Document Detail


Hydrogen sulfide activates Ca²⁺ sparks to induce cerebral arteriole dilatation.
MedLine Citation:
PMID:  22508960     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hydrogen sulfide (H₂S) is a gaseous vasodilator produced by endothelial cells. Mechanisms by which H₂S induces vasodilatation are unclear. We tested the hypothesis that H₂S dilates cerebral arterioles by modulating local and global intracellular Ca²⁺ signals in smooth muscle cells. High-speed confocal imaging revealed that Na₂S, an H₂S donor, increased Ca²⁺ spark frequency ∼1.43-fold and decreased global intracellular Ca²⁺ concentration ([Ca²⁺]i) by ∼37 nM in smooth muscle cells of intact piglet cerebral arterioles. In contrast, H₂S did not alter Ca²⁺ wave frequency. In voltage-clamped (-40 mV) cells, H₂S increased the frequency of iberiotoxin-sensitive, Ca²⁺ spark-induced transient Ca²⁺-activated K⁺ (KCa) currents ∼1.83-fold, but did not alter the amplitude of these events. H₂S did not alter the activity of single KCa channels recorded in the absence of Ca²⁺ sparks in arteriole smooth muscle cells. H₂S increased SR Ca²⁺ load ([Ca²⁺]SR), measured as caffeine (10 and 20mM)-induced [Ca²⁺]i transients, ∼1.5-fold. H₂S hyperpolarized (by ∼18 mV) and dilated pressurized (40 mmHg) cerebral arterioles. Iberiotoxin, a KCa channel blocker, reduced H₂S-induced hyperpolarization by ∼51%. Iberiotoxin and ryanodine, a ryanodine receptor channel inhibitor, reduced H₂S-induced vasodilatation by ∼38 and ∼37%, respectively. In summary, our data indicate that H₂S elevates [Ca²⁺]SR, leading to Ca²⁺ spark activation in cerebral arteriole smooth muscle cells. The subsequent elevation in transient KCa current frequency leads to membrane hyperpolarization, a reduction in global [Ca²⁺]i and vasodilatation.
Authors:
Guo Hua Liang; Qi Xi; Charles W Leffler; Jonathan H Jaggar
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural     Date:  2012-04-16
Journal Detail:
Title:  The Journal of physiology     Volume:  590     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-07-12     Completed Date:  2012-11-29     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  2709-20     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arterioles / drug effects,  physiology
Brain / blood supply*,  drug effects,  physiology
Calcium / physiology*
Hydrogen Sulfide / pharmacology*
Membrane Potentials / drug effects
Myocytes, Smooth Muscle / drug effects*,  physiology
Potassium Channels, Calcium-Activated / physiology
Ryanodine Receptor Calcium Release Channel / physiology
Sarcoplasmic Reticulum / physiology
Swine
Vasodilation / drug effects*
Grant Support
ID/Acronym/Agency:
HL110347/HL/NHLBI NIH HHS; HL34059/HL/NHLBI NIH HHS; HL42851/HL/NHLBI NIH HHS; HL67061/HL/NHLBI NIH HHS; HL94378/HL/NHLBI NIH HHS; R01 HL042851/HL/NHLBI NIH HHS; R01 HL110347/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Potassium Channels, Calcium-Activated; 0/Ryanodine Receptor Calcium Release Channel; 7440-70-2/Calcium; 7783-06-4/Hydrogen Sulfide
Comments/Corrections
Comment In:
J Physiol. 2012 Jul 15;590(Pt 14):3213-4   [PMID:  22826300 ]

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


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