Document Detail


Adenosine receptor regulation of coronary blood flow in Ossabaw miniature swine.
MedLine Citation:
PMID:  20855445     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Adenosine clearly regulates coronary blood flow (CBF); however, contributions of specific adenosine receptor (AR) subtypes (A(1), A(2A), A(2B), A(3)) to CBF in swine have not been determined. ARs generally decrease (A(1), A(3)) or increase (A(2A), A(2B)) cyclic adenosine monophosphate, a major mediator of vasodilation. We hypothesized that A(1) antagonism potentiates coronary vasodilation and coronary stent deployment in dyslipidemic Ossabaw swine elicits impaired vasodilation to adenosine that is associated with increased A(1)/A(2A) expression. The left main coronary artery was accessed with a guiding catheter allowing intracoronary infusions. After placement of a flow wire into the left circumflex coronary artery the responses to bolus infusions of adenosine were obtained. Steady-state infusion of AR-specific agents was achieved by using a small catheter fed over the flow wire in control pigs. CBF was increased by the A(2)-nonselective agonist 2-phenylaminoadenosine (CV1808) in a dose-dependent manner. Baseline CBF was increased by the highly A(1)-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), but not changed by other AR-specific agents. The nonselective A(2) antagonist 3,7-dimethyl-1-propargylxanthine and A(2A)-selective antagonist 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM241385) abolished adenosine-induced CBF, whereas A(2B) and A(3) antagonism had no effect. Dyslipidemia and stenting decreased adenosine-induced CBF ∼70%, whereas A(1), A(2A), and A(2B) mRNA were up-regulated in dyslipidemic versus control >5-fold and there was no change in the ratio of A(1)/A(2A) protein in microvessels distal to the stent. In control Ossabaw swine A(1) antagonism by DPCPX positively regulated basal CBF. Impaired adenosine-induced CBF after stenting in dyslipidemia is most likely caused by the altered balance between A(1) and A(2A) signaling, not receptor expression.
Authors:
Xin Long; Eric A Mokelke; Zachary P Neeb; Mouhamad Alloosh; Jason M Edwards; Michael Sturek
Related Documents :
474775 - Early changes in collateral blood flow during myocardial infarction in conscious dogs.
6830405 - Regional cerebral blood flow in schizophrenics. tests using the xenon xe 133 inhalation...
125025 - Regional cerebral blood flow in patients with chronic subdural hematomas.
9627735 - Bilateral mydriasis during laparoscopic surgery.
12672905 - Bcg promotes cord blood monocyte-derived dendritic cell maturation with nuclear rel-b u...
10598615 - Local coupling of cerebral blood flow to cerebral glucose metabolism during inhalationa...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-09-20
Journal Detail:
Title:  The Journal of pharmacology and experimental therapeutics     Volume:  335     ISSN:  1521-0103     ISO Abbreviation:  J. Pharmacol. Exp. Ther.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-18     Completed Date:  2011-02-03     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  0376362     Medline TA:  J Pharmacol Exp Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  781-7     Citation Subset:  IM    
Affiliation:
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana 46202-5120, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adenosine / pharmacology
Adenosine A2 Receptor Agonists / administration & dosage,  pharmacology
Adenosine A2 Receptor Antagonists / administration & dosage,  pharmacology
Animals
Cholesterol / blood
Coronary Circulation / drug effects,  physiology*
Dietary Fats / pharmacology
Gene Expression / genetics
Hemodynamics / physiology
Hyperlipidemias / blood,  chemically induced,  metabolism,  physiopathology
Lipoproteins / blood
Male
Microvessels / metabolism
Receptor, Adenosine A1 / physiology
Receptor, Adenosine A2A / physiology
Receptor, Adenosine A2B / physiology
Receptor, Adenosine A3 / physiology
Receptors, Purinergic P1 / physiology*
Stents / adverse effects
Swine
Swine, Miniature / physiology*
Triglycerides / blood
Up-Regulation / genetics
Grant Support
ID/Acronym/Agency:
HL062552/HL/NHLBI NIH HHS; RR013223/RR/NCRR NIH HHS; UL1-RR025761/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Adenosine A2 Receptor Agonists; 0/Adenosine A2 Receptor Antagonists; 0/Dietary Fats; 0/Lipoproteins; 0/Receptor, Adenosine A1; 0/Receptor, Adenosine A2A; 0/Receptor, Adenosine A2B; 0/Receptor, Adenosine A3; 0/Receptors, Purinergic P1; 0/Triglycerides; 57-88-5/Cholesterol; 58-61-7/Adenosine

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


Previous Document:  Dopamine transporter-dependent and -independent striatal binding of the benztropine analog JHW 007, ...
Next Document:  Induction of insulin-producing cells derived from endometrial mesenchymal stem-like cells.