The renal haemodynamic and excretory actions of prostacyclin and 6-oxo-PGF1α in anaesthetized dogs

Intrarenal arterial (i.a.) infusions of prostacyclin (PGI₂) at 30–300 ng/min to anaesthetized dogs reduced renal vascular resistance (RVR) and filtration fraction (FF), increased mean renal blood flow (MRBF) but did not alter mean arterial pressure (MAP) or glomerular filtration rate (GFR). The urinary excretion of sodium (U_NaV), potassium (U_KV) and chloride ions (U_ClV) were increased through inhibition of net tubular ion reabsorption. PGI₂ (3000 ng/min, i.a.) reduced MAP and increased heart rate. Intravenous (i.v.) infusions of PGI₂ (3000 ng/min) reduced MAP, GFR, FF, urine volume and ion excretion, with elevation of heart rate. The measured variables were unaltered by 6-oxo-PGF_1α (10,000 ng/min i.a.). Treatment of the dogs witht he PG synthetase inhibitor meclofenamic acid (2.5 mg/kg i.v.), did not antagonise the elevation of MRBF to PGI₂ (300 ng/min i.a.). Thus the renal effects of PGI₂ were due to a direct action rather than through conversion to 6-oxo-PGF_1α or through stimulation of endogenous renal PG biosynthesis and release.