This project examines the physiologic consequences of glomerular injury in rats, both due to mechanical, non-immunologic obstructin of a portion of the glomerular capillary loops (microspheres) as well as that due to immunologically induced inflammation (nephrotoxic serum nephritis). The studies will examine the relative roles of the renin-angiotensin and prostaglandin systems and extracellular fluid volume in the adaptive changes in glomerular hemodynamic tending to preserve glomerular filtration rate (GFR) in disease. The studies will also examine the mechanism of disordered autoregulaton of renal plasma flow and GFR in glomerular disease, including the operating characteristics of tubuloglomerular feedback in diseased compared to normal kidneys. The relative contributions of decreased GFR, proximal, distal and collecting duct sodium readsorption to the expansion of ECF volume seen in acute proliferative glomerulonephritis induced by nephrotoxic serum will be studied by micropuncture techniques.