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Endogenous adipose-derived factors diminish coronary endothelial function via inhibition of nitric oxide synthase

Gregory A Payne1, Léna Borbouse, Ian N Bratz

  • 1Department of Cellular and Integrative Physiology, School of Medicine, Indiana University, Indianapolis, IN 46202, USA.

Microcirculation (New York, N.Y. : 1994)
|June 25, 2008
PubMed

Insights

Adipose tissue releases factors that impair blood vessel function by inhibiting nitric oxide (NO) production. This finding links obesity to vascular disease by affecting endothelial-dependent vasodilation.

Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Obesity Research

Background:

  • Obesity is linked to vascular disease, with adipocytokines potentially mediating this connection.
  • The precise impact of adipose-derived factors on coronary vascular function remains unclear.

Purpose of the Study:

  • To investigate the mechanisms by which endogenous adipose-derived factors influence coronary vascular endothelial function.
  • To determine if adipose tissue affects endothelial-dependent and independent vasodilation.

Main Methods:

  • Studied isolated canine coronary arteries and coronary blood flow in anesthetized dogs.
  • Exposed vessels and blood flow to adipose tissue or adipose-conditioned buffer.
  • Utilized bradykinin for endothelial-dependent vasodilation and sodium nitroprusside for endothelial-independent vasodilation.
  • Assessed nitric oxide (NO) production and oxidative stress markers.

Main Results:

  • Adipose tissue impaired endothelial-dependent vasodilation to bradykinin but not endothelial-independent vasodilation to sodium nitroprusside.
  • Adipose tissue reduced baseline and bradykinin-stimulated nitric oxide (NO) production.
  • Inhibition of NO synthase with L-NAME mimicked the effect of adipose tissue, and blocking NO synthase abolished adipose tissue's impact.
  • Oxidative stress was not the cause of impaired vasodilation.

Conclusions:

  • Adipose tissue releases factors that selectively inhibit endothelial-dependent vasodilation.
  • These factors act by suppressing nitric oxide synthase-mediated NO production.
  • This mechanism provides insight into how obesity contributes to vascular dysfunction.

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