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In clinical renal transplantation studies, recipients of a renal graft from a donor with a genetic predisposition to hypertension had higher blood pressures and required more antihypertensive treatment than recipients of a renal graft from a normotensive donor. In addition, blood pressure normalization in patients suffering from essential hypertension by bilateral nephrectomy and subsequent transplantation of a kidney from a normotensive donor has been reported. The interpretation of these data may be limited by the large number of different factors that can contribute to post-transplantation hyertension in human renal transplant recipients.In experimental renal transplantation studies the contribution of individual factors to post-transplantation hypertension can be independently assessed. Besides immunological graft rejection and hypertension-induced damage to the renal graft, a genetic predisposition to hypertension in the kidney donor has been demonstrated to be associated with post-transplantation hypertension in the recipient. Thus, normotensive recipients of a renal graft from a genetically hypertensive donor consistently developed post-transplantation hypertension in four different animal models of genetic hypertension. Furthermore, in genetically hypertensive rats bilateral nephrectomy together with transplantation of a kidney from a normotensive donor has been shown to be associated with a decrease in blood pressure.Conclusions:Hypertension following renal transplantation may be due to a variety of factors, including immunological graft rejection, hypertension-induced damage to the renal transplant and a genetic predisposition to hypertension of the kidney donor. The finding that blood pressure is transplanted with the renal graft in genetic hypertension suggests a genetically determined alteration to the kidney as a major factor in the aetiology of primary hypertension. The nature of this factor is just beginning to be understood. Renal transplantation studies in rat models of genetic hypertension, combined with the tools of molecular biology, may help to provide further insights into the role of the kidney in primary hypertension.