The present study was designed to investigate the development of blood pressure and renal sodium handling in recipients of renal grafts from adult stroke-prone spontaneously hypertensive rats (SHRSP), normotensive Wistar-Kyoto (WKY) rats, and borderline hypertensive F1hybrids bred from SHRSP and WKY rats. Unilaterally nephrectomized F1hybrids served as renal graft recipients. The second native kidney was removed 7 days after transplantation. Starting on the day of transplantation, renal graft recipients were put on a standard diet for 7 days followed by a low salt diet (0.18% salt) for 10 days and a high salt diet (1.8% salt) for another 14 days. In recipients of a renal graft from SHRSP donors, systolic blood pressure rose progressively from 140±4 mm Hg before to 190±7 mm Hg 4 weeks after transplantation. In contrast, in recipients of a renal graft from WKY rat donors, blood pressure fell during the same time from 139±7 mm Hg to 120±4 mm Hg. Blood pressure did not change significantly in recipients of a renal graft from F1hybrid donors (132±4 versus 138±7 mm Hg). With transition from a low salt to high salt diet, all rats exhibited renal sodium retention. The accumulating amount of sodium retained by the renal graft was significantly higher in recipients of an SHRSP kidney than in recipients of a WKY rat kidney at all days on the high salt diet. It was also higher in recipients of an SHRSP kidney versus recipients of an F1hybrid kidney on days 8 through 14 on the high salt diet and in recipients of an F1hybrid kidney versus recipients of a WKY rat kidney on days 1 through 5 on the high salt diet. On the low salt diet, urinary aldosterone excretion was lower in recipients of an SHRSP kidney compared with recipients of a WKY rat kidney. On the high salt diet, it was similar in both groups. Urinary corticosterone excretion was similar in both groups on the low salt diet and increased significantly on the high salt diet in recipients of an SHRSP kidney but not in recipients of a WKY rat kidney. At the end of the protocol, glomerular filtration rate, renal plasma flow, plasma sodium concentration, and fractional sodium excretion were not significantly different among groups. These results confirm our previous finding that recipients of a renal graft from SHRSP donors developed posttransplantation hypertension, whereas blood pressure actually decreased in recipients of a renal graft from WKY rat donors. In addition, the data demonstrate that posttransplantation hypertension in recipients of an SHRSP kidney is associated with increased renal sodium retention.