SPONTANEOUS AND AGONIST-INDUCED CONTRACTIONS AND ENDOTHELIUM-DEPENDENT RELAXATION IN AORTAE FROM SHRSP AND WKY RATS UNDER VARIOUS LEVELS OFPASSIVE FORCE

Citation
F. Sekiguchi et al., SPONTANEOUS AND AGONIST-INDUCED CONTRACTIONS AND ENDOTHELIUM-DEPENDENT RELAXATION IN AORTAE FROM SHRSP AND WKY RATS UNDER VARIOUS LEVELS OFPASSIVE FORCE, Clinical and experimental pharmacology and physiology, 23(6-7), 1996, pp. 483-489
Citations number
43
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
03051870
Volume
23
Issue
6-7
Year of publication
1996
Pages
483 - 489
Database
ISI
SICI code
0305-1870(1996)23:6-7<483:SAACAE>2.0.ZU;2-7
Abstract
1. The influence of the passive force on the contraction and endotheli um-dependent relaxation in aortae of normotensive Wister Kyoto (WKY) r ats and stroke-prone spontaneously hypertensive rats (SHRSP) Here comp ared. 2. Force changes of endothelium-intact and -removed preparations were measured isometrically by a force-displacement transducer, Endot helium-dependent relaxation was observed by applying acetylcholine to the preparation precontracted in the presence of 5 x 10(-7) mol/L nora drenaline. 3. The preparations showed spontaneously developed tension (tone) that increased with the increase in the passive force. The effe ct of passive force was greater in preparations from SHRSP. Contractio n initiated by noradrenaline was also increased by passive force up to 30 mN, then showed a tendency to decrease.4. Endothelium-dependent re laxation was depressed as the passive force was increased. Preparation s from SHRSP showed impaired endothelium-dependent relaxation and were influenced by passive force to a lesser degree when compared with pre parations from WKY rats. 5. Relaxation by sodium nitroprusside was inf luenced by passive force to a much lesser extent than that by acetylch oline. 6. Indomethacin potentiated endothelium-dependent relaxation an d blocked the effect of passive force in both preparations. 7. The dif ference in relaxation and the effect of passive force is primarily cau sed by the difference in the release of endothelium-derived contractin g factor, which is thought to be a product of the cyclo-oxygenase path way of the arachidonic acid cascade.