Matsudaira T, Kogo H, Satoh T
Jpn J Pharmacol. 1985 Jan;37(1):51-7. doi: 10.1254/jjp.37.51.
A possible role of prostaglandin E2 (PGE2) in the regulation of blood pressure in spontaneously hypertensive rats (SHR) was investigated. The inhibition of PG synthesis by chronic indomethacin treatment accelerated the elevation of blood pressure with the tendency to decrease renal PGE2. We, therefore, confirmed that PGE2 in SHR may play a role in the antihypertensive mechanism. In this connection, the participation of renal PGE2 in the retardation of the development of hypertension in male SHR induced by orchiectomy was examined. Urinary PGE2 which reflects the renal PGE2 level tended to keep a higher level in the castrated group. Urinary electrolytes excretion also inclined to augment in the castrated group throughout the experiment. These results indicate that renal PGE2 may participate in the gonads-mediated blood pressure regulation system, although the mechanism of the retardation of spontaneous hypertension induced by orchiectomy remains obscure.
研究了前列腺素E2（PGE2）在自发性高血压大鼠（SHR）血压调节中的可能作用。长期用吲哚美辛治疗抑制PG合成会加速血压升高，并伴有肾PGE2降低的趋势。因此，我们证实SHR中的PGE2可能在降压机制中起作用。就此而言，研究了肾PGE2在去势诱导的雄性SHR高血压发展延缓中的作用。反映肾PGE2水平的尿PGE2在去势组中倾向于保持较高水平。在整个实验过程中，去势组的尿电解质排泄也有增加的倾向。这些结果表明，肾PGE2可能参与性腺介导的血压调节系统，尽管去势诱导的自发性高血压延缓机制仍不清楚。
