Hypertension in Obesity and NIDDM: Role of Insulin and Sympathetic Nervous System

  1. Lewis Landsberg, MD
  1. Department of Medicine, Harvard Medical School, and Beth Israel Hospital, Dana-Thorndike Research Laboratories Boston, Massachusetts
  1. Address correspondence and reprint requests to Lewis Landsberg, MD, Department of Medicine, Northwestern Memorial Hospital, 250 East Superior Street, Wesley Pavilion, Room 296, Chicago, IL 60611


An important link exists between obesity, noninsulin-dependent diabetes mellitus (NIDDM), and hypertension. Most patients with NIDDM are obese; the incidence of hypertension in obesity and NIDDM is substantial, approaching 50% in some studies. Furthermore, hypertension is known to contribute to the increased cardiovascular morbidity and mortality in patients with obesity and NIDDM. Despite the obvious clinical importance, the pathogenesis of hypertension in obesity and NIDDM remains poorly understood. Recent studies have identified hyperinsulinemia and insulin resistance as important threads that tie hypertension, obesity, and NIDDM together. The hypothesis is developed that insulin-mediated sympathetic stimulation contributes to blood pressure elevation in both obesity and NIDDM. Recruited as a mechanism to limit weight gain and restore energy balance, insulin resistance and sympathetic stimulation increase blood pressure by enhancing renal Na+ reabsorption and stimulating the cardiovascular system. In this article, we review the evidence on which this hypothesis is based.

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