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Renal mechanisms and the sympathetic nervous system contribute to the development of arterial hypertension. Renal transplantation experiments in spontaneously hypertensive rats (SHRs) were performed to investigate how the sympathetic nervous system and the kidneys interact during the development and maintenance of hypertension. Our findings indicate that the rise in arterial pressure that occurs after transplantation of a kidney from a SHR into normotensive recipients is not mediated by elevations in sympathetic activity. However, chronic reductions in sympathetic tone reduce the rise in arterial pressure which can be induced by SHR renal grafts in normotensive recipients. Untreated SHRs transplanted with a kidney from sympathectomized donors have lower arterial pressure and reduced sodium sensitivity of arterial pressure compared to SHRs transplanted with a kidney from hydralazine-treated donors. It is concluded that chronic non-adapting changes in sympathetic activity modulate the degree to which renal mechanisms can cause hypertension in SHRs. Severe reduction in sympathetic tone during early ontogeny causes long-term changes in renal function that mitigate hypertension development in SHRs even when the extrarenal neuro-hormonal environment is restored.
Olaf Grisk (2004) studied this question.