Elevated sympathetic activity changes renal function and accelerates the development of hypertension. Principles of sympatho-renal interactions in chronic hypertension are reviewed. Alterations in the ontogeny of the sympathetic nervous system and the kidney, inherited abnormalities in sensory receptor function and exaggerated responsiveness to mental stress contribute to inappropriately high sympathetic activity in primary or essential hypertension. Careful characterization of clinical study populations shows that elevated sympathetic activity and "essential" hypertension are not unequivocally associated. Prospective clinical studies which investigate a broader array of physiological functions and experiments in recombinant inbred rodents with less traumatic nerve recording techniques than currently available will help to define under which conditions elevated sympathetic activity is indeed a cause of primary hypertension. Signals arising from the kidney which activate the renin–angiotensin system and afferent renal nerves increase sympathetic activity. These mechanisms importantly contribute to the pathogenesis of hypertension secondary to renal artery stenosis and end-stage renal disease.
Copyright (C) 2004, European Society of Cardiology
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