Frusemide releases renin in the rat kidney when prostacyclin synthesis is suppressed

1 The effect of inhibiting prostaglandin (PG) synthesis on basal and frusemide‐stimulated renin secretion was examined in the rat isolated perfused kidney. The stable PGI2 derivative, 6‐keto PGF1α, was measured by radioimmunoassay in urine collected from the kidney. 2 Treatment of rats with indomethacin (3.0 mg kg−1) reduced 6‐keto PGF1α excretion from 121.3 ± 39.1(n = 9) to 15.5 ± 6.6 (n = 9) pg min−1 (P < 0.02) but had no effect on basal renin secretion. Renal perfusion pressure, flow rate and vascular resistance were similar in treated and control rats. Mean urine flow was lower after treatment. 3 Infusion of frusemide (250 μg min−1) did not alter 6‐keto PGF1α excretion in control or indomethacin‐treated (P > 0.05) rats. Although renin secretion was increased during frusemide infusion, there was no significant difference between control (1,806 ± 384 ng angiotensin I (AI) min−1) and treated (2,310 ± 554 ng AI min−1) rats (P > 0.05). Propranolol, at a dose (8 pig min−1) which suppressed renin secretion after isoprenaline stimulation, had no effect on the response to frusemide in indomethacin‐treated rats. 4 These results demonstrate that frusemide‐stimulated renin secretion in the rat kidney does not require intact renal PGI2 synthesis and is independent of β‐adrenergic mechanisms.