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MR Cernadas, A Lopez-Farre, A Riesco, MJ Gallego, G Espinosa, E Digiuni, L Hernando, S Casado and C Caramelo
Laboratorio de Nefrologia Fundacion Jimenez Diaz, Universidad Autonoma, Madrid, Spain.
The present study examined the mechanisms of the renal effect of the NO- donor aminoacid, L-Arg and different non-NO-donor aminoacids, namely L- Asn, L-Ala, L-Gly L-Gln administered separately. In conscious, unrestricted Wistar rats, a bolus of L-Arg produced a short-lasting decrease in mean arterial pressure. No variations in mean arterial pressure were found with either L-Gly, L-Asn, L-Ala or L-Gln. This effect of L-Arg was inhibited by NwNLA, methylene blue and atropine and not affected by meclofenamate. Simultaneously, a dose-response diuretic and natriuretic effect was observed with all the aminoacids. In further experiments with L-Arg and L-Gly, this effect was associated with increased glomerular filtration rate, renal plasma flow, fractional sodium and free water excretion and urinary cyclic guanosine monophosphate. These effects of L-Arg and L-Gly were inhibited by NwNLA. On the contrary, no inhibition by NwNLA was detected on the diuretic, natriuretic and renal hemodynamic effects of L-Gln, and the diuretic and natriuretic effects of L-Asn or L-Ala. Our results show that all the assayed aminoacids were endowed of diuretic and natriuretic capabilities. Such effects were apparently related with a NO-mediated mechanism in the case of L-Arg and L-Gly, but not in the case of L-Gln, L-Asn or L-Ala, therefore suggesting that more than one mechanism is involved in the renal effect of the different aminoacids. Simultaneously, only L-Arg produced a NO-, cyclic guanosine monophosphate-dependent hypotensive effect, which was not shared by the other assayed aminoacids.
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