自发性高血压大鼠主动脉对前列腺素H_2反应的增加先于前列腺素H合酶1表达的变化(英文)

Increased response to prostaglandin H_2 precedes changes in PGH synthase-1 expression in the SHR aorta

AIM: To determine the expression of PGH synthase-1and the sensitivity of vascular smooth muscle to PGH_2in the aorta from the SHR at an age when noendothelium-dependent contractions to acetylcholine areobserved under control conditions. METHODS: Allexperiments were performed in parallel on aortas from20-wk-old SHR and Wistar-Kyoto normotensive rats(WKY). Rings, with or without endothelium, weresuspended in conventional organ chambers for therecording of changes in isometric force. Theexpression of PGH Synthase-1 was evaluated by

AIM: To determine the expression of PGH synthase-1 and the sensitivity of vascular smooth muscle to PGH2 in the aorta from the SHR at an age when no endothelium-dependent contractions to acetylcholine are observed under control conditions. METHODS: All experiments were performed in parallel on aortas from 20-wk-old SHR and Wistar-Kyoto normotensive rats (WKY). Rings, with or without endothelium, were suspended in conventional organ chambers for the recording of changes in isometric force. The expression of PGH synthase-1 was evaluated by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. RESULTS: Under control conditions acetylcholine did not cause contractions of rings with or without endothelium. However, in the presence of nitro-L-arginine (NLA, an inhibitor of nitric-oxide synthase ), it evoked endothelium-dependent contraction in the SHR but not in the WKY aortas. The expression of PGH synthase-1 was comparable in the aortas of both strains (with and without endothelium). PGH2 caused greater contractions in rings without endothelium from the SHR than those from WKY, while U46,619 evoked a comparableresponse, in aortas from both strains. CONCLUSION: In the aorta of 20-wk-old SHR, endothelium-dependent contractions to acetylcholine are observed only when the production of nitric oxide is prevented. They are associated with an augmented sensitivity of the smooth muscle to PGH2, but not with an increased expression of PGH synthase-1.