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Blood pressure regulation in chronic hypotensive and hypertensive patients with chronic renal failure
Insights
Blood pressure regulation in uremic patients on hemodialysis is complex. Abnormalities stem from altered cardiac index and total peripheral resistance relative to hematocrit, influenced by the renin-angiotensin system and autonomic dysfunction.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Internal Medicine
Background:
- Uremic patients (UP) on long-term hemodialysis often exhibit complex blood pressure (BP) regulation issues.
- Anemia is a common comorbidity in UP, potentially influencing cardiovascular parameters.
- The interplay between cardiac index (CI), total peripheral resistance (TPR), and hematocrit (Ht) in uremia requires further elucidation.
Purpose of the Study:
- To investigate the regulatory mechanisms of blood pressure in uremic patients undergoing long-term hemodialysis.
- To identify the roles of cardiac index, total peripheral resistance, hematocrit, plasma renin activity, and autonomic function in BP abnormalities.
Main Methods:
- Comparison of cardiovascular parameters (CI, TPR) and hematocrit between uremic patients (subgrouped into hypertensive, normotensive, and hypotensive) and normal controls.
- Correlation analysis between hematocrit and CI/TPR.
- Measurement of plasma renin activity (PRA) and extracellular fluid volume.
- Assessment of hemodynamic changes during hemodialysis and renin secretion responsiveness.
Main Results:
- Uremic patients exhibited higher CI (especially hypertensive) and lower TPR (hypotensive) relative to hematocrit compared to controls.
- Plasma renin activity was elevated in uremic patients, correlating positively with TPR, suggesting its role in BP regulation.
- Autonomic dysfunction was implicated in chronic hypotension in hypotensive uremic patients due to blunted renin response during dialysis.
Conclusions:
- Blood pressure abnormalities in uremic patients are primarily driven by altered TPR and CI relative to hematocrit, modulated by the renin-angiotensin system.
- Elevated PRA contributes to higher TPR in uremic patients.
- Autonomic dysfunction plays a role in the development and maintenance of hypotension in a subset of uremic patients.
Abstract:
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.