Glomerular bemodynamics were studied by mJcropuncture technique in the undipped kidney in rats in which modest two kidney Goldblatt hypertension was maintained for 4 weeks and in normotensive controls. Both groups ingested less than 2 mEq Na+/day. In hypertensive rats at micropuncture, mean hydrostatic pressure was elevated both systemically (128 ± 5 vs 113 ± 3 mm Hg, p < 0.05) and within glomerular capillaries (55 ± 2 vs 48 ± 1 mm Hg, p < 0.05), resulting in an Increase in the transglomerular hydrostatic pressure gradient (40 ± 2 TS 33 ± 1 mm Hg, p < 0.05). The glomerular capillary permeability coefficient, however, was decreased in the hypertensive rats (0.063 ± 0.017 vs 0.115 ± 0.011 nl/s/g kw/mm Hg, p < 0.05), resulting in no change in nephron filtration rate (38.9 ± 2.3 TS 39.9 ± 2.5 nl/min/g kw). Nephron plasma flow also remained unchanged (154 ± 10 vs 140 ± 7 ml/mln/g kw). In separate studies in this model of hypertension, saralasin infusion demonstrated a peripheral effect of circulating angiotensin II which was increased over controls. Kidney mass and GFR were not different between clipped and undipped kidneys. No consistent abnormalities were observed by light or electron microscopy either in glomeruli or in vessels in the undipped kidney. This study demonstrates that glomerular bemodynamics may be altered early In the course of modest hypertension in this model without altering blood flow or fUtration rate. The deaease in glomerular capillary area and/or permeability (LpA) in the hypertensive rats could be either a result of the increased effect of circulating angiotensin II or the direct effect of glomerular capillary hypertension. (Hypertension 4: 51–57, 1982)