A semiquantitative glomerular damage index (GDI) was determined for overall (O), superficial (S), and juxtamedullary (JM) glomeruli in four models of experimental hypertension in the rat to assess the severity and distribution of injury in light of present day knowledge of glomerular hemodynamics. After a four week period of similar hypertension, comparison of Group 1 (renal ablation) with Group 2 (aortic ligature) revealed OGDIs of 0.420 ± 0.064 (SEM) vs. 0.062 ± 0.019, P < 0.0001, SGDIs of 0.250 ± 0.071 vs. 0.035 ± 0.007, P < 0.0089, and JGDIs of 0.455 ± 0.071 vs. 0.155 ± 0.036, P , 0.002. Within Group 1 the SGDI and JMGDI were not significantly different but within Group 2 the SGDI was less (P , 0.005) than the JMGDI. Arterial/arteriolar damage was comparable in both groups. After an eight week period of similar hypertension, comparison of Group 3 (deoxycorticosterone-saline) with Group 4( stroke-prone spontaneously hypertensive rats) showed OGDIs of 0.301 ± 0.065 vs. 0.128 ± 0.023, P < 0.025, SGDIs of 0.289 ± 0.096 vs. 0.072 ± 0.015, P < 0.044, and JMGDIs of 0.394 ± 0.083 vs. 0.307 ± 0.062, NS. Within Group 3 the SGDI and JMGDI were not significantly different, but within Group 4 the SGDI was less (P < 0.002) than the JMGDI. Vascular damage in the two groups was comparable. Taking into account known physiologic data, the findings are consistent with the idea that increased preglomerular resistance is protective of glomeruli, whereas decreased resistance with increased pressure and/or flow is injurious. The greater vulnerability of the JM glomeruli in Groups 2 and 4 suggests some breakdown in control of glomerular hemodynamics.
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