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The Role of Sympathetic Nervous Activity in Chronic Renal Failure

Journal of Clinical and Basic Cardiology 2001; 4 (3): 179-182

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Fig. 1: SNS-‹beraktivitšt - Niereninsuffizienz Fig. 2: SNS-‹beraktivitšt - Niereninsuffizienz Fig. 3A-B: Noradrenalinfreisetzung - Moxonidin Fig. 4: Noradrenalin - Angiotensin II Fig. 5: SNS - Co-Transmitter



Keywords: chronische NiereninsuffizienzCo-TransmitterKardiologieproliferationRenin-Angiotensin-Systemsympathisches Nervensystemcardiologychronic renal failurecotransmittersproliferationrenin-angiotensin systemsympathetic

Cardiovascular morbidity and mortality are extremely high in patients with chronic renal failure. Preventing progression of chronic renal failure and reducing the cardiovascular risk of uraemic patients are major challenges for nephrologists. In the past the renin-angiotensin system has been the main focus of research and therapy efforts. Today we know that sympathetic overactivity plays an important role for progression and prognosis in chronic renal disease. Afferent signals arising from the damaged kidneys due to the activation of mechanoreceptors and chemoreceptors lead to efferent sympathetic nervous activation. This results in an enhanced release of the sympathetic neurotransmitters noradrenaline, ATP and NPY at important neuroeffector junctions in heart, kidney and blood vessels. All three sympathetic cotransmitter are able to induce vasoconstriction and to stimulate proliferative processes. Recently it was shown in an animal model of chronic renal failure that inhibition of sympathetic nervous activity by moxonidine ameliorates disease progression. This effect was independent from blood pressure reductions and likely due to reduced cotransmitter release. Thus, interference with sympathetic overactivity may provide a new therapeutic avenue to follow in clinical medicine to prolong the interval between chronic and end-stage renal failure.
 
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