Document Detail


Sympathetic nerve stimulation induces local endothelial Ca2+ signals to oppose vasoconstriction of mouse mesenteric arteries.
MedLine Citation:
PMID:  22140050     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It is generally accepted that the endothelium regulates vascular tone independent of the activity of the sympathetic nervous system. Here, we tested the hypothesis that the activation of sympathetic nerves engages the endothelium to oppose vasoconstriction. Local inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) signals ("pulsars") in or near endothelial projections to vascular smooth muscle (VSM) were measured in an en face mouse mesenteric artery preparation. Electrical field stimulation of sympathetic nerves induced an increase in endothelial cell (EC) Ca(2+) pulsars, recruiting new pulsar sites without affecting activity at existing sites. This increase in Ca(2+) pulsars was blocked by bath application of the α-adrenergic receptor antagonist prazosin or by TTX but was unaffected by directly picospritzing the α-adrenergic receptor agonist phenylephrine onto the vascular endothelium, indicating that nerve-derived norepinephrine acted through α-adrenergic receptors on smooth muscle cells. Moreover, EC Ca(2+) signaling was not blocked by inhibitors of purinergic receptors, ryanodine receptors, or voltage-dependent Ca(2+) channels, suggesting a role for IP(3), rather than Ca(2+), in VSM-to-endothelium communication. Block of intermediate-conductance Ca(2+)-sensitive K(+) channels, which have been shown to colocalize with IP(3) receptors in endothelial projections to VSM, enhanced nerve-evoked constriction. Collectively, our results support the concept of a transcellular negative feedback module whereby sympathetic nerve stimulation elevates EC Ca(2+) signals to oppose vasoconstriction.
Authors:
Lydia W M Nausch; Adrian D Bonev; Thomas J Heppner; Yvonne Tallini; Michael I Kotlikoff; Mark T Nelson
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-12-02
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  302     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-02-01     Completed Date:  2012-03-20     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H594-602     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of Vermont College of Medicine, Burlington, VT05405, USA. Mark.Nelson@uvm.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / metabolism
Calcium Signaling / physiology*
Connexins / genetics
Endothelium, Vascular / metabolism
Feedback, Physiological / physiology
Inositol 1,4,5-Trisphosphate Receptors / metabolism
Intermediate-Conductance Calcium-Activated Potassium Channels / metabolism
Mesenteric Arteries / innervation*,  physiology*
Mice
Mice, Inbred C57BL
Mice, Transgenic
Muscle, Smooth, Vascular / metabolism
Receptors, Adrenergic, alpha / metabolism
Sympathetic Nervous System / physiology*
Vasoconstriction / physiology*
Grant Support
ID/Acronym/Agency:
P01-HL-095488-01/HL/NHLBI NIH HHS; R01-HL-44455/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Connexins; 0/Inositol 1,4,5-Trisphosphate Receptors; 0/Intermediate-Conductance Calcium-Activated Potassium Channels; 0/Itpr1 protein, mouse; 0/Receptors, Adrenergic, alpha; 0/connexin 40; 7440-70-2/Calcium
Comments/Corrections

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