SOURCE OF KIDNEY DETERMINES BLOOD-PRESSURE IN YOUNG RENAL TRANSPLANTED RATS

Recipients of a renal graft from adult stroke-prone spontaneously hypertensive rat (SHRSP) but not normotensive Wistar-Kyoto rat (WKY) donors have been shown to develop posttransplantation hypertension. To investigate whether hypertension would also travel with the kidneys from young prehypertensive SHRSP and whether the age-related increase in blood pressure in F1 hybrids (F1H) bred from SHRSP and WKY parents was attenuated by early bilateral nephrectomy and transplantation of a WKY kidney, we transplanted kidneys from 14 male SHRSP and 16 WKY donors aged 35-42 days to young male F1H. Recipients had both native kidneys removed. Fifteen unilaterally nephrectomized nontransplanted F1H served as controls. At the time when kidneys were harvested for transplantation, systolic blood pressures in young SHRSP and WKY donors were not significantly different (114 +/- 5 vs. 113 +/- 3 mmHg). After transplantation, recipients of an SHRSP kidney rapidly developed posttransplantation hypertension with systolic blood pressures above 180 mmHg at 3 mo after transplantation. In contrast, systolic blood pressure in recipients of a WKY kidney rose only slightly with increasing age and remained significantly lower than in nontransplanted controls. Transplanted rats exhibited normal weight gain, and renal function (glomerular filtration rate, renal blood flow) in grafted kidneys was well preserved; plasma renin activity was reduced compared with nontransplanted controls. These data demonstrate that 1) hypertension can be transmitted to normotensive recipients by transplantation of a kidney from young prehypertensive SHRSP donors and 2) the age-related increase in arterial pressure in F1H is attenuated by early bilateral nephrectomy and transplantation of a WKY kidney. They support the hypothesis that a primary defect in the kidney plays a major role in the etiology of genetic hypertension.