Endothelium dependent hyperpolarization-type relaxation compensates for attenuated nitric oxide-mediated responses in subcutaneous arteries of diabetic patients

Mokhtar SS 1 , Vanhoutte PM 2 , Leung SW 2 , Yusof MI 3 , Wan Sulaiman WA 4 , Mat Saad AZ 4 Show all authors , Suppian R 5 , Rasool AH 6

Affiliations 

  • 1 Pharmacology Vascular Laboratory, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, Kota Bharu, Malaysia
  • 2 Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
  • 3 Department of Orthopaedic, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, Kota Bharu, Malaysia
  • 4 Reconstructive Sciences Unit, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, Kota Bharu, Malaysia
  • 5 School of Health Sciences, Universiti Sains Malaysia, Health Campus, Kota Bharu, Malaysia
  • 6 Pharmacology Vascular Laboratory, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, Kota Bharu, Malaysia. Electronic address: [email protected]
Nitric Oxide, 2016 Feb 29;53:35-44.
PMID: 26768833 DOI: 10.1016/j.niox.2015.12.007

Abstract

Diabetes impairs endothelium-dependent relaxations. The present study evaluated the contribution of different endothelium-dependent relaxing mechanisms to the regulation of vascular tone in subcutaneous blood vessels of humans with Type 2 diabetes mellitus. Subcutaneous arteries were isolated from tissues of healthy controls and diabetics. Vascular function was determined using wire myography. Expressions of proteins were measured by Western blotting and immunostaining. Endothelium-dependent relaxations to acetylcholine were impaired in arteries from diabetics compared to controls (P = 0.009). Acetylcholine-induced nitric oxide (NO)-mediated relaxations [in the presence of an inhibitor of cyclooxygenases (COX; indomethacin) and small and intermediate conductance calcium-activated potassium channel blockers (UCL1684 and TRAM 34, respectively)] were attenuated in arteries from diabetics compared to controls (P 

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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