title: Spontaneous and agonist-induced contractions and endothelium-dependent relaxation in aortae from SHRSP and WKY rats under various levels of passive force.
abstract: 1. The influence of the passive force on the contraction and endothelium-dependent relaxation in aortae of normotensive Wistar Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP) were compared. 2. Force changes of endothelium-intact and -removed preparations were measured isometrically by a force-displacement transducer. Endothelium-dependent relaxation was observed by applying acetylcholine to the preparation precontracted in the presence of 5 x 10(-7) mol/L noradrenaline. 3. The preparations showed spontaneously developed tension (tone) that increased with the increase in the passive force. The effect of passive force was greater in preparations from SHRSP. Contraction initiated by noradrenaline was also increased by passive force up to 30 mN, then showed a tendency to decrease. 4. Endothelium-dependent relaxation was depressed as the passive force was increased. Preparations from SHRSP showed impaired endothelium-dependent relaxation and were influenced by passive force to a lesser degree when compared with preparations from WKY rats. 5. Relaxation by sodium nitroprusside was influenced by passive force to a much lesser extent than that by acetylcholine. 6. Indomethacin potentiated endothelium-dependent relaxation and blocked the effect of passive force in both preparations. 7. The difference in relaxation and the effect of passive force is primarily caused by the difference in the release of endothelium-derived contracting factor, which is thought to be a product of the cyclo-oxygenase pathway of the arachidonic acid cascade.
authors.affiliation: Faculty of Pharmaceutical Sciences, Kinki University, Osaka, Japan.
authors.forename: F
authors.initials: F
authors.lastname: Sekiguchi
authors.forename: T
authors.initials: T
authors.lastname: Adachi
authors.forename: H
authors.initials: H
authors.lastname: Matsubara
authors.forename: K
authors.initials: K
authors.lastname: Matsuda
authors.forename: K
authors.initials: K
authors.lastname: Kita
authors.forename: K
authors.initials: K
authors.lastname: Shimamura
authors.forename: S
authors.initials: S
authors.lastname: Sunano
mesh_terms: D000109:Acetylcholine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D002561:Cerebrovascular Disorders / Q000235:genetics / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000502:physiology*; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D016859:Lipoxygenase Inhibitors / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D016859:Lipoxygenase Inhibitors; D014665:Vasodilator Agents; D009599:Nitroprusside; D000109:Acetylcholine; D009638:Norepinephrine; D007213:Indomethacin