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Updated: May 5, 2026

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Prolonged AMP-activated protein kinase induction impairs vascular functions

Saadet Turkseven1, Elif Ertuna

  • 1Ege University, Faculty of Pharmacy, Department of Pharmacology, Bornova-Izmir 35100, Turkey.

Canadian Journal of Physiology and Pharmacology
|December 3, 2013
PubMed

Insights

Prolonged activation of AMP-activated protein kinase (AMPK) impairs vascular function by reducing endothelium-dependent relaxation and decreasing endothelial nitric oxide synthase (eNOS) expression. This suggests AMPK activation may negatively impact cardiovascular health.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Regulation
  • Vascular Physiology

Background:

  • AMP-activated protein kinase (AMPK) is a key regulator of cellular metabolism.
  • AMPK's role in vascular function is controversial, with potential implications for diseases like type 2 diabetes and cardiovascular conditions.

Purpose of the Study:

  • To investigate the impact of prolonged AMPK activation on specific vascular functions.
  • To elucidate the mechanisms underlying AMPK's effects on endothelium-dependent and -independent relaxation and vascular contractility.

Main Methods:

  • Thoracic aortic rings from rats were treated with the AMPK activator AICAR (5-aminoimidazole-4-carboxamide-1-4-ribofuranoside) and the inhibitor compound C.
  • Dose-response curves were generated for acetylcholine (endothelium-dependent), nitroglycerine (endothelium-independent), and noradrenaline (vasoconstrictor).
  • Endothelial nitric oxide synthase (eNOS) protein expression was quantified.

Main Results:

  • AICAR treatment significantly inhibited endothelium-dependent relaxation, an effect reversed by compound C.
  • AICAR enhanced the contractile response to noradrenaline.
  • AICAR treatment led to a reduction in eNOS protein expression.

Conclusions:

  • Prolonged AMPK activation impairs endothelial function.
  • This impairment may be mediated by reduced eNOS expression or increased degradation.
  • Findings suggest a potential detrimental role of sustained AMPK activation in vascular health.

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