ISSN:
1440-1681
Quelle:
Blackwell Publishing Journal Backfiles 1879-2005
Thema:
Medizin
Notizen:
1. Experiments were designed to determine the effects of low concentrations (5–500 nmol/L) of naftidrofuryl, a 5-hydroxytryptamine (5-HT) antagonist, on renal functions and prostanoid synthesis responses to noradrenaline (NA) and 5-HT. Isolated kidneys of 8 week old male spontaneously hypertensive rats were perfused at a constant flow rate in a single-pass system.2. In baseline conditions, naftidrofuryl did not modify the renal vascular resistance and the glomerular filtration rate (GFR), although it elicited a significant but not dose-dependent increase in the venous excretion of 6-keto-prostaglandin (PG) F1α and thromboxane (Tx)B2, the stable end-products of PGI2 and TxA2, respectively.3. NA increased renal vascular resistance and GFR in a dose-dependent manner and enhanced the venous excretion of 6-keto-PGF1α and TxB2. Naftidrofuryl significantly attenuated the effects of NA on renal vascular resistance, abolished those on GFR and enhanced, at the highest concentration (500 nmol/L) only, those on 6-keto-PGF1α excretion.4. 5-HT increased renal vascular resistance but not GFR. It did not change the sodium excretion and the release of 6-keto-PGF1α and TxB2. Naftidrofuryl blunted the RVR response to 5-HT without change in the prostanoid release. The inhibitory action of naftidrofuryl was not modified by indomethacin which, by itself, prevented the vasoconstrictor response to 5-HT.5. It is concluded that, in isolated perfused kidneys of SHR, naftidrofuryl inhibits the contractile response to 5-HT and NA; this effect is not dependent upon changes in synthesis of PGI2 or TxA2 and the vasoconstrictor effect of 5-HT involves the release of a cyclooxygenase metabolite that differs from TXA2.
Materialart:
Digitale Medien
URL:
http://dx.doi.org/10.1111/j.1440-1681.1993.tb01648.x
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