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Published on: June 16, 2014
Relationships between urinary electrolytes excretion and central hemodynamics, and arterial stiffness in hypertensive
Weizhong Han1, Xiao Han2, Ningling Sun3
1Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Shandong, China.
Insights
High sodium intake is linked to increased central blood pressure and arterial stiffness in hypertensive individuals. Reducing dietary salt may improve cardiovascular health by lowering these risk factors.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Hypertension Research
Background:
- High sodium intake is a known contributor to hypertension development and worsening.
- The precise links between urinary electrolyte excretion, central hemodynamics, and arterial stiffness remain debated.
- Understanding these relationships is crucial for managing hypertension and its complications.
Purpose of the Study:
- To investigate the associations between salt intake, central aortic pressure, and arterial stiffness indicators.
- To clarify the independent relationships of urinary sodium and potassium excretion with central hemodynamics and arterial stiffness.
Main Methods:
- A study involving 431 untreated hypertensive patients.
- Collection and analysis of 24-hour urinary samples for electrolyte excretion.
- Measurement of central hemodynamics and brachial-ankle pulse wave velocity (baPWV).
Main Results:
- Mean 24-hour urinary sodium excretion was 166.6±70.0 mmol/24 h.
- Increased urinary sodium excretion correlated with higher central blood pressure and baPWV.
- Urinary sodium was independently associated with elevated central systolic blood pressure, central diastolic blood pressure, augmentation index, and baPWV.
Conclusions:
- Significant correlations exist between high dietary sodium intake and adverse central hemodynamics and arterial elasticity.
- Urinary sodium excretion is a significant independent predictor of central hemodynamic parameters and arterial stiffness in hypertensive patients.
- Further interventional studies are warranted to confirm the causal effect of salt intake on central hemodynamics in hypertensive populations.
Abstract:
High sodium intake plays an important role in the onset and exacerbation of hypertension. However, the relationships between urinary electrolytes excretion and central hemodynamics and between urinary electrolyte excretion and arterial stiffness are still the subject of debate. This study sought to clarify the associations of salt intake with central aortic pressure and arterial stiffness indicators. A total of 431 untreated hypertensive individuals were recruited into the study. Twenty-four-hour urinary samples were collected to measure the excretion of urinary electrolytes. Central hemodynamics parameters and brachial-ankle pulse wave velocity (baPWV) were measured. We evaluated the independent relationship between urinary sodium or potassium excretion and the abovementioned indices. The mean 24-h urinary sodium of all subjects was 166.6±70.0 mmol/24 h. With increases in urinary sodium excretion, central blood pressure and baPWV values markedly increased. Multiple regression analysis showed that urinary sodium was independently associated with increases in central systolic blood pressure, central diastolic blood pressure, the augmentation index, and baPWV. Significant correlations were identified between high dietary sodium and central hemodynamics and between high dietary sodium and arterial elasticity. Prospective interventional studies in hypertensive patients may be required to determine the effect of salt intake on central hemodynamics.
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