吲达帕胺对自发性高血压大鼠组织6-酮-PGF_(1α)、PGE_2、PGF_(2α)合成及对血浆 TXB_2的影响

The Influence of Indapamide on 6-keto-PGF_(1α),PGE_2,and PGF_(2α) Synthesis and Plasma TXB_2 Levels in Spontaneously Hypertensive Rats

观察自发性高血压大鼠(SHR)服用降压药吲达帕胺后,在血压下降的同时,体内前列腺素系统的变化,并与对照组及正常大鼠比较。结果表明,SHR体内缩血管前列腺素(PGE_2和PGF_2a)合成量较正常大鼠升高,这可能与SHR高血压的出现和维持密切相关。SHR服用吲达帕胺后体内PGI_2合成呈增加趋势,而PGE_2及PGF_2a合成急剧下降,表明在SHR,前列腺素系统,尤其是PGE_2及PGF_2a,在吲达帕胺的降压过程中发挥着一定作用。

The influence of indapamide on the prostaglandin system was studied in spontaneously hypertensive rats (SHR) and compared with SHR control and normal WKY rats. The results show that the synthesis of vasoconstrictive prostaglandins (PGE2 and PGF2a) in the renal medullary tissues of SHR is higher than that of normal rats, and this may have something to do with the development and maintenance of high blood pressure in SHR. After indapamide administration, the synthesis of prostacyclin in SHR aorta increased significantly as compared with the SHR control group, whereas PGE2 and PGF2a production in renal medullary tissues decreased markedly. The results support the idea that the prostaglandin system, especially PGE2 and PGF2a, plays an important role in the antihypertensive mechanism of indapamide.