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Published on: June 16, 2014
Endothelin-1 and nitric oxide in patients on chronic hemodialysis
Monika Tomić1, Kresimir Galesić, Ivica Markota
1Department of Internal Medicine, Mostar University Hospital Center, Mostar, Bosnia and Herzegovina.
Insights
Endothelin-1 levels are elevated in chronic hemodialysis patients and correlate with higher blood pressure, even with ACE inhibitor use. Nitric oxide also influences blood pressure during dialysis.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Pharmacology
Background:
- Hypertension is a common complication in patients undergoing chronic hemodialysis (CHD).
- The roles of endothelin-1 (ET-1) and nitric oxide (NO) in dialysis-induced hemodynamic changes are not fully elucidated.
- Angiotensin-converting enzyme (ACE) inhibitors are frequently used in hypertensive patients, but their interaction with ET-1 and NO in CHD requires further investigation.
Purpose of the Study:
- To investigate the involvement of ET-1 and NO in the pathogenesis of hypertension in CHD patients.
- To correlate plasma concentrations of ET-1 and NO with the severity of arterial hypertension.
- To assess the influence of ACE inhibitor therapy on the relationship between ET-1, NO, and blood pressure in CHD patients.
Main Methods:
- Plasma concentrations of ET-1 and NO were measured in 30 CHD patients and 20 healthy controls before and after hemodialysis.
- Blood pressure measurements were correlated with ET-1 and NO levels.
- The effect of ACE inhibitors on these correlations was analyzed.
Main Results:
- CHD patients exhibited significantly higher ET-1 plasma concentrations than controls, both before and after dialysis.
- A significant decrease in ET-1 levels was observed post-hemodialysis.
- Positive correlation between ET-1 and systolic blood pressure was noted after dialysis, independent of ACE inhibitors.
- In patients on ACE inhibitors, higher ET-1 levels correlated with increased systolic blood pressure, and diastolic blood pressure showed a tendency to increase with ET-1 and decrease with NO post-dialysis.
Conclusions:
- ET-1 and NO play a significant role in the hemodynamic alterations of blood pressure during hemodialysis.
- Elevated ET-1 contributes to hypertension in CHD patients.
- Further research is warranted to fully understand the interplay of ET-1, NO, and ACE inhibitors in managing hypertension in dialysis patients.
Aim:
To establish the role of endothelin-1 and nitric oxide in the pathogenesis of hypertension in patients on chronic hemodialysis by correlating endothelin-1 and NO plasma concentrations to the level of arterial hypertension with respect to angiotensin-converting enzyme (ACE) inhibitor therapy.
Methods:
We determined plasma concentrations of endothelin-1 and NO in patients on chronic hemodialysis (CHD) before and after hemodialysis treatment. The study included 30 CHD patients and 20 healthy participants as controls. Correlation to blood pressure was determined, as well as the effect of ACE inhibitors on the relationship between both endothelin-1 and NO in correlation with arterial hypertension.
Main Findings:
Endothelin-1 plasma concentration was significantly higher in CHD patients before hemodialysis treatment than in healthy controls. Endothelin-1 plasma concentration was also significantly higher in CHD patients after hemodialysis than in healthy controls. There was a significant decrease in endothelin-1 plasma concentration after hemodialysis in comparison with its values before hemodialysis. In CHD patients, a positive correlation was found between endothelin-1 plasma concentration and systolic blood pressure after hemodialysis, irrespective of ACE inhibitors therapy. In CHD patients taking ACE inhibitors, systolic blood pressure increased with increasing endothelin-1 plasma concentration before as well as after hemodialysis. In patients taking ACE inhibitors, there was a tendency for diastolic blood pressure to increase with an increase in endothelin-1 plasma concentration after hemodialysis and to decrease with an increase in NO plasma concentration.
Conclusion:
NO and endothelin-1 play a significant role in etiology of the hemodynamic changes of blood pressure during the dialysis.
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