CONFLICTING RESULTS ABOUT THE ROLE OF NITRIC OXIDE IN DIALYSIS INDUCED HYPOTENSION

This study was planned to investigate the possible role of endogenous nitric oxide (NO) in acute hypotension during hemodialysis. Twenty-seven patients who had normal blood pressure before hemodialysis(HD) were included in this study. None of the patients was receiving antihypertensive drugs. The patients were dialysedfor 4 hour three times a week using hemophane membranes and a bicarbonate-based dilysate in our hemodialysis centre. The participants did not eat during dialysis. In all cases, blood pressures were recorded at every hour and for the measurement of plasma nitrate, blood samples were collected before the start of dialysis, at 2 hours after the start of dialysis (middialysis) and after the end of dialysis. On the basis of their blood pressure responses during hemodialysis, the patients were divided into two groups: 16 patients who had hypotensive episodes during hemodialysis were defined as those in whom mean arterial pressure (MAP) decreased more than 10 mmHg. The remain patients (n=11) were included in the other group named normotensive patients. In the first group, MAP were 83.8±16.2 mmHg and 65.8 ± 15.2 mmHg before and after hemodialysis respectively (p=0.001 ). In the second group, MAP were 88.9±8.9 mmHg and 87.8±9 mmHg before and after dialysis, respectively (p=0.43 ). Ultrafiltration rate was not differ between hypotensive and normotensive groups (p=0.34). Plasma nitrate levels at the initiation of hemodialysis did not differ significantly between hypotensive (76.4±69.7mmol/L) and normotensive (63.2±34.9 mmol/L) patients (p=0.9). In addition, nitric oxide production markedly decreased during hemodialysis into each groups (from 76.4±69.7 to 32.6±19.3 p=0.000 in the first group, from 63.2±34.9 to 33.8±13, p=0.006 in the second group) and did not found any correlation between NO production and MAP after hemodialysis (p=0.2). Our present results appear to conflict with previous studies showing that enhanced NO biosynthesis may contribute to hemodialysis induced hypotension. Although the number of patients is not enough, we suggest that the role of NO in dialysis-induced hypotension is still unclear.