PMID- 9415272
OWN - NLM
STAT- MEDLINE
DCOM- 19980213
LR  - 20190512
IS  - 0008-6363 (Print)
IS  - 0008-6363 (Linking)
VI  - 36
IP  - 1
DP  - 1997 Oct
TI  - Evidence for a role for both the adenosine A1 and A3 receptors in protection of 
      isolated human atrial muscle against simulated ischaemia.
PG  - 52-9
AB  - OBJECTIVE: Adenosine receptor activation has been implicated in the mechanism of 
      ischaemic preconditioning protection. Evidence suggests adenosine A1 receptor 
      involvement, and possibly A3 receptor involvement in the rabbit. This study 
      investigated the roles of these receptors in human preconditioning. Human A1- and 
      A3-selective compounds were chosen based on Ki values for inhibition of 
      N6-(4-amino-3-[125I]iodobenzyl)adenosine (125I-ABA) binding to stably expressed 
      recombinant human A1 and A3 receptors. Cyclopentyladenosine (CPA), a 194-fold 
      selective A1 agonist, and iodobenzylmethylcarboxamidoadenosine (IBMECA), a 
      10-fold selective A3 agonist were used alone and in combination with 
      dipropylcyclopentylxanthine (DPCPX) a 62-fold selective A1 antagonist. METHODS: 
      Human atrial trabeculae were superfused with oxygenated Tyrode's solution. After 
      stabilisation, muscles underwent one of 8 protocols (n = 6 per group), followed 
      by 90 min of simulated ischaemia and 120 min of reoxygenation. The experimental 
      endpoint was recovery of contractile function, presented as percentage baseline 
      function. RESULTS: 5 nM CPA (52.2 +/- 3.1%), 30 nM IBMECA (49.7 +/- 3.8%) and 
      preconditioning (55.3 +/- 2.5%) produced similar functional recoveries at 120 min 
      of reoxygenation; significantly different to controls (27.7 +/- 1.0%; P < 0.05, 
      ANOVA). When DPCPX (200 nM) was added prior to 5 nM CPA, protection was lost 
      (31.8 +/- 0.9%), but when added prior to 30 nM IBMECA, muscles continued to be 
      significantly protected (41.5 +/- 2.3%). CONCLUSIONS: In human atrium both A1 and 
      A3 receptor stimulation appears to mimic ischaemic preconditioning. This may 
      represent the first evidence for A3 receptor involvement in 'pharmacological' 
      preconditioning of human myocardium.
FAU - Carr, C S
AU  - Carr CS
AD  - Hatter Institute, Department of Academic and Clinical Cardiology, University 
      College London Hospitals, UK.
FAU - Hill, R J
AU  - Hill RJ
FAU - Masamune, H
AU  - Masamune H
FAU - Kennedy, S P
AU  - Kennedy SP
FAU - Knight, D R
AU  - Knight DR
FAU - Tracey, W R
AU  - Tracey WR
FAU - Yellon, D M
AU  - Yellon DM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Cardiovasc Res
JT  - Cardiovascular research
JID - 0077427
RN  - 0 (Dinucleoside Phosphates)
RN  - 0 (Purinergic P1 Receptor Agonists)
RN  - 0 (Purinergic P1 Receptor Antagonists)
RN  - 0 (Receptor, Adenosine A3)
RN  - 0 (Receptors, Purinergic P1)
RN  - 0 (Xanthines)
RN  - 152918-18-8 (N(6)-(3-iodobenzyl)-5'-N-methylcarboxamidoadenosine)
RN  - 2382-66-3 (cytidylyl adenosine)
RN  - 9PTP4FOI9E (1,3-dipropyl-8-cyclopentylxanthine)
RN  - K72T3FS567 (Adenosine)
SB  - IM
MH  - Adenosine/analogs & derivatives/pharmacology
MH  - Dinucleoside Phosphates/pharmacology
MH  - Heart Atria/drug effects/*metabolism
MH  - Humans
MH  - In Vitro Techniques
MH  - Ischemic Preconditioning, Myocardial
MH  - Models, Biological
MH  - Myocardial Contraction/drug effects
MH  - Myocardial Ischemia/metabolism/*prevention & control
MH  - Myocardial Reperfusion
MH  - Purinergic P1 Receptor Agonists
MH  - Purinergic P1 Receptor Antagonists
MH  - Receptor, Adenosine A3
MH  - Receptors, Purinergic P1/*physiology
MH  - Xanthines/pharmacology
EDAT- 1998/02/12 00:00
MHDA- 1998/02/12 00:01
CRDT- 1998/02/12 00:00
PHST- 1998/02/12 00:00 [pubmed]
PHST- 1998/02/12 00:01 [medline]
PHST- 1998/02/12 00:00 [entrez]
AID - S0008636397001600 [pii]
AID - 10.1016/s0008-6363(97)00160-0 [doi]
PST - ppublish
SO  - Cardiovasc Res. 1997 Oct;36(1):52-9. doi: 10.1016/s0008-6363(97)00160-0.