changes in RVR correlated with the ratio of excretion of vasodilator PG (PGE2 + 6kPGF1 alpha) to TXB2 (r = -0.74). Indomethacin administration blunted, but did not abolish, the Cl-induced increase in RVR. In conclusion, (1) AA evokes the release of PGs, especially prostacyclin, into renal cortex; (2) hypercholoremia increases RVR and evokes a rather selective release of renal TX; (3) the production of vasodilator PGs by AA may attenuate Cl-induced renal vasoconstriction; (4) renal vasodilator and vasoconstrictor PGs can be released relatively independently--their balance could modulate RVR during activation of the TG response.