Ylitalo P, Pitkäjärvi T, Metsä-Ketelä T, Vapaatalo H
Prostaglandins Med. 1978 Dec;1(6):479-88. doi: 10.1016/0161-4630(78)90118-0.
The influence of oral indomethacin treatment (75 mg daily for a week) on urinary excretion of prostaglandin (PG) F2alpha, plasma renin activity (PRA), blood pressure (BP) and electrolyte excretion (Na+ and K+) was studied in 21 patients with untreated essential hypertension (9 women and 12 men, aged from 40 to 45 years). PGF2alpha excretion and PRA were markedly suppressed by indomethacin in both sexes. A close correlation was found between the decreases in PGF2alpha excretion and PRA. 13,14dihydro-15keto-PGF2alpha (a metabolite of PGF2alpha) excretion also tended to be lowered during the indomethacin treatment. BP tended to increase but urine volume and electrolyte excretion were unchanged during the indomethacin period. The results suggest that in essential hypertension inhibition of the PG synthesis causes a concomitant suppression in PRA and may slightly increase BP.
在21例未经治疗的原发性高血压患者(9名女性和12名男性,年龄40至45岁)中,研究了口服消炎痛治疗(每日75毫克,持续一周)对前列腺素(PG)F2α尿排泄、血浆肾素活性(PRA)、血压(BP)和电解质排泄(Na +和K +)的影响。消炎痛显著抑制了两性的PGF2α排泄和PRA。PGF2α排泄和PRA的降低之间存在密切相关性。在消炎痛治疗期间,13,14-二氢-15-酮-PGF2α(PGF2α的一种代谢产物)排泄也趋于降低。消炎痛治疗期间血压趋于升高,但尿量和电解质排泄没有变化。结果表明,在原发性高血压中,PG合成的抑制会导致PRA的同时抑制,并可能使血压略有升高。