Sympathetic overactivity and arterial hypertension in renal failure.
In the past, it had been presumed that hypertension in chronic renal disease can be explained by the dual effects of sodium retention and inappropriate activity of the renin-angiotensin system. Recent experimental and clinical data provide strong evidence that the increase in blood pressure is to a large part due to sympathetic overactivity which is triggered by afferent signals emanating from the kidney and resetting sympathetic tone by stimulation of hypothalamic centres. The sequelae of sympathetic overactivity extend beyond their effects on blood pressure and include accelerated progression of renal failure and presumably increased cardiac arrhythmia.
Orth
S R
SR
Department of Nephrology, Ruperto Carola University Heidelberg, Germany.
Amann
K
K
Strojek
K
K
Ritz
E
E
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D001794:Blood Pressure; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D007031:Hypothalamus / Q000503:physiopathology; D007668:Kidney / Q000294:innervation*; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D000319:Adrenergic beta-Antagonists