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| Content Provider | Springer Nature Link |
|---|---|
| Author | Willems, Laura Headrick, John P. |
| Copyright Year | 2006 |
| Abstract | There is mixed evidence adenosine receptors (ARs) may enhance myocardial contractility, although this remains contentious. We assessed inotropic actions of adenosine (50 μM) and selective AR activation with 100 nM N 6-cyclohexyladenosine (CHA; A1AR agonist), 25 nM 2-[p-(2-carboxyethyl) phenethylamino]-5′-N-ethylcarboxamidoadenosine (CGS-21680; A2AAR agonist) and 100 nM 2-chloro-N 6-(3-iodobenzyl)-adenosine-5′-N-methyluronamide (Cl-IB-MECA; A3AR agonist) in mouse hearts perfused at constant pressure, constant flow, or conditions of stable flow and pressure (following maximal nitroprusside-mediated dilatation at constant flow). Adenosine and CGS-21680 significantly (although modestly) increased force in constant-pressure perfused hearts (≤10 mmHg elevations in systolic pressure), effects paralleled by coronary vasodilatation (≤10 ml min−1 g−1 elevations in flow). Neither CHA nor Cl-IB-MECA altered force or flow. With constant-flow perfusion, adenosine and CGS-21680 reduced systolic pressure in parallel with perfusion pressure. When changes in coronary flow and pressure were prevented, CGS-21680 failed to alter contractility. However, adenosine still enhanced systolic pressure up to 10 mmHg. Relations between flow, perfusion pressure and ventricular force evidence substantial Gregg effects in murine myocardium: systolic force increases transiently by approximately 1 mmHg ml−1 min−1 g−1 rise in flow during the first minutes of hyperaemia and in a sustained manner (by ∼1 mmHg mmHg−1) during altered perfusion pressure. These effects contribute to inotropism with AR agonism when flow/pressure is uncontrolled. In summary, we find no evidence of direct A1 or A3AR-mediated inotropic responses in intact myocardium. Inotropic actions of A2AAR agonism appear entirely Gregg-related. Nonetheless, the endogenous agonist adenosine exerts a modest inotropic action independently of flow and perfusion pressure. The basis of this response remains to be identified. |
| Starting Page | 433 |
| Ending Page | 441 |
| Page Count | 9 |
| File Format | |
| ISSN | 00316768 |
| Journal | Pflügers Archiv |
| Volume Number | 453 |
| Issue Number | 4 |
| e-ISSN | 14322013 |
| Language | English |
| Publisher | Springer-Verlag |
| Publisher Date | 2006-10-28 |
| Publisher Place | Berlin, Heidelberg |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Adenosine Adenosine receptor Coronary flow Myocardial contractility Gregg phenomenon Mouse heart Human Physiology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Physiology Physiology (medical) Clinical Biochemistry |
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