Effects of Captopril on the Urinary Excretion of Prostanoids and Kallikrein in Spontaneously Hypertensive Rats
| Autor: | Säynävälammi P |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Male
medicine.medical_specialty Captopril Prostacyclin Toxicology Excretion chemistry.chemical_compound Spontaneously hypertensive rat Rats Inbred SHR Internal medicine Renin medicine Animals cardiovascular diseases Pharmacology Dose-Response Relationship Drug biology Chemistry Prostanoid Angiotensin-converting enzyme Kallikrein Kinin Rats Thromboxane B2 Endocrinology Hypertension Prostaglandins cardiovascular system biology.protein Kallikreins lipids (amino acids peptides and proteins) circulatory and respiratory physiology medicine.drug |
| Zdroj: | Acta Pharmacologica et Toxicologica. 59:285-290 |
| ISSN: | 0001-6683 |
| DOI: | 10.1111/j.1600-0773.1986.tb00170.x |
| Popis: | The possible roles of vasodilatory prostanoids and the kallikrein-kinin system in the antihypertensive 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 PGF2 alpha and TxB2 tended to be enhanced. A clear increase, significant with all doses of captopril, occurred in the urinary excretion of 6-keto-PGF1 alpha. Kallikrein excretion in urine was suppressed by the two larger doses of captopril. The markedly augmented urinary excretion of 6-keto-PGF1 alpha, 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. |
| Databáze: | OpenAIRE |
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