American Society of Hypertension Self-Assessment GuideTreatment: special conditions: Metabolic syndrome: obesity and the hypertension connection
Section snippets
Insulin Resistance (IR)
IR is the decreased ability of insulin to affect glucose uptake by cells biologically. The result of this process is an increased secretion of insulin required to stimulate glucose transport into the muscle and fat cells and suppresses hepatic glucose production. The increased insulin secretion is necessary in order to maintain normal physiologic serum glucose levels. This condition may result in diabetes mellitus type II when this excess secretion can no longer meet the increased metabolic
Sympathetic Nervous System (SNS)
The increased SNS activity remains controversial in obesity and the MS but may increase BP, heart rate, and cardiac output and induce renal tubular sodium reabsorption, changes that may be explained by alpha and beta adrenergic receptor stimulation followed by an increase in renin.
Renin–Angiotensin–Aldosterone System (RAAS) Activity
Higher expression of RAAS is present in human adipose tissue, components that may play a paracrine, autocrine, and/or endocrine role in the relationship between obesity/MS and hypertension. It is increasingly being recognized that adipocytes may produce a significant amount of exogenous aldosterone.
Lipotoxicity, Inflammatory Cytokines, and Leptin
The MS and obesity exacerbate the release of non–esterified free fatty acid (FFA). These changes increase the beta and non–beta oxidative metabolism of FA. The release of products of lipid peroxidation and triglycerides and the decreased production of adiponectin originated by the excess of FFA causes lipotoxicity, which is characterized by apoptosis and fibrosis in the liver, pancreatic islets, heart, and tubulointerstitial inflammation with fibrosis in the kidneys. The increase in FFA also
Systemic Hemodynamic Changes and Fluid–Volume Distribution
Individuals with obesity–hypertension have an increased total blood volume that is largely redistributed to the cardiopulmonary area, which causes an augmented venous return, greater ventricular filling, and increased cardiac output. Total peripheral resistance is less elevated than expected for the degree of hypertension and is “inappropriately” normal. The high stroke volume in obese hypertensive subjects is caused by increased intravascular volume and normal heart rate.
Structural Cardiovascular Changes
Obesity has been associated with an increase in left ventricular (LV) wall thickness, an increase in overall LV mass, and a high prevalence of LV hypertrophy. These changes and the previously mentioned volume overload independent of the BP effect induce concentric–eccentric LV hypertrophy. A higher BMI is also independently associated with increased atrial fibrillation.
Hemodynamic and Structural Kidney Changes
Obese subjects have increased renal flow, decreased or unchanged renal vascular resistance, increased glomerular filtration rate, hyperperfusion, and glomerular hyperfiltration. Epidemiologic studies found that each component of the MS was associated with the increased prevalence of chronic kidney disease and microalbuminuria. Obese subjects had a high incidence of glomerulomegaly and “secondary” focal segmental glomerulosclerosis with a more indolent pattern of progression than in patients
Treatment Lifestyle Modification
The low–sodium Dietary Approaches to Stop Hypertension (DASH) trial and other studies with a low–calorie diet and/or salt restriction (no more than 6 g/day sodium chloride) have been effective in decreasing hypertension in the obese population. The Mediterranean diet, which has similarities to the DASH diet with an emphasis on consumption of fruit and non–starchy vegetables, lean meats and fish, and monounsaturated fats found in tree nuts and olive oil, has more recently been suggested to have
Pharmacological Approach
(Table 1) The ideal pharmacologic approach to treat subjects with obesity or the MS and hypertension will be to correct the metabolic–endocrine and hemodynamic changes, and protect the cardiac, renal, and end–organ changes without enhancing the existing metabolic characteristics. The most commonly used therapeutic agents and their potential metabolic consequences are listed below:
- 1.
Angiotensin–converting enzyme inhibitors and angiotensin receptor blockers: block the RAAS; may reduce plasma levels
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