Regulation of blood pressure in chronic renal failure: determinants of hypertension and dialysis-related hypotension

Abstract

Regulation of blood pressure is of crucial importance in the management of patients with chronic renal failure. In the predialysis phase, hypertension is common. Apart from volume overload and an inappropriately activated renin-angiotensin system, overactivity of the sympathetic nervous system appears to play a role as well. Sympathetic outflow may be enhanced by elevated Angiotensin II levels. Maintenance treatment with angiotensin converting enzyme inhibition normalizes sympathetic overactivity in hypertensive patients with chronic renal failure. In view of the unfavourable role of increased sympathetic activity in cardiovascular disease and prognosis, normalization of sympathetic outflow may be a new treatment goal. Hemodialysis is often complicated by sudden hypotension, causing considerable distress and morbidity. Reduction of blood volume causes sympatho-excitation, vasoconstriction and tachycardia. Sudden hypotension, however, is accompanied by acute withdrawal of sympathetic activity, vasodilation and relative bradycardia, also known as the Bezold-Jarisch reflex. Subtle fluctuations in vasomotor tone in hypovolemic conditions can elicit this reflex. In a series of experiments we showed that reduction of blood volume plays a pivotal role in the pathogenesis of hypovolemic hypotension. Autonomic neuropathy and dysfunction of the central opioid system have been proposed as causative mechanisms in dialysis-related hypotension. We, however, could not confirm a pathogenetic role for either mechanism.