Secondary Hypertension: Obesity and the Metabolic Syndrome

Abstract

The epidemic of obesity in the United States and around the world is intensifying in severity and scope and has been implicated as an underlying mechanism in systemic hypertension. Obese hypertensive individuals characteristically exhibit volume congestion, relative elevation in heart rate, and high cardiac output with concomitant activation of the renin‐angiotensin‐aldosterone system. When the metabolic syndrome is present, insulin resistance and hyperinsulinemia may contribute to hypertension through diverse mechanisms. Blood pressure can be lowered when weight control measures are successful, using, for example, caloric restriction, aerobic exercise, weight loss drugs, or bariatric surgery. A major clinical challenge resides in converting short‐term weight reduction into a sustained benefit. Pharmacotherapy for the obese hypertensive patient may require multiple agents, with an optimal regimen consisting of inhibitors of the renin‐angiotensin‐aldosterone system, thiazide diuretics, β‐blockers, and calcium channel blockers if needed to attain contemporary blood pressure treatment goals.

Traffic-related Air Pollution and Blood Pressure in Elderly Subjects With Coronary Artery Disease

“…39 Potential mechanisms of obesity-pollutant interactions may include an enhancement of the proinflammatory and autonomic effects of air pollution by factors thought to be involved in obesity-hypertension linkages (endothelial dysfunction, renin-angiotensin system activation, insulin resistance, adipokines, sympathetic activation, and oxidative stress). 40 Similar to our results for BP, the coronary artery disease panel study also found stronger heart-rate variability associations among subjects not using β -blockers. 38 …”

A Randomized Trial of a Low-Carbohydrate Diet vs Orlistat Plus a Low-Fat Diet for Weight Loss

“…18 Another mechanism may be related to lower serum insulin levels seen with the LCKD; hyperinsulinemia has been associated with sodium reten- tion, proliferation of vascular smooth muscle, increased sympathetic nervous system activity, and diminished release of nitric oxide from the endothelium. 31,32 In a meta-analysis of studies comparing the LCKD with an LFD, changes in systolic and diastolic blood pressure favored the LCKD but reached statistical significance for systolic blood pressure only. 2 In the OmniHeart Study, both the high-protein and high-monounsaturated fat diets (the LCKD is high in these macronutrients) lowered systolic and diastolic blood pressures more than the highcarbohydrate, low-fat diet.…”

Low‐Carbohydrate Diet Review

“…In addition, the high circulating levels of insulin that accompany insulin resistance related to obesity have been associated with sodium retention, proliferation of vascular smooth muscle, increased sympathetic nervous system activity, and diminished release of nitric oxide from the endothelium. [33][34][35] Frequently, the improvements seen in blood pressure with patients eating a LC diet are attributed to the weight loss effects of the diet, 12,14 but recent results demonstrate that improvements in blood pressure may be independent of weight loss and related to other mechanisms, as noted below.…”