Tonic activation of the sympathetic nervous system is a major factor contributing to hypertension in patients with chronic renal failure. Besides its role in blood pressure regulation, sympathetic overactivity causes structural and functional alterations of the myocardium and large artery walls. Altogether, these factors contribute substantially to the increased cardiovascular morbidity and mortality in patients with chronic renal disease. Moreover, increased sympathetic outflow in conjunction with increased oxidative stress causes progression of renal disease thereby accelerating the course towards the need of renal replacement therapy. The origin of increased sympathetic outflow in patients with renal disease still has not been fully elucidated. There is sound evidence that signals arising from the diseased kidneys - mediated via renal afferent nerves – cause tonic activation of efferent sympathetic nerve fibres. Renal ischemia with release of adenosine and renal chemoreceptor activation, accumulation of angiotensin II and fibroproliferative scarring with renal mechanoreceptor dysfunction may be involved in the activation of renal afferences. Sympathetic overactivity in renal disease can be diminished by blockers of the renin angiotensin aldosterone system, by adrenoreceptor blockers and by substances inhibiting central sympathetic outflow such as imidazolines. These drugs not only reduce sympathetic nerve activity, they attenuate cardiovascular pathology and they slow the progression of renal disease. A combination of these drugs in patients with chronic renal failure seems promising and warrants randomized large-scale studies.
Keywords: Sympathetic nerve activity, chronic renal failure, kidney transplantation, renin angiotensin aldosteron system, large artery structure and function
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