Renal effects of aprotinin after 24 hours of unilateral ureteral obstruction
| Autor: | W. J. Newman, W. E. Yarger, Paul E. Klotman |
|---|---|
| Rok vydání: | 1987 |
| Předmět: |
Male
medicine.medical_specialty Captopril Physiology Renal function Vasodilation Kidney urologic and male genital diseases Thromboxane A2 chemistry.chemical_compound Aprotinin Internal medicine Animals Medicine Dose-Response Relationship Drug urogenital system business.industry Angiotensin II Rats Inbred Strains Rats Endocrinology chemistry Regional Blood Flow Renal blood flow cardiovascular system medicine.symptom business hormones hormone substitutes and hormone antagonists Vasoconstriction Glomerular Filtration Rate Ureteral Obstruction circulatory and respiratory physiology medicine.drug |
| Zdroj: | American Journal of Physiology-Renal Physiology. 253:F1006-F1014 |
| ISSN: | 1522-1466 1931-857X |
| DOI: | 10.1152/ajprenal.1987.253.5.f1006 |
| Popis: | We have previously demonstrated that, after the release of 24-h unilateral ureteral obstruction (UUO), glomerular filtration rate (GFR), and renal blood flow (RBF) are reduced because of increased production of the potent vasoconstrictors thromboxane A2 (TxA2) and angiotensin II (ANG II). Captopril, which blocks ANG II production, increases GFR and RBF. Sequential administration of aprotinin, a kallikrein inhibitor, has an additive effect to further decrease renal vasoconstriction, even though kinins are generally thought to be vasodilators. Therefore, we assessed mechanisms by which aprotinin might improve renal function of previously obstructed anesthetized rats. When given alone to UUO rats, aprotinin improved renal hemodynamics. Since kinins stimulate TxA2 production by UUO kidneys perfused in vitro, our data suggest that aprotinin improved postobstructive function by decreasing kinin-stimulated TxA2 production, although this may not be its only effect. Aprotinin also improved postobstructive function, even if TxA2 formation was blocked with indomethacin. But when both ANG II and TxA2 formation were blocked by the simultaneous administration of captopril and indomethacin, aprotinin had no effect. This suggests that aprotinin may also affect ANG II formation. These pharmacological effects of aprotinin suggest that the kallikrein-kinin system may also contribute to postobstructive renal vasoconstriction by stimulating the production of both vasoconstrictor eicosanoids and ANG II. |
| Databáze: | OpenAIRE |
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