Long-term arterial pressure in spontaneously hypertensive rats is set by the kidney

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Abstract
We investigated whether arterial pressure in spontaneously hypertensive rats (SHR) can be normalized by a kidney graft from normotensive histocompatible donors. In addition, the effect of differential genetic predisposition to hypertension of recipients of an SHR kidney on the development of post-transplantation hypertension was studied. SHR were transplanted with a kidney from congenic rats (BB.1K) homozygous for a 2 cM segment of SHR chromosome 20, including the major histocompatibility complex class Ia and class II genes. BB.1K and F1 hybrids (F1H, SHR × Wistar–Kyoto rats) were transplanted with an SHR kidney and the development of renal post-transplantation hypertension was monitored. Thirty days after renal transplantation, mean arterial pressure (MAP) was 116 ± 4 mmHg in SHR with a BB.1K kidney (n = 8) versus 168 ± 2 mmHg in sham-operated SHR (n = 10);P < 0.001. Cumulative renal sodium balance (mmol/100 g body weight) over 21 days after bilateral nephrectomy was 6.8 ± 0.6 in SHR with a BB.1K kidney versus 10.8 ± 1.6 in sham-operated SHR (P < 0.05). Within 60 days of transplantation, MAP increased in BB.1K and in F1H transplanted with an SHR kidney (n = 7 per group) by 38 ± 5 mmHg and 43 ± 8 mmHg, respectively. In SHR, arterial pressure can be normalized by a kidney graft from normotensive donors. The genetic predisposition of the recipients to hypertension does not modify the rate and the extent of the arterial pressure rise induced by an SHR kidney graft.