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- W2019075360 abstract "Abstract: The possible roles of vasodilatory prostanoids and the kallikrein-kinin system in the antihyperten-sive action of the angiotensin-converting enzyme (kininase II) inhibitor captopril were examined in spontaneously hypertensive rats. Captopril (20, 50 or 100 mg/kg daily orally) reduced blood pressure markedly and dose-dependently. It also increased water consumption and urine excretion, measured on the 5th day of treatment. The 24-hr urinary excretion of PGE2 was not changed, whereas that of PGF2α and TxB2 tended to be enhanced. A clear increase, significant with all doses of captopril, occurred in the urinary excretion of 6-keto-PGF1α. Kallikrein excretion in urine was suppressed by the two larger doses of captopril. The markedly augmented urinary excretion of 6-keto-PGF1α, the stable metabolite of vasodilatory prostacyclin (PGI2), suggests that increased prostacyclin production may participate in the antihypertensive mechanism of captopril. Vasodilatory kinins can also contribute, since the captopril-induced decrease in kallikrein may reflect accumulation of kinins due to their reduced metabolism." @default.
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- W2019075360 date "2009-03-13" @default.
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- W2019075360 title "Effects of Captopril on the Urinary Excretion of Prostanoids and Kallikrein in Spontaneously Hypertensive Rats" @default.
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- W2019075360 doi "https://doi.org/10.1111/j.1600-0773.1986.tb00170.x" @default.
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