Journal of the American Society of Hypertension
Volume 1, Issue 2 , Pages 120-134, March 2007

Understanding essential hypertension from the perspective of the cardiometabolic syndrome

  • Poorna R. Karuparthi, MD

      Affiliations

    • Department of Internal Medicine, University of Missouri, Columbia, Missouri, USA
    • Corresponding Author InformationCorresponding author: Poorna R. Karuparthi, MD, Department of Internal Medicine, University of Missouri, Columbia, Missouri 65201. Tel: 573-529-6638.
  • ,
  • Preethi Yerram, MD

      Affiliations

    • Department of Internal Medicine, University of Missouri, Columbia, Missouri, USA
    • Veteran Affairs Medical Center, Columbia, Missouri, USA
  • ,
  • Guido Lastra, MD

      Affiliations

    • Department of Internal Medicine, University of Missouri, Columbia, Missouri, USA
    • Veteran Affairs Medical Center, Columbia, Missouri, USA
  • ,
  • Melvin R. Hayden, MD

      Affiliations

    • Department of Internal Medicine, University of Missouri, Columbia, Missouri, USA
    • Division of Endocrinology Diabetes and Metabolism, University of Missouri, Columbia, Missouri, USA
  • ,
  • James R. Sowers, MD

      Affiliations

    • Division of Endocrinology Diabetes and Metabolism, Diabetes Center, Arizona Health Sciences, Tucson, Arizona, USA

Received 16 December 2006; accepted 19 January 2007.

Abstract 

Hypertension (HTN) is an important modifiable risk factor for major health problems such as coronary heart disease, stroke, congestive heart failure, end-stage renal disease, and peripheral vascular disease. Because of the associated morbidity and mortality, and the cost to society, HTN is an important public health challenge. HTN is frequently associated with other cardiovascular disease risk factors constituting the cardiometabolic syndrome, which individually and synergistically influence the pathophysiology of HTN, and the resultant increased redox stress contributes to the remodeling changes in key organs such as the heart and kidney. Remodeling at the subcellular level, and extracellular matrix in the heart and kidney of the hypertensive Ren2 transgenic rat model of tissue angiotensin II overexpression (TG(mREN-2)27), compared with the Sprague Dawley control rat model, has been observed by light and electron microscopy and are discussed. A better understanding of the pathophysiology of HTN may provide clinician and researcher, tools to effectively investigate and manage this complicated disease process.

Keywords: Metabolic syndrome, microalbuminuria, endothelial dysfunction, insulin resistance, hyperinsulinemia

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 Conflict of interest: none.

PII: S1933-1711(07)00018-6

doi:10.1016/j.jash.2007.01.006

Journal of the American Society of Hypertension
Volume 1, Issue 2 , Pages 120-134, March 2007