Document Detail


ATP is the predominant sympathetic neurotransmitter in rat mesenteric arteries at high pressure.
MedLine Citation:
PMID:  17510179     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Most studies of neurovascular transmission in isolated small mesenteric arteries have used either isometric recording techniques or measured vasoconstriction in vessels with no distending pressure. Here we have used pressure myography to assess the contribution of noradrenaline and ATP to sympathetic neurotransmission in rat second-order mesenteric arteries. In arteries pressurized to 30 or 90 mmHg, activation of sympathetic axons with trains of electrical stimuli (50 pulses, 0.5-10 Hz) evoked frequency-dependent vasoconstrictions that increased in amplitude at higher pressure. In the presence of the P2-receptor antagonist suramin (0.1 mM), the amplitude of vasoconstrictions to trains at 2 and 10 Hz did not differ at 30 and 90 mmHg. In contrast, in the presence of the alpha(1)-adrenoceptor antagonist prazosin (0.1 microm) vasoconstrictions at 90 mmHg were larger than those at 30 mmHg. At both pressures, the combination of prazosin and suramin virtually abolished constrictions. The purinergic component of vasoconstriction (prazosin-resistant) was almost abolished by the L-type Ca(2+) channel antagonist nifedipine (1 microm). Increasing pressure from 30 to 90 mmHg decreased the resting membrane potential and increased the amplitude of purinergic excitatory junction potentials. These findings indicate that the contribution of ATP to neurovascular transmission increases when the pressure is raised from 30 to 90 mmHg, which is similar to the pressure second-order mesenteric arteries experience in vivo, and that Ca(2+) influx through L-type Ca(2+) channels is largely responsible for purinergic activation of the vascular smooth muscle.
Authors:
Nicole M Rummery; James A Brock; Poungrat Pakdeechote; Vera Ralevic; William R Dunn
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-05-17
Journal Detail:
Title:  The Journal of physiology     Volume:  582     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2007 Jul 
Date Detail:
Created Date:  2007-07-16     Completed Date:  2007-08-20     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  745-54     Citation Subset:  IM    
Affiliation:
School of Biomedical Sciences, University of Nottingham, Nottingham NG7 2UH, UK.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / analogs & derivatives,  pharmacology,  physiology*
Animals
Axons / physiology
Calcium Channels / physiology
Electric Stimulation
Electrophysiology
Male
Mesenteric Arteries / drug effects,  innervation,  physiology*
Myography
Neurotransmitter Agents / physiology*
Nifedipine / pharmacology
Norepinephrine / physiology
Pressure
Rats
Rats, Wistar
Vasoconstriction / physiology
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
//Wellcome Trust
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Neurotransmitter Agents; 0/Vasodilator Agents; 21829-25-4/Nifedipine; 51-41-2/Norepinephrine; 56-65-5/Adenosine Triphosphate; 7292-42-4/alpha,beta-methyleneadenosine 5'-triphosphate
Comments/Corrections

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


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