Chronic pyelonephritis and hypertensive vascular disease often coexist clinically, and a primary and causal role in the relationship usually has been attributed to the renal inflammatory disease. In experimental pyelonephritis, however, where the sequence of events and the presence of other complicating factors can be controlled, such a causal role has not been clearly established. A number of investigators have noted development of hypertension in rats with chronic pyelonephritis, but this has been either mild, of low and irregular incidence, or associated with unilateral nephrectomy, or hydronephrosis, or both (1-3). On the other hand, in our previous studies in rats, in which renal infection was produced by a nonobstructive technique that results in damage to the kidney only by the inflammatory process, chronic pyelonephritis, from any one of several different bacterial species, has not been followed by significant hypertension or vascular disease. Nor have the development of renal failure or the additional insults of infection with a mixed bacterial flora and reduction of renal mass by unilateral nephrectomy produced hypertension in this model (4, 5). Such animals, however, do show a greater response than normal rats to the hypertensive influences of salt and desoxycorticosterone (6). Similarly, Guze and Kalmanson have demonstrated the failure of hypertension to develop in rats with chronic nonobstructive pyelonephritis produced by repeated injections of Enterococci alone and with Escherichia coli (7).