Blood pressure regulation in chronic hypotensive and hypertensive patients with chronic renal failure.

We studied the regulatory mechanism of blood pressure in uremic patients (UP) treated with long-term hemodialysis. The cardiac index (CI) was higher in UP than in normal control (NC). Total peripheral resistance (TPR) in hypertensive (U-Hyper) and normotensive (U-Normo) uremic patients was almost the same as that in NC but TPR in hypotensive uremic patients (U-Hypo) was lower than in NC. High CI in U-Hyper and low TPR in U-Hypo seem to be the causes of their blood pressure abnormalities. All patients had severe anemia. There was a significant positive correlation between hematocrit (Ht) and TPR in UP as well as in NC. The regression line of correlation between Ht (x axis) and TPR (y axis) in UP was shifted to the left from that of NC, suggesting TPR was higher even in U-Hypo than in NC. There was a significant negative correlation between Ht and CI in UP as well as in NC. The regression line of correlation between Ht (x axis) and CI (y axis) in UP was shifted to the left from that in NC, suggesting that CI was lower even in U-Hyper than that in NC. Therefore, higher TPR relative to Ht in U-Hyper and lower CI relative to Ht in U-Hypo may actually be principal causes of their blood pressure abnormalities. Circulating plasma volume and extracellular fluid volume were significantly higher in UP even after hemodialysis but there was no significant difference among subgroups of uremia. Plasma renin activity (PRA) was higher in UP than in NC. However, PRA in U-Hypo was significantly lower than that in U-Hyper or U-Normo. PRA in UP, even in U-Hypo, was inappropriately high relative to sodium/volume status. There was a significant positive correlation between TPR and PRA in UP. Therefore, higher TPR in UP relative to Ht than NC might be a result of elevated PRA. The level of blood pressure in UP seems to be regulated mainly by renin-angiotensin system. All patients were dialysed under the same condition. Heart rate and TPR increased after dialysis in U-Hyper and U-Hypo. However, no change occurred in these parameters throughout dialysis in U-Hypo. The responsiveness of renin secretion upon dialysis was lower in U-Hypo than in other two groups. Therefore, autonomic dysfunction may partly contribute to the development and maintenance of chronic hypotension in U-Hypo.