Journal
BIOMOLECULES
Volume 12, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/biom12070889
Keywords
endothelium; nitric oxide; proteinase-activated receptor 2; ageing; cardiovascular system
Categories
Funding
- Canadian Institutes of Health Research [PJT-162199]
- Natural Sciences and Engineering Research Council of Canada [RGPIN 4536-2017]
- Western University's School of Graduate Studies
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Ageing is associated with reduced production of nitric oxide in the femoral artery. This study examined the endothelium-dependent relaxation in the saphenous artery and its caudal branches. The results showed that ageing decreased the responsiveness of the arteries to specific agonists and the sensitivity to nitric oxide.
Ageing is associated with reduced endothelium-derived nitric oxide (NO) production in the femoral artery of Sprague Dawley (SD) rats. In the current study, we examined endotheliumdependent relaxation (EDR) in the saphenous artery and its caudal branches. We used acetylcholine and the Proteinase-Activated receptor-2 (PAR2)-specific agonist (2fLIGRLO) with nitroarginine methylester (L-NAME) to assess EDR in two groups of male SD rats (age in weeks: young, 10-12; old, 27-29). Acetylcholine and 2fLIGRLO were potent NO-dependent relaxant agents in all arteries. For all arteries, EDR by acetylcholine decreased significantly in old compared to young SD rats. Interestingly, PAR2-induced EDR of proximal saphenous artery segments and caudal branches decreased significantly in old compared to young, but did not differ for the in-between middle and distal ends of the saphenous artery. L-NAME treatment increased subsequent contractions of proximal and middle segments of saphenous arteries by phenylephrine and U46619 in young, but not in old, SD rats. We conclude the SD saphenous artery and caudal branches exhibit regional characteristics that differ in response to specific EDR agonists, endothelial NO synthase inhibitor, and changes to endothelium function with increased age, which are, in part, attributed to decreased sensitivity of vascular smooth muscle to the gaseous transmitter NO.
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