Potassium protection against lesions of the renal tubules, arteries, and glomeruli and nephron loss in salt-loaded hypertensive Dahl S rats.
Dahl S rats (20/group) were given three Purina diets for 24 weeks: 4% NaCl-no added potassium (BP 171 mm Hg); 4% NaCl-3.8% K citrate (BP 174 mm Hg); 4% NaCl-2.6% KCl (BP 173 mm Hg). The added potassium did not lower blood pressure (BP) but strikingly reduced microscopic renal lesions. Focal tubular dilation was scored blindly (100, severest lesions; 0, normal). Scores were: renal cortex: no potassium (41); K citrate (20); KCl (22), 50% improvement p less than 0.001; outer medulla: no potassium (79); K citrate (54); KCl (58), 30% improvement p less than 0.001; renal papilla: no potassium (49); K citrate (28); KCl (28), 43% improvement, p less than 0.001. Both K citrate and KCl also eliminated the thickened walls and relatively narrowed lumens of the hypertensive renal arterioles, without lowering BP. In these same rats, the wall thickness of arterioles from 20 normotensive salt-resistant (R) rats on 4% NaCl averaged 18.9 mu vs 26.1 mu in arterioles from 18 hypertensive salt-sensitive (S) rats on 4% NaCl with no added potassium. Adding either KCl or K citrate to the 4% NaCl diet strikingly reduced the wall thickness to that found in the R rat, even though the BP was not reduced at all. Potassium did not lower the high BP but apparently reduced the severity of the arteriolar lesions resulting from that high BP.(ABSTRACT TRUNCATED AT 250 WORDS)
- Copyright © 1984 by American Heart Association