Document Detail

TEA inhibits ACh-induced EDRF release: endothelial Ca(2+)-dependent K+ channels contribute to vascular tone.
MedLine Citation:
PMID:  8092278     Owner:  NLM     Status:  MEDLINE    
The effects of K(+)-channel blockers on the acetylcholine (ACh)-induced relaxation of vascular smooth muscle, intracellular free Ca2+ concentration ([Ca2+]i) elevation, and ACh-evoked outward K+ current of endothelial cells of rabbit aorta were studied using bioassay, spectrofluorimetry, and patch-clamp techniques, respectively. In bioassay experiments, ACh caused relaxation of endothelium-denuded aortic rings in a concentration-dependent manner when perfused through an endothelium-intact donor segment of aorta but not when perfused directly onto the recipient aortic ring. ACh-induced relaxation was inhibited by perfusion of tetraethylammonium ions (TEA; 5 mM) through the donor but not by perfusion directly onto the recipient segment. Glibenclamide had no effect on ACh-induced relaxation of the bioassay ring in either situation. ACh increased [Ca2+]i at the endothelial surface of aortic strips but not at the adventitial surface. TEA inhibited ACh-induced [Ca2+]i elevation, whereas glibenclamide had no effect. In patch-clamp experiments with freshly isolated endothelial cells, ACh evoked a biphasic outward current which was completely abolished by TEA (3 mM). It is concluded that Ca(2+)-dependent K+ channels are important for increasing [Ca2+]i during agonist stimulation and consequently for the synthesis/release of endothelium-derived relaxing factors (EDRFs). Furthermore, endothelial ATP-sensitive K+ channels do not contribute to ACh-induced relaxation or evoke an increase in endothelial [Ca2+]i of rabbit thoracic aorta.
E Demirel; J Rusko; R E Laskey; D J Adams; C van Breemen
Related Documents :
3492648 - Stimulatory effect of acetylcholine on immunoreactive corticotropin-releasing factor re...
9732388 - Potentiation and inhibition of nicotinic acetylcholine receptors by spermine in the te6...
497898 - Interactions of methylxanthines, nonxanthine phosphodiesterase inhibitors, and calcium ...
2797218 - Regulation of acetylcholine receptor function by the phorbol ester tpa in rat skeletal ...
2065718 - Cholinergic inositol phosphate formation in striatal neurons is mediated by distinct me...
11247758 - Contributions of prostacyclin and nitric oxide to carbon monoxide-induced cerebrovascul...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  267     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1994 Sep 
Date Detail:
Created Date:  1994-10-19     Completed Date:  1994-10-19     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1135-41     Citation Subset:  IM    
Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, Florida 33101.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Acetylcholine / pharmacology*
Aorta / cytology,  drug effects,  physiology
Biological Assay
Calcium / metabolism,  physiology
Endothelium, Vascular / cytology,  metabolism*
Intracellular Membranes / metabolism
Nitric Oxide / antagonists & inhibitors*
Potassium Channel Blockers
Potassium Channels / physiology*
Tetraethylammonium Compounds / pharmacology*
Vasodilation / drug effects
Vasomotor System / physiology*
Grant Support
Reg. No./Substance:
0/Potassium Channel Blockers; 0/Potassium Channels; 0/Tetraethylammonium Compounds; 10102-43-9/Nitric Oxide; 51-84-3/Acetylcholine; 66-40-0/Tetraethylammonium; 7440-70-2/Calcium

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

Previous Document:  Leukocyte sequestration in the microvasculature in normal and low flow states.
Next Document:  Microvascular volume changes induced by exercise, heat exposure, or endotoxin injection.