6533b7d0fe1ef96bd1259f97
RESEARCH PRODUCT
Experimental diabetes induces hyperreactivity of rabbit renal artery to 5-hydroxytryptamine
Francisco Javier Miranda AlonsoJosé Antonio Alabadí FerrerSilvia LlorénsRosa F. Ruiz De ApodacaJosé M. Centeno GuilEnrique Alborch Domínguezsubject
DiabetisArtèriesEndoteli vascularÒxid nítricdescription
The influence of diabetes on the response of isolated rabbit renal arteries to 5-hydroxytryptamine (5-HT) was examined. 5-HT induced a concentration-related contraction that was higher in arteries from diabetic rabbits than in arteries from control rabbits. Endothelium removal did not significantly modify 5-HT contractions in arteries from control rabbits but enhanced the response to 5-HT in arteries from diabetic rabbits. Incubation with NG-nitro-L-arginine (L-NA) enhanced contractions to 5-HT in arteries from control and diabetic rabbits. In arteries with endothelium, this L-NA enhancement was lower in diabetic rabbits than in control rabbits. In arteries without endothelium, incubation with L-NA enhanced the maximal contractions to 5-HT in control rabbits but did not in diabetic rabbits. Indomethacin inhibited 5-HT-induced contraction of arteries from control rabbits and enhanced the maximal contraction to 5-HT of arteries from diabetic rabbits. In summary, diabetes enhances contractile response of rabbit renal artery to 5-HT. In control animals, this response is regulated by both endothelial and non-endothelial (neuronal) nitric oxide (NO) and by a vasoconstrictor prostanoid. Diabetes impairs the release of non-endothelial NO and the vasoconstrictor prostanoid
year | journal | country | edition | language |
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2002-01-01 |