Spontaneously hypertensive rats (SHR) develop proteinuria and glomerular lesions during the first year of their life. To determine whether an intrarenal hemodynamic abnormality might participate in the pathogenesis of these lesions, normotensive Wistar-Kyoto (WKY) and SHR rats were subjected to acute pressure increase with phenylephrine infusion (2.5 and 5 micrograms X kg-1 X min-1), and renal blood flow (RBF), afferent and efferent arteriolar resistances, glomerular filtration rate (GFR), and glomerular capillary hydrostatic pressure were measured or calculated. The results indicate that the two strains responded differently to the pressure rise. Thus, although the increment in renal perfusion pressure and afferent arteriolar resistance increased similarly in the two strains, efferent resistance increased only in the SHR (7.2 +/- 1.6 vs. 9.0 +/- 2.1 units, P less than 0.02) but decreased in the WKY (5.3 +/- 0.8 vs. 4.0 +/- 0.5 units, P less than 0.05). This was associated with a decreased RBF of SHR (8.31 +/- 0.71 vs. 7.22 +/- 0.57 ml X min-1 X g kidney-1, P less than 0.05) but stable RBF in WKY (7.36 +/- 0.55 vs. 7.79 +/- 0.51 ml X min-1 X g kidney-1); GFR remained unchanged in both strains. Calculated glomerular hydrostatic pressure, however, increased in the SHR (43.6 +/- 3.0 vs. 48.5 +/- 2.2 mmHg, P less than 0.05) but decreased in the WKY (33.2 +/- 2.5 vs. 28.8 +/- 1.7 mmHg, P less than 0.01). The observed higher base-line glomerular pressure in the SHR and a greater rise with phenylephrine infusion may participate in the pathogenesis of the SHR glomerular lesions and proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)