[Pathophysiology of blood pressure variability in patients with chronic renal failure under maintenance hemodialysis].
The rise of blood pressure is negatively related with the glomerullar filtration rate(GFR) in patients with terminal renal failure. Hypertension may be a mechanism to maintain renal blood flow and GFR constant by the increased driving force of blood to the kidney. Elevated levels of a so-called third factor, now designated as endogenous digitalis, are found in those patients. The most likely candidate of the endogenous digitalis is ouabain, which causes hypertension with chronic administration. On the other hand, extreme hypotension often occurs during maintenance hemodialysis, and since hemodynamic alterations closely resemble endotoxin shock, the involvement of nitric oxide(NO) over-production has been suggested. When we measured nitrate anion as the final metabolite of NO, the concentration was significantly higher in patients with marked hypotension during hemodialysis than those without hypotension. Since reflex tachycardia was not observed during hypotension, we speculated that those patients had autonomic disturbances, and assessed autonomic function by heart rate spectral analysis. Although the high frequency spectral power, regarded as the vagal tone, was not significantly different between the groups, low/high frequency spectral power ratio, which was thought to be a sympathetic component, was significantly lower in patients with hypotension during hemodialysis than that in patients without hypotension. We speculated that NO synthase may be induced by the stimuli to monocytes by tubes and dialyser membrane made of synthetic materials leading to the over production of NO during and after regular hemodialysis. Thus, cytokines may be the mediator of the induction of NO synthase. Dilated capacitance vessels decrease the venous return to the heart, which may be the direct cause of dialysis-induced hypotension.
Takahashi
H
H
Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University, Moriguchi 570-8507.
Masaki
H
H
Nishimura
M
M
D001341:Autonomic Nervous System / Q000503:physiopathology; D001794:Blood Pressure; D016207:Cytokines / Q000502:physiology; D006801:Humans; D007022:Hypotension / Q000209:etiology*; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D006435:Renal Dialysis / Q000009:adverse effects*
D016207:Cytokines; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase