Tuncel Meryem, Augustyniak Robert, Zhang Weiguo, Toto Robert D, Victor Ronald G
Hypertension Division, Department of Internal Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Room J4.134, Dallas, TX 75390-8586, USA.
Curr Hypertens Rep. 2002 Jun;4(3):229-36. doi: 10.1007/s11906-002-0012-7.
Hypertension is a common complication of chronic renal failure, accelerating the deterioration in renal function and constituting an important risk factor for the excessive cardiovascular morbidity and mortality. However, there are large gaps in our understanding of the pathogenesis and treatment of renal hypertension. Although this hypertension traditionally is thought to be largely volume dependent, an increasing body of literature suggests that there is an important sympathetic neural component. Microneurographic studies have demonstrated sympathetic overactivity without baroreflex impairment in both hypertensive chronic hemodialysis patients as well as in those with less advanced renal insufficiency. In a small group of patients with moderate chronic renal insufficiency and renin-dependent hypertension, sympathetic overactivity was normalized during antihypertensive monotherapy with the angiotensin converting enzyme inhibitor enalapril, but exacerbated by antihypertensive therapy with the dihydropyridine calcium channel blocker amlodipine. These results implicate a potentially important role for the sympathetic nervous system in explaining recent trial data suggesting an added renoprotective effect of antihypertensive agents that block the renin-angiotensin system. Future clinical trials are needed to determine whether normalization of sympathetic activity should constitute an important therapeutic goal to improve renal and cardiovascular outcomes in patients with chronic renal failure.
