Tubular cell damage is an important mediator of interstitial fibrosis in chronic renal diseases. Glomerular and tubular damage in genetic hypertension was therefore studied. Tubular and glomerular damage was investigated in 10, 40 and 70 week old SHR and WKY and compared with glomerular capillary pressure (P_GC) and glomerulosclerosis in superficial (OC) and juxtamedullary (JMC). Tubular vimentin was used as criterion of tubular damage. Variation in tubular diameter was measured during change in perfusion pressure and ureter ligation was used to demonstrate the relation between tubular pressure and appearance of vimentin positive cells. Tubular and glomerular damage were most pronounced in JMC and greater in SHR than in WKY. It was absent in 10 week old WKY, and significantly higher in JMC of SHR compared to WKY at 70 weeks of age. Numbers of vimentin positive segments:18 ± 9 vs.38 ± 7 % in JMC of 70 weeks old WKY and SHR (p<0.02) and glomerulosclerosis was seen in 8 ± 3 vs. 19 ± 5 % of glomeruli in JMC of 70 weeks old WKY and SHR, respectively (p<0.01). PGC was 45 ± 3 mmHg in JMC of WKY and 57 ± 3 mmHg in JMC of 70 week old SHR (p<0.001). Tubular diameter variation was greatest in SHR (p<0.05) during pressure variation. Proteinuria was present only in 40 and 70 weeks old SHR, and did not correlate with tissue damage. Tubular and glomerular damage in both strains develop in parallel and may be caused by a common mechanism, which may be glomerular capillary and tubular wall stretch during acute blood pressure variation which is greatest in JMC in SHR.