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Frusemide releases renin in the rat kidney when prostacyclin synthesis is suppressed
Author(s) -
Barden Anne E.,
Mahoney Denis P.,
Tunney Anne M.,
Vandongen Robert
Publication year - 1984
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1984.tb10785.x
Subject(s) - endocrinology , medicine , renin–angiotensin system , chemistry , kidney , furosemide , radioimmunoassay , prostacyclin , propranolol , prostaglandin , excretion , stimulation , angiotensin ii , perfusion , blood pressure
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 PGI 2 derivative, 6‐keto PGF 1α , was measured by radioimmunoassay in urine collected from the kidney. 2 Treatment of rats with indomethacin (3.0 mg kg −1 ) reduced 6‐keto PGF 1α 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 PGF 1α 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 PGI 2 synthesis and is independent of β‐adrenergic mechanisms.