Document Detail


Effect of the vascular endothelium on contractions induced by noradrenaline and phenylephrine in perforating branch of the human internal mammary artery.
MedLine Citation:
PMID:  14581717     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The effects of noradrenaline (Nor) and phenylephrine (Phe) on the isolated, non-precontracted perforating branch of the human internal mammary artery (HIMA) were investigated. Nor and Phe induced concentration-dependent contractions of intact and endothelium-denuded arterial rings with no statistically significant differences between the pEC(30) and maximal response values. The pretreatment of arterial rings with indomethacin had no effect on Nor- and Phe-induced contractions of both, intact and endothelium-denuded preparations. The pre-addition of L-NMMA did not affect contractions of perforating branch of the HIMA evoked by Nor, but provoked significant potentiation of Phe-induced contractions of perforating branch of the HIMA both intact and denuded of endothelium only at Phe concentration higher than 3 x 10(-6)M. The effects of selective alpha1-adrenoceptor antagonist, prazosin and selective alpha2-adrenoceptor antagonist, rauwolscine were concentration-dependent, and they induced a significant shift to the right (for both studied antagonists) of the concentration-response curves for Nor in both preparations with or without endothelium. The effects of prazosin and rauwolscine on the concentration-response curves for Phe were similar. In conclusion, this study has shown that Nor and Phe induce concentration-dependent contractions of the perforating branch of the HIMA. Removal of the endothelium did not modify this effect. Products of cyclooxygenase pathway had no influence on Nor and Phe action. Endothelium derived nitric oxide (NO) had no modulatory effect of Nor-induced contractions, but inhibition of NO synthesis provoked potentiation of Phe-induced contractions either in intact or endothelium-denuded preparations. The mechanism of this effect remains still unclear. On the basis of differential affinity of the antagonists and affinities of Nor and Phe themselves, we suggest that alpha1-adrenoceptor subtype is probably involved in the Nor- and Phe-induced contraction of the perforating branch of the HIMA both intact or denuded of endothelium.
Authors:
Srdan Pesić; Leposava Grbović; Aleksandar Jovanović; Miroslav Radenković; Dragica Stojić
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article    
Journal Detail:
Title:  Polish journal of pharmacology     Volume:  55     ISSN:  1230-6002     ISO Abbreviation:  Pol J Pharmacol     Publication Date:    2003 Jul-Aug
Date Detail:
Created Date:  2003-10-28     Completed Date:  2004-08-06     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9313882     Medline TA:  Pol J Pharmacol     Country:  Poland    
Other Details:
Languages:  eng     Pagination:  581-93     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Medical Faculty, 81 Braće Tasković, 18000 Nis, Yugoslavia. srdjan@medfak.ni.ac.yu
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Antagonists / pharmacology
Adult
Dose-Response Relationship, Drug
Endothelium, Vascular / physiology*
Enzyme Inhibitors / pharmacology
Female
Humans
Indomethacin / pharmacology
Mammary Arteries / drug effects*,  physiology
Middle Aged
Nitric Oxide Synthase / antagonists & inhibitors
Norepinephrine / pharmacology*
Phenylephrine / pharmacology*
Prazosin / pharmacology
Vasoconstriction / drug effects*
Vasoconstrictor Agents / pharmacology*
Yohimbine / pharmacology
omega-N-Methylarginine / pharmacology
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Antagonists; 0/Enzyme Inhibitors; 0/Vasoconstrictor Agents; 146-48-5/Yohimbine; 17035-90-4/omega-N-Methylarginine; 19216-56-9/Prazosin; 51-41-2/Norepinephrine; 53-86-1/Indomethacin; 59-42-7/Phenylephrine; EC 1.14.13.39/Nitric Oxide Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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