Mechanisms of hypertension in the cardiometabolic syndrome

Redon J., Cifkova R., Laurent S., Nilsson P., Narkiewicz K., Erdine S., ...More

JOURNAL OF HYPERTENSION, vol.27, pp.441-451, 2009 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Review
  • Volume: 27 Issue: 3
  • Publication Date: 2009
  • Doi Number: 10.1097/hjh.0b013e32831e13e5
  • Title of Journal : JOURNAL OF HYPERTENSION
  • Page Numbers: pp.441-451


Arterial hypertension is often part of a constellation of anthropometric and metabolic abnormalities that occur simultaneously to a higher degree than would be expected by chance alone, supporting the existence of a discrete disorder, the so-called metabolic syndrome. It is the result of interactions among a large number of interconnected mechanisms, which eventually lead to both an increase in cardiovascular and renal risk, and the development of diabetes. Mechanisms involved in the metabolic syndrome are obesity, insulin resistance, and a constellation of independent factors, which include molecules of hepatic, vascular, and immunologic origin with pro-inflammatory properties. At each of these key points are interactions of demographics, lifestyle, genetic factors, and environmental fetal programming. Superimposing upon these are infections or chronic exposure or both to certain drugs that can also make their contribution. Skeletal muscle and the liver, not adipose tissue, are the two key insulin-response tissues involved in maintaining glucose balance, although abnormal insulin action in the adipocytes also plays a role in development of the syndrome. Factors commonly associated with and partly dependent on obesity, insulin resistance, such as overactivity of the sympathetic, stimulation of the renin-angiotensin-aldosterone systems, abnormal renal sodium handling, endothelial dysfunction, and large vessels' alterations, may play a key role in the blood pressure elevation of the syndrome. J Hypertens 27:441-451 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.