The Effect of a Reduced Sodium Intake on Post-Renal Transplantation Hypertension in Rats

Abstract

1. In an experimental model of post-renal transplantation hypertension in rats, we studied the effect of a reduction of sodium intake on the development of this type of hypertension. 2. Systolic blood pressure, plasma- renin concentration and renal function were measured regularly in recipients of an allogeneic kidney transplant that had previously undergone active immunological enhancement. 3. Transplant recipients on a normal diet showed a rise in systolic blood pressure during the second week after transplantation. The systolic blood pressure of recipients on a low sodium diet remained normotensive throughout the 15 weeks follow-up period. 4. The plasma renin concentration was low in the hypertensive recipients on a normal diet, as compared with unilaterally nephrectomized controls. Although the plasma renin concentration of recipients on a low sodium diet fell below that of unilaterally nephrectomized controls on a low sodium diet, it was higher than that of recipients on a normal diet. 5. The renal function of transplant recipients was greatly reduced compared with that of control rats. The glomerular filtration rate was reduced to a greater extent than the effective renal plasma flow. 6. In a separate experiment it was revealed that a similar reduction in the glomerular filtration rate of kidneys permanently damaged by temporary ischaemia did not result in an increase in the systolic blood pressure. 7. Survival up to 6 weeks after transplantation was the same for both groups of recipients. Recipients on a low sodium diet, however, showed a better 15 weeks survival, probably owing to the absence of hypertension in this group. 8. The prevention of the development of hypertension by means of a reduction of sodium intake, points to an involvement of sodium retention in this post-transplantation hypertension model.

Effect of Cyclosporin A on the Development of Posttransplantation Hypertension in Rat Renal Allograft Recipients

“…Either sodium restriction or the prevention of chronic rejection, i.e., a more successful immunosuppression, should prevent the development of hypertension. As shown in the present and a previous study [3] we found both to be effective.…”

“…From the present and previously published results [2,3,11] we postulate that in our rat model of postrenal trans plantation hypertension the increase in SBP is the result of the following chain of events. Pretreatment with donor strain blood partially suppresses the rejection process, leading to a chronic type of rejection.…”

“…The transplantation technique, using endto-side anastomosis, is not prone to the development of artery stenosis. Furthermore, the blood pressure re sponse to a reduction in salt intake and the presence of an intact native kidney convinced us that the posttransplan tation hypertension model was at variance with the 1-kidney-I-clip Goldblatt hypertension in rats [3]. Conse quently, rejection remains as the most likely cause for the rise in SBP.…”

“…Treatment with donor strain blood prior to transplantation was used to prolong graft sur vival. This posttransplantation hypertension was asso ciated with a reduced renal function and a low plasma renin concentration [2], The latter was considered to result from sodium retention, and in a subsequent experi ment it was shown that a reduction in the daily sodium intake prevented the development of hypertension [3].…”

Renal Transplantation Modulates Expression and Function of Receptors and Transporters of Rat Proximal Tubules

“…Non-immunologic factors are increasingly regarded as important for the prognosis of the transplant. In humans, investigations of changes on the tubular level are hardly possible, and only a few functional studies in animals are available (12)(13)(14)(15)(16)(17)(18)(19)(20). No direct data exist on expression and function of transporters and receptors involved in transport after renal transplantation.…”