Document Detail


Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine: role of BK channels.
MedLine Citation:
PMID:  20833953     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The objectives of this study were to determine the role of calcium-activated, small (SK), intermediate (IK), and large (BK) conductance potassium channels in initiating the development of an anti-inflammatory phenotype elicited by preconditioning with an exogenous hydrogen sulfide (H(2)S) donor, sodium hydrosulfide (NaHS). Intravital microscopy was used to visualize rolling and firmly adherent leukocytes in vessels of the small intestine of mice preconditioned with NaHS (in the absence and presence of SK, IK, and BK channel inhibitors, apamin, TRAM-34, and paxilline, respectively) or SK/IK (NS-309) or BK channel activators (NS-1619) 24 h before ischemia-reperfusion (I/R). I/R induced marked increases in leukocyte rolling and adhesion, effects that were largely abolished by preconditioning with NaHS, NS-309, or NS-1619. The postischemic anti-inflammatory effects of NaHS-induced preconditioning were mitigated by BKB channel inhibitor treatment coincident with NaHS, but not by apamin or TRAM-34, 24 h before I/R. Confocal imaging and immunohistochemistry were used to demonstrate the presence of BKα subunit staining in both endothelial and vascular smooth muscle cells of isolated, pressurized mesenteric venules. Using patch-clamp techniques, we found that BK channels in cultured endothelial cells were activated after exposure to NaHS. Bath application of the same concentration of NaHS used in preconditioning protocols led to a rapid increase in a whole cell K(+) current; specifically, the component of K(+) current blocked by the selective BK channel antagonist iberiotoxin. The activation of BK current by NaHS could also be demonstrated in single channel recording mode where it was independent of a change in intracellular Ca(+) concentration. Our data are consistent with the concept that H(2)S induces the development of an anti-adhesive state in I/R in part mediated by a BK channel-dependent mechanism.
Authors:
Mozow Y Zuidema; Yan Yang; Meifang Wang; Theodore Kalogeris; Yajun Liu; Cynthia J Meininger; Michael A Hill; Michael J Davis; Ronald J Korthuis
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-09-10
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-01     Completed Date:  2010-11-29     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1554-67     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Apamin / pharmacology
Cells, Cultured
Electrophysiological Phenomena
Endothelium, Vascular / cytology,  drug effects,  physiopathology
Humans
Hydrogen Sulfide / pharmacology,  therapeutic use*
Inflammation / physiopathology,  prevention & control*
Intestine, Small / blood supply*
Ischemia / complications*,  physiopathology
Ischemic Preconditioning*
Large-Conductance Calcium-Activated Potassium Channels / drug effects,  physiology*
Male
Mice
Mice, Inbred C57BL
Models, Animal
Peptides / pharmacology
Phenotype*
Pyrazoles / pharmacology
Grant Support
ID/Acronym/Agency:
AA-014945/AA/NIAAA NIH HHS; HL-071796/HL/NHLBI NIH HHS; HL-082816/HL/NHLBI NIH HHS; HL-092241/HL/NHLBI NIH HHS; R01 HL092241/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Large-Conductance Calcium-Activated Potassium Channels; 0/Peptides; 0/Pyrazoles; 0/TRAM 34; 129203-60-7/iberiotoxin; 24345-16-2/Apamin; YY9FVM7NSN/Hydrogen Sulfide
Comments/Corrections

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