Cardiovascular Disease: Obesity Mechanisms in Hypertension
Article Outline
Every clinician is sure to find something new, interesting, or stimulating in this cardiovascular issue. Whether learning that hearts truly can be broken, discovering stiff arteries, determining the best cardiac stress tests for women, connecting infectious and cardiovascular diseases (CVD), or processing findings on metabolic syndrome in college students, this issue is sure to get the blood pumping.
The United States has the highest CVD (hypertension, myocardial infarction, heart failure, arrhythmias, stroke, etc) and obesity rates in the world. In keeping with the journal's 2009 obesity theme, I chose to highlight the pathophysiological mechanisms of obesity relative to hypertension (HTN), rather than discussing the importance of weight management.
Haynes1 proposes that obesity contributes to HTN development through overactivation of the sympathetic nervous system (SNS). The SNS stimulates alpha-receptors in the smooth muscles of blood vessels, which causes vasoconstriction (restricted blood flow) in skin, skeletal muscle, heart, and gastrointestinal systems. The SNS can also increase blood flow by stimulating beta-receptors, causing vasodilation. The body maintains a delicate balance between alpha- and beta-receptor stimulation in order to promote homeostasis. Evidence suggests that obese people have increased SNS activity, increased norephinephrine levels, and enhanced sodium retention, as well as increased vasoconstriction. Further, Kidambi et al2 proposed that central obesity may cause an increase in cortisol levels (stress hormone involved in SNS activation) in certain tissue (ie, liver, adipose, muscle), which leads to insulin resistance and increased aldosterone levels (promotes sodium retention), leading to elevated blood pressure.
Haynes1 also suggests that the protein leptin stimulates the SNS, contributing to the development of HTN. Leptin, which is secreted by adipose tissue, works in the hypothalamus to regulate appetite, energy, and SNS activity. Leptin normally causes weight loss, but obese people appear to be resistant to this positive action. Research suggests increased SNS activity, and increased norephinephrine and leptin in obese people leads to enhanced sodium retention and increased endothelial nitrous oxide, which contributes to vasoconstriction.
Fat in the abdominal region (a metabolic syndrome criterion) may be a more important indicator of cardiovascular risks than estimates of total body fat. However, researchers found that all body fat measures, including waist circumference, total fat, and body mass index, were associated with arterial stiffness, an indicator of cardiovascular risk.3 Stiffening of the arteries represents another mechanism whereby obesity might contribute to HTN. Obesity has also been implicated as a contributor to the body's inflammatory response associated with CVD.
The mechanisms whereby obesity contributes to CVD are complex and multifaceted, so let's work together to prevent and manage this risk factor.
References
- . Role of leptin in obesity-related hypertension . Exp Physiol . 2007;90(5):683–688
- Association of adrenal steroids with hypertension and the metabolic syndrome in blacks . Hypertension . 2007;49(3):704–711
- . Elevated aortic pulse wave velocity, a marker of arterial stiffness, predicts cardiovascular events in well-functioning older adults . Circulation . 2005;111(25):3384–3390
PII: S1555-4155(09)00503-0
doi:10.1016/j.nurpra.2009.09.003
© 2009 American College of Nurse Practitioners. Published by Elsevier Inc. All rights reserved.
