Osanai T, Matsumura H, Kikuchi T, Minami O, Yokono Y, Akiba R, Eidou H, Konta A, Kanazawa T, Onodera K
Second Department of Internal Medicine, Hirosaki University School of Medicine, Japan.
Jpn Circ J. 1990 May;54(5):507-14. doi: 10.1253/jcj.54.507.
The purpose of this study was to clarify how the metabolism of vascular prostacyclin (PGI2) and thromboxane (TX) A2 in spontaneously hypertensive rats (SHR) is involved in aging and development of hypertension. We removed the aortic walls from 5-week-old and 20 to 25-week-old SHR and age-matched Wistar Kyoto rats (WKY). At 5 weeks of age, there was no significant difference in basal and maximal (arachidonic acid 0.1 mM) 6-keto-PGF1 alpha production between SHR and WKY, but the TXB2 generation in the SHR aortic wall was markedly enhanced as compared with that in WKY. At 20 to 25 weeks of age, the SHR aortic wall synthesized about 1.5 times more 6-keto-PGF1 alpha in the basal condition and twice as much as in the maximal condition as did the WKY wall. However there was no significant difference in TXB2 production between SHR and WKY. Age-dependent increase of vascular 6-keto-PGF1 alpha was greater in SHR than in WKY. Moreover, the maximal/basal 6-keto-PGF1 alpha production ratio increased with age in SHR, but not in WKY. The synthesis of vascular TXB2 was enhanced with age in WKY, but did not change with age in SHR. These data suggest that not only the enhanced basal generation of vascular 6-keto PGF1 alpha but also a much greater reservoir of 6-keto-PGF 1 alpha synthesis in SHR was induced by both hypertension and maturity. The increased production of vascular TXB2 in young SHR may affect the development of hypertension.
本研究的目的是阐明自发性高血压大鼠(SHR)中血管前列环素(PGI2)和血栓素(TX)A2的代谢如何参与衰老和高血压的发展。我们从5周龄以及20至25周龄的SHR和年龄匹配的Wistar Kyoto大鼠(WKY)身上取下主动脉壁。在5周龄时,SHR和WKY之间基础和最大(花生四烯酸0.1 mM)6-酮-PGF1α生成量无显著差异,但SHR主动脉壁中TXB2的生成与WKY相比明显增强。在20至25周龄时,SHR主动脉壁在基础状态下合成的6-酮-PGF1α约为WKY壁的1.5倍,在最大状态下则是WKY壁的两倍。然而,SHR和WKY之间TXB2生成量无显著差异。SHR中血管6-酮-PGF1α随年龄的增加比WKY更大。此外,SHR中最大/基础6-酮-PGF1α生成比率随年龄增加,而WKY则不然。WKY中血管TXB2的合成随年龄增强,而SHR中则不随年龄变化。这些数据表明,高血压和成熟不仅诱导了SHR中血管6-酮-PGF1α基础生成的增强,还诱导了6-酮-PGF1α合成的更大储备。年轻SHR中血管TXB2生成的增加可能影响高血压的发展。