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Journal of the American Society of Nephrology, Vol 7, 338-344, Copyright © 1996 by American Society of Nephrology
REGULAR ARTICLES |
X Wu, JW Scholey and H Sonnenberg
Department of Physiology, University of Toronto, Ontario, Canada.
Inbred Dahl salt-sensitive (S) and sal-resistant (R) rats were fed with either high (4% K; HK) or low (0.2% K; LK) potassium diets (both contained 8% salt, 2.5% calcium, 0.8% magnesium, and 2.0% PO4) for 4 wk. During the last week, systolic blood pressure was measured in conscious animals. External diameter of renal vessels (ED) was used to divide renal vessels into four subgroups: less than 25 microns; greater than 25 microns but less than 55 microns; greater than 55 microns but less than 150 microns; and greater than 150 microns. Luminal diameter (LD), cross-sectional wall area (WAC) and wall-tolumen ratio (W/L) were measured or calculated. Glomerular volume (VG) was measured. Data showed that blood pressures of S rats were significantly higher than those of R rats on both diets. Reduced dietary potassium was associated with increased blood pressure in both strains. Changes in renal vessels were characterized by bigger lumen and greater wall area in S rats, compared with R rats, especially in the smallest vessels. Low potassium intake was associated with reduced lumen diameter and enlarged W/L ratio with or without changing WAC in both strains. VG showed no significant differences between strains or between diets. It was concluded that in addition to the genetically determined differences in renal vascular structure between S and R rats, dietary potassium depletion may engender further renal injury, exacerbating hypertension.
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