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Departments of 1 Nephrology and 2 Pathology, Instituto Nacional de Cardiologia I Chavez, 14080 Mexico City, Mexico; 3 Division of Nephrology, Baylor College of Medicine, Houston, Texas 77030; and 4 Hospital Universitario and Universidad del Zulia, Maracaibo, Venezuela
Mildly hyperuricemic rats
develop renin-dependent hypertension and interstitial renal disease.
Hyperuricemia might also induce changes in glomerular hemodynamics.
Micropuncture experiments under deep anesthesia were performed in
Sprague-Dawley rats fed a low-salt diet (LS group), fed a low-salt diet
and treated with oxonic acid (OA/LS group), and fed a low-salt diet and
treated with oxonic acid + allopurinol (OA/LS/AP group) for 5 wk.
The OA/LS group developed hyperuricemia and hypertension compared with
the LS group: 3.1 ± 0.2 vs. 1.1 ± 0.2 mg/dl
(P < 0.01) and 143 ± 4 vs. 126 ± 2 mmHg
(P < 0.01). Hyperuricemic rats developed increased
glomerular capillary pressure compared with the LS rats: 56.7 ± 1.2 vs. 51.9 ± 1.4 mmHg (P < 0.05). Pre- and
postglomerular resistances were not increased. Histology showed
afferent arteriolar thickening with increased 
-smooth muscle actin
staining of the media. Allopurinol prevented hyperuricemia (1.14 ± 0.2 mg/dl), systemic (121.8 ± 2.8 mmHg) and glomerular
hypertension (50.1 ± 0.8 mmHg), and arteriolopathy in oxonic
acid-treated rats. Linear regression analysis showed that glomerular
capillary pressure and arteriolar thickening correlated positively with
serum uric acid and systolic blood pressure. Glomerular hypertension
may be partially mediated by an abnormal vascular response to systemic hypertension due to arteriolopathy of the afferent arteriole.
uric acid; arteriolopathy; renal hemodynamics; micropuncture; hypertension
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