Objective: To investigate if blood volume expansion, increased sodium retention, changes in neurohumoral arterial pressure control, or altered extrarenal resistance vessel function contribute to the development of renal post-transplantation hypertension.
Methods: F1-hybrids (F1H) obtained from crossing spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats received either an SHR or an F1H kidney graft. Groups consisted of 8-12 animals and were investigated between days 1 and 14 after renal transplantation in three sets of experiments including arterial pressure recordings, plasma volume measurements, metabolic studies, and small vessel myography.
Results: Two days after completion of bilateral nephrectomy, arterial pressure was elevated by 15-20 mmHg in recipients of an SHR kidney, compared with syngeneically transplanted controls. There was no evidence for increased sodium and fluid retention during the early development of renal post-transplantation hypertension despite a 35% reduced creatinine clearance in recipients of an SHR kidney. The plasma renin-angiotensin-aldosterone system was similarly suppressed in both recipients of an SHR kidney and controls. The arterial pressure response to ganglionic blockade did not differ between groups and there was no evidence for changes in extrarenal resistance vessel function, which could be involved in the genesis of this form of hypertension.
Conclusions: None of the investigated mechanisms was altered in a way that might help to explain the rapid and consistent development of hypertension in recipients of an SHR kidney. We conclude that post-transplantation hypertension in recipients of an SHR kidney is due to mechanisms other than those investigated in the present study.