Experimental diabetes induces hyperreactivity of rabbit renal artery to 5-hydroxytryptamine.

6533b832fe1ef96bd129ad39

RESEARCH PRODUCT

Experimental diabetes induces hyperreactivity of rabbit renal artery to 5-hydroxytryptamine.

Rosa F Ruiz De Apodaca José A. Alabadí Silvia Llorens Francisco J. Miranda José M. Centeno Enrique Alborch

subject

Male medicine.medical_specialty Serotonin Contraction (grammar)Endothelium Indomethacin In Vitro Techniques Nitroarginine Diabetes Mellitus Experimental chemistry.chemical_compound Nitroarginine Renal Artery Internal medicine medicine.artery Alloxan medicine Animals Renal artery Enzyme Inhibitors Pharmacology Dose-Response Relationship Drug business.industry Prostanoid Drug Synergism medicine.anatomical_structure Endocrinology chemistry Vasoconstriction Circulatory system Rabbits medicine.symptom Nitric Oxide Synthase business Vasoconstriction Blood vessel

description

Abstract 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 N G -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
2002-04-09	European journal of pharmacology

10.1016/s0014-2999(02)01438-3 https://pubmed.ncbi.nlm.nih.gov/11937101

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