Abstract
Alterations in the β-adrenergic receptor adenylyl cyclase pathway are well known in heart failure. To determine if an alteration in this pathway occurs during the reversible phase of cardiac allograft rejection, we used a rat heterotopic heart transplant model. Lewis rats received either isografts or Lewis Brown Norway allografts. Cardiac grafts and native hearts were explanted 4, 5, or 6 days later. Receptor-mediated modulation of adenylyl cyclase activity was investigated using isoproterenol, forskolin, and the muscarinic and adenosine receptor agonists carbachol and R-N6-(C2-phenyl-isopropyl)-adenosine (R-PIA), respectively. Allografts demonstrated evidence of histological rejection and a significantly impaired response to forskolin and isoproterenol on all days: {A table is presented} (% increase in cAMP in response to forskolin or isoproterenol ± standard error. All results P < 0.03 except Day 4 forskolin and Day 5 isoproterenol.) No significant difference was noted between isografts and allografts stimulated with carbachol and R-PIA. These data suggest that a primary alteration in adenylyl cyclase activity may be a component of the molecular basis of reversible contractile dysfunction in cardiac allograft rejection.
Original language | English (US) |
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Pages (from-to) | 472-475 |
Number of pages | 4 |
Journal | Journal of Surgical Research |
Volume | 52 |
Issue number | 5 |
DOIs | |
State | Published - May 1992 |
Externally published | Yes |
ASJC Scopus subject areas
- Surgery