Production of prostaglandin E2 (PGE2) and prostacyclin (PGI2) as 6-ketoprostaglandin F(1α) (PGF(1α)) 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°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-PGF(1α) production in superficial (PGE2 from 0.44 ± 0.32 to 5.46 ± 3.77 pg/period and 6-keto-PGF(1α) 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-PGF(1α) 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-PGF(1α) production only in superficial afferent arterioles (from 4.4 ± 0.8 to 17.3 ± 3.1 pg/period). Angiotensin II-stimulated 6-keto-PGF(1α) 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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Issue number||5 (23/5)|
|State||Published - 1988|
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