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Obesity and essential hypertension. Hemodynamics, intravascular volume, sodium excretion, and plasma renin activity
Insights
Obesity is linked to higher cardiac output and expanded intravascular volume, but maintains normal hemodynamic relationships. Despite lower peripheral resistance, increased volume burdens the hypertensive left ventricle.
Area of Science:
- Cardiovascular Physiology
- Obesity Research
- Hypertension Studies
Background:
- Obesity is associated with altered systemic hemodynamics and fluid balance.
- Understanding these changes is crucial for managing hypertension in obese individuals.
- Previous research has yielded conflicting results regarding intravascular volume and hemodynamics in obesity.
Purpose of the Study:
- To investigate the relationship between systemic hemodynamics, intravascular volume, and plasma renin activity in lean, overweight, and obese subjects with varying degrees of hypertension.
- To clarify how obesity affects cardiac output, peripheral resistance, and intravascular volume.
- To determine if established pathophysiological correlations hold true in the context of obesity and hypertension.
Main Methods:
- Studied 135 subjects across a spectrum of body weights (lean to distinctly overweight) and blood pressure levels (normotensive to established essential hypertension).
- Measured systemic hemodynamics (cardiac output, peripheral resistance), intravascular volume, and plasma renin activity.
- Analyzed correlations between these parameters, considering corrections for body size (height and weight).
Main Results:
- Obese subjects exhibited higher cardiac output and lower peripheral resistance compared to lean subjects, except in borderline hypertension.
- Intravascular volume was increased in obese individuals, particularly when corrected for height.
- Significant positive correlations were found between intravascular volume and cardiac output, and inverse correlations with peripheral resistance, even after accounting for obesity's influence on blood volume.
- Sodium excretion was higher in obese subjects.
Conclusions:
- The pathophysiological relationship between systemic hemodynamics and intravascular volumes remains consistent in obesity, despite expanded circulating volume.
- Lower peripheral resistance in obesity may offer some protection against systemic vascular disease.
- However, the increased circulating volume in obese hypertensive individuals imposes an additional load on the left ventricle due to heightened venous return and afterload.
Abstract:
Systemic hemodynamics, intravascular volume, and plasma renin activity were determined in 135 lean, midly obese, or distinctly overweight subjects who were normotensive or had borderline or established essential hypertension. Cardiac output (but not index) was higher and peripheral resistance lower in obese than in lean subjects, except in borderline hypertension. Intravascular volume was increased in obese patients, and more so when corrected for body height; correction for body weight led to relative volume contraction. Intravascular volume correlated directly with cardiac output in the entire population, as well as in the subgroups. Intravascular volume correlated inversely with total peripheral resistance in all subjects and in each subgroup. Both correlations remained significant when an approximation was used to correct influences of obesity on total blood volume. Sodium excretion was higher in obese than in lean subjects. Thus, despite the expanded intravascular volume in obesity, the pathophysiologic relationship between systemic hemodynamics and intravascular volumes remains unchanged. Relatively low peripheral resistance in obesity may decrease the risk of systemic vascular disease. Nevertheless, since circulating volume is increased, the greater venous return adds an additional load to a left ventricle that is already burdened by a high afterload caused by arterial hypertension.