Enhanced adenosine A2B mediated coronary response in reserpinised rat heart.

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Title Enhanced adenosine A2B mediated coronary response in reserpinised rat heart.
Author Rose'Meyer, Roselyn; Harrison, Glenn; Headrick, John Patrick
Journal Name Naunyn-Schmiedeberg's Archives of Pharmacology
Editor M C Michel
Year Published 2003
Place of publication Germany
Publisher Springer-Verlag
Abstract In this study, we investigated the effect of noradrenaline depletion on contractile recovery in rat isolated heart following myocardial ischaemia. Groups tested included control tissues and hearts from reserpinised rats. Reserpine 1 mg/kg s.c. was injected into rats 18 to 24 h prior to experiments. Hearts underwent 15 min global normothermic ischaemia followed by 30 min reperfusion. Functional data (end diastolic pressure (EDP), heart rate (HR), left ventricular developed pressure (LVDP), dP/dtmax, dP/dtmin) showed that contractile function following ischaemia-reperfusion is unaffected by reserpinisation. However, pre- and post-ischaemic coronary flow rates (CFR) were increased by 16 to 38% in hearts from reserpinised rats versus control hearts. Pre-ischaemic CFRs in control hearts (11.17-0.67 ml/inm1.g tissuem1, n=9) were significantly lower then CFRs derived from reserpinised rat hearts (14.57-0.72 ml/minm1/g tissuem1, n=10). Post-ischaemic reactive hyperaemia was evident in all groups. CFRs in reserpinised hearts remained elevated when compared to pre-ischaemic values through reperfusion (P<0.05). Reserpine treatment did not significantly alter pre- or post-ischaemic adenosine efflux. The A2B adenosine receptor antagonist alloxazine (10 wM) attenuated pre- and post-ischaemic CFRs in both control and reserpinised hearts (P<0.05) without altering the hyperaemic response while the A2A adenosine receptor antagonist 8-(3-chlorostyryl) caffeine (1 wM) did not alter CFRs in both groups. The A3 adenosine receptor antagonist MRS1191 (0.1 wM) increased CFR in control and reserpinised hearts (P<0.05). Catecholamine depletion with reserpinisation enhances the responsiveness of the coronary resistance vessels to endogenous adenosine through activation of the A2B adenosine receptor.
Peer Reviewed Yes
Published Yes
Alternative URI http://dx.doi.org/10.1007/s00210-002-0678-z
Volume 367
Page from 266
Page to 273
ISSN 0028-1298
Date Accessioned 2004-03-19
Date Available 2010-07-30T07:19:03Z
Language en_AU
Research Centre Griffith Health Institute; Heart Foundation Research Centre
Faculty Griffith Health Faculty
Subject PRE2009-Cardiology (incl. Cardiovascular Diseases)
URI http://hdl.handle.net/10072/6191
Publication Type Journal Articles (Refereed Article)
Publication Type Code c1

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