title: Effects of endothelium-derived hyperpolarizing factor and nitric oxide on endothelial function in femoral resistance arteries of spontaneously hypertensive rats.
abstract: In hypertension, endothelium-dependent relaxation is attenuated and this attenuation contributes to the increased peripheral resistance. However, the role of endothelium-derived hyperpolarizing factor (EDHF) in the arteries of hypertensive rats remains unclear. Therefore, the aim of this study was to evaluate the role of EDHF in the femoral resistance arteries of hypertensive rats. The femoral resistance arteries were isolated from 5-, 15- and 25-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar Kyoto rats (WKY). Changes in internal diameter were examined with videomicroscopy. EDHF-mediated dilatation was determined by differences between the degree of acetylcholine (ACh)-induced dilatation in the presence of NG-monomethy-L-arginine (L-NMMA) plus a prostaglandin I2 inhibitor (indomethacin) and the degree of such dilatation in the presence of L-NMMA, indomethacin and KCl. Charybdotoxin (CTx) and apamin (a Ca2+-activated K+ channel [KCa] inhibitor)-sensitive EDHF dilatation was also compared between in 5-, 15- and 25-week-old SHR and WKY. ACh-induced vasodilatation was not different between 5-week-old SHR and WKY. There was no difference between NO- and EDHF-mediated vasodilatation in 5-week-old rats. ACh-induced vasodilatation was weaker in 15-week-old SHR than in WKY. NO-mediated vasodilatation did not differ between the two groups. EDHF-mediated dilatation was attenuated in SHR but not in WKY. ACh-induced dilatation was weaker in 25-week-old SHR than in WKY. NO- and EDHF-mediated vasodilatation were attenuated in SHR but not WKY. EDHF-mediated vasodilatation was attenuated before the loss of NO-mediated vasodilatation in the femoral resistance arteries of SHR. The attenuation of this vasodilatation was mediated by the CTx plus apamin-sensitive EDHF.
authors.affiliation: Department of Internal Medicine, Division of Coronary Heart Disease, Hyogo College of Medicine, Japan.
authors.forename: Yoshitomo
authors.initials: Y
authors.lastname: Mori
authors.forename: Mitsumasa
authors.initials: M
authors.lastname: Ohyanagi
authors.forename: Satsuki
authors.initials: S
authors.lastname: Koida
authors.forename: Atsunori
authors.initials: A
authors.lastname: Ueda
authors.forename: Kai
authors.initials: K
authors.lastname: Ishiko
authors.forename: Tadaaki
authors.initials: T
authors.lastname: Iwasaki
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000503:physiopathology*; D001685:Biological Factors / Q000502:physiology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005263:Femoral Artery / Q000187:drug effects / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D009569:Nitric Oxide / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D001685:Biological Factors; D014665:Vasodilator Agents; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide; D000109:Acetylcholine