INHIBITION OF RABBIT RENAL PROSTAGLANDIN-E2 BIOSYNTHESIS BY CHRONIC POTASSIUM-DEFICIENCY

  • 1 January 1981
    • journal article
    • research article
    • Vol. 97  (2) , 205-212
Abstract
To test the hypothesis that renal PG [prostaglandin] may mediate the renal functional defect of K depletion, rabbits were placed on normal K and K-deficient diets for 7 wk, and measurements were made of urinary PGE2 excretion; renal cortical, medullary and papillary PGE2 content; and in vitro, de novo PGE2 biosythesis. In the 6th wk maximal urinary osmolality declined significantly, from 1118 .+-. 44 mosmol/kg of H2O in controls to 666 .+-. 25 in K-deficient animals, accompanied by a corresponding decrease in urinary excretion of K from 12.2 .+-. 0.7 meq/24 h to 0.93 .+-. 0.1 and in muscle K content from 39.0 .+-. 1.0 meq/100 g to 22.3 .+-. 1.9. By 3 wk urinary excretion of PGE2 was significantly lower in hypokalemic animals than in controls. Renal cortical, medullary and papillary PGE2 tissue content decreased significantly, from 0.061 .+-. 0.01 .mu.g/g to 0.022 .+-. 0.005, 0.73 .+-. 0.09 .mu.g/g to 0.267 .+-. 0.036, and 8.6 .+-. 1.04 .mu.g/g to 4.6 .+-. 1.4, respectively. In vitro PGE2 biosynthesis by cortical, medullary and papillary slices from normal animals was 0.102 .+-. 0.01, 9.55 .+-. 1.7, and 25.5 .+-. 2.8 .mu.g per 30 min, whereas corresponding values from hypokalemic rabbits were 0.04 .+-. 0.006, 3.9 .+-. 0.747, and 14.0 .+-. 1.25 .mu.g/g per 30 min, respectively. Apparently renal slices from hypokalemic rabbits synthesize much less PGE2 in vitro than do normal controls. Enhanced PGE2 synthesis evidently does not mediate the renal concentrating defect of chronic K deficiency but decreased renal PGE2 production may underlie the impairment in renal hemodynamics known to exist in this condition.