期刊
BIOLOGICAL & PHARMACEUTICAL BULLETIN
卷 39, 期 3, 页码 384-393出版社
PHARMACEUTICAL SOC JAPAN
DOI: 10.1248/bpb.b15-00821
关键词
cyclooxygenase; endothelium; femoral artery; hypertension; contraction
资金
- JSPS KAKENHI [26460107, 15K21419, 15K07975]
- Grants-in-Aid for Scientific Research [15K21419, 26460107, 15K07975] Funding Source: KAKEN
We investigated the relationship between noradrenaline (NAd)-induced contractions, endothelial function, and hypertension in femoral arteries isolated from spontaneously hypertensive rats (SHR). In the femoral arteries of SHR, vs. age-matched control Wistar Kyoto (WKY) rats, contractions induced by NAd were increased. These effects were enhanced by endothelial denudation, which abolished the differences between the two groups. NAd-induced contractions were enhanced by nitric oxide (NO) synthase inhibition, and further increased by the blockade of endothelium-derived hyperpolarizing factor (EDHF). Conversely, NAd-induced contractions were inhibited by cyclooxygenase (COX) inhibition. In addition, in SHR arteries, acetylcholine-induced relaxation was reduced, and components of endothelium-derived factors were altered, such as increased COX-derived vasoconstrictor prostanoids, reduced EDHF, and preserved NO-mediated relaxation. In the femoral arteries of SHR, the production of prostanoids [6-keto prostaglandin (PG)F-1a (a metabolite of prostacyclin (PGI(2)), PGE(2), and PGF(2a)] and COX-2 protein were increased compared with that in WKY rats. By contrast, contractions induced by beraprost (a stable PGI(2) analogue), PGE(2), and U46619 (thromboxane/prostanoid receptor agonist) were similar between the SHR and WKY groups. Thus, NAd-induced femoral arterial contractions are augmented in SHR resulting from endothelial dysfunction and increased COX-derived vasoconstrictor prostanoid levels.
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