Obesity associated hypertension: New insights into mechanism

Young Sun Kang

Research output: Contribution to journalReview article

71 Citations (Scopus)

Abstract

With excess nutrition, the burden of obesity is a growing problem worldwide. The imbalance between energy intake and expenditure leads to variable disorders as all major risk factors for cardiovascular disease. There are many hypothetical mechanisms to explain obesity-associated hypertension. Activation of the RAAS is a key contributing factor in obesity. Particularly, the RAAS in adipose tissue plays a crucial role in adipose tissue dysfunction and obesity-induced inflammation. The phenotypic changes of adipocytes occur into hypertrophy and an inflammatory response in an autocrine and paracrine manner to impair adipocyte function, including insulin signaling pathway. Adipose tissue produce and secretes several molecules such as leptin, resistin, adiponectin, and visfatin, as well as cytokines such as TNF-α, IL-6, MCP-1, and IL-1. These adipokines are stimulated via the intracellular signaling pathways that regulate inflammation of adipose tissue. Inflammation and oxidative stress in adipose tissue are important to interact with the microvascular endothelium in the mechanisms of obesity-associated hypertension. Increased microvascular resistance raises blood pressure. Therefore, a regulatory link between microvascular and perivascular adipose tissue inflammation and adipokine synthesis are provided to explain the mechanism of obesity-associated hypertension.

Original languageEnglish
Pages (from-to)46-52
Number of pages7
JournalElectrolyte and Blood Pressure
Volume11
Issue number2
DOIs
Publication statusPublished - 2013 Dec

Keywords

  • Hypertension
  • Insulin resistance
  • Microvascular dysfunction
  • Obesity
  • Renin-angiotensin-aldosterone system (RAAS)

ASJC Scopus subject areas

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'Obesity associated hypertension: New insights into mechanism'. Together they form a unique fingerprint.

  • Cite this