Production of prostaglandin E2 (PGE2) and prostacyclin (PGI2) as 6-ketoprostaglandin F1 alpha (PGF1 alpha) in isolated canine superficial and juxtamedullary afferent arterioles was measured in the basal state and after administration of angiotensin II and bradykinin. Individual afferent arterioles were obtained by microdissection, and pooled collections were incubated at 37 degrees C for two consecutive 30-min periods. Prostaglandin content of the incubation media was measured by radioimmunoassay and expressed as picograms prostaglandin per incubation vial per 30-min period. Bradykinin (10(-7) M) produced significant stimulation of both PGE2 and 6-keto-PGF1 alpha production in superficial (PGE2 from 0.44 +/- 0.32 to 5.46 +/- 3.77 pg/period and 6-keto-PGF1 alpha from 6.5 +/- 5.0 to 104.5 +/- 25.5 pg/period) and juxtamedullary afferent arterioles (PGE2 from 0.31 +/- 0.06 to 7.47 +/- 1.55 pg/period and 6-keto-PGF1 alpha from 12.0 +/- 0.01 to 184.4 +/- 14.8 pg/period). Angiotensin II in concentrations of 10(-12) M to 10(-7) M produced no stimulation of prostaglandin production. Angiotensin II (10(-6) M) produced significant stimulation of 6-keto-PGF1 alpha production only in superficial afferent arterioles (from 4.4 +/- 0.8 to 17.3 +/- 3.1 pg/period). Angiotensin II-stimulated 6-keto-PGF1 alpha production was blocked by saralasin (2 X 10(-6) M). A heterogeneous renal vascular response to angiotensin II is demonstrated, since the latter stimulated PGI2 production in superficial afferent arterioles only. PGI2 could potentially antagonize the vasoactive effect of angiotensin II in superficial afferent arterioles.