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

Authors
Citation
G. Ligtenberg, Regulation of blood pressure in chronic renal failure: determinants of hypertension and dialysis-related hypotension, NETH J MED, 55(1), 1999, pp. 13-18
Citations number
36
Categorie Soggetti
General & Internal Medicine
Journal title
NETHERLANDS JOURNAL OF MEDICINE
ISSN journal
03002977 → ACNP
Volume
55
Issue
1
Year of publication
1999
Pages
13 - 18
Database
ISI
SICI code
0300-2977(199907)55:1<13:ROBPIC>2.0.ZU;2-D
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 ren in-angiotensin system, overactivity of the sympathetic nervous system appea rs to play a role as well. Sympathetic outflow may be enhanced by elevated Angiotensin II levels. Maintenance treatment with angiotensin converting en zyme inhibition normalizes sympathetic overactivity in hypertensive patient s with chronic renal failure. In View of the unfavourable role of increased sympathetic activity in cardiovascular disease and prognosis, normalizatio n of sympathetic outflow may be a new treatment goal. Hemodialysis is often complicated by sudden hypotension, causing considerab le distress and morbidity. Reduction of blood volume causes sympatho-excita tion, vasoconstriction and tachycardia. Sudden hypotension, however, is acc ompanied by acute withdrawal of sympathetic activity, vasodilation and rela tive bradycardia, also known as the Bezold-Jarisch reflex. Subtle fluctuati ons in vasomotor tone in hypovolemic conditions can elicit this reflex. in a series of experiments we showed that reduction of blood Volume plays a pi votal role in the pathogenesis of hypovolemic hypotension. Autonomic neurop athy and dysfunction of the central opioid system have been proposed as cau sative mechanisms in dialysis-related hypotension. We, however, could not c onfirm a pathogenetic role for either mechanism. (C) 1999 Elsevier Science B.V. All rights reserved.