Document Detail

Calcium-activated potassium channels in native endothelial cells from rabbit aorta: conductance, Ca2+ sensitivity and block.
MedLine Citation:
PMID:  1484364     Owner:  NLM     Status:  MEDLINE    
1. Isolated native endothelial cells, obtained by treatment of rabbit aortic endothelium with papain and dithiothreitol, were voltage clamped, and single channel (unitary) and spontaneous transient outward currents (STOCs) were recorded from both whole cells and excised membrane patches. 2. In inside-out patches, the reversal potential of unitary currents was dependent on the extracellular K+ concentration and had a single-channel slope conductance of 220 pS in symmetrical 140 mM-K+ solutions. The open-state probability (Po) of the unitary K+ currents was sensitive to the intracellular Ca2+ concentration with half-maximal activation at approximately 1 microM at +20 mV. The ionic selectivity and Ca2+ sensitivity indicate that a large conductance, Ca(2+)-activated K+ channel is present in freshly dissociated rabbit aortic endothelial cells. 3. The frequency and amplitude of whole-cell unitary currents and amplitude of spontaneous transient outward currents were voltage-dependent. Whole-cell outward K+ currents evoked by depolarizing voltage ramps had amplitudes often corresponding to the simultaneous opening of more than five single Ca(2+)-activated K+ channels. Lowering the intracellular EGTA concentration tenfold, and hence the Ca2+ buffering capacity of the cell, increased unitary K+ current activity and shifted the relationship between Po and membrane potential by approximately -20 mV. 4. Bradykinin (1 microM), adenosine 5'-triphosphate (3 microM) and acetylcholine (3 microM) applied extracellularly evoked a biphasic increase in N Po (where N is number of channels activated) of the Ca(2+)-activated K+ channel studied in the whole-cell recording configuration. The development of a biphasic response to agonist stimulation requires a source of extracellular Ca2+. The sustained increase in N Po of the Ca(2+)-activated K+ channel was attenuated upon the removal of external Ca2+ (Mg2+ replacement) or in the presence of the Ca2+ entry blocker, Ni2+, and the potassium channel blockers tetrabutylammonium (TBA) or tetraethylammonium (TEA). 5. Unitary and spontaneous transient outward currents were inhibited by extracellularly applied TEA (0.5 mM), TBA (0.5-5 mM) and charybdotoxin (100 nM). Ca(2+)-activated K+ currents were blocked completely by 5 mM-TEA, whereas 3,4-diaminopyridine (1 mM), Ba2+ (10 mM) and apamin (0.1-1 microM) did not abolish these K+ currents. 6. The K+ channel opener cromakalim (10 microM) evoked a sustained increase in N Po of the Ca(2+)-activated K+ channels which was not potentiated by the addition of bradykinin. Glibenclamide (10 microM) alone increased N Po and partially inhibited the cromakalim-induced increase in N Po with respect to control.(ABSTRACT TRUNCATED AT 400 WORDS)
J Rusko; F Tanzi; C van Breemen; D J Adams
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of physiology     Volume:  455     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  1992 Sep 
Date Detail:
Created Date:  1993-02-17     Completed Date:  1993-02-17     Revised Date:  2010-09-07    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  601-21     Citation Subset:  IM    
Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, FL 33101.
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MeSH Terms
Acetylcholine / pharmacology
Adenosine Triphosphate / pharmacology
Benzopyrans / pharmacology
Bradykinin / pharmacology
Calcium / metabolism*
Egtazic Acid / pharmacology
Endothelium, Vascular / metabolism*
Glyburide / pharmacology
Membrane Potentials / drug effects,  physiology
Potassium / metabolism
Potassium Channels / drug effects,  metabolism*
Pyrroles / pharmacology
Quaternary Ammonium Compounds / pharmacology
Vasodilator Agents / pharmacology
Grant Support
Reg. No./Substance:
0/Benzopyrans; 0/Potassium Channels; 0/Pyrroles; 0/Quaternary Ammonium Compounds; 0/Vasodilator Agents; 10238-21-8/Glyburide; 10549-76-5/tetrabutylammonium; 51-84-3/Acetylcholine; 56-65-5/Adenosine Triphosphate; 58-82-2/Bradykinin; 67-42-5/Egtazic Acid; 7440-09-7/Potassium; 7440-70-2/Calcium; 94470-67-4/Cromakalim

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