Abstract 16451: Centrally Administered Ghrelin Enhances Acetylcholine Release from Cardiac Vagal Nerve Endings
Introduction: It has been reported that central ghrelin acts cardioprotectively through the inhibition of sympathetic nerve activity. Although activation of cardiac vagal nerve also acts cardioprotectively, the effects of central ghrelin on cardiac vagal nerve remain unknown. We applied microdialysis technique to the heart and investigated the effects of centrally administered ghrelin on norepinephrine (NE) and acetylcholine (ACh) release from cardiac autonomic nerve endings.
Methods: Microdialysis probe was implanted in the right atrium near the sinoatrial node of anesthetized rabbits and was perfused with Ringer's solution containing a cholinesterase inhibitor, eserine. After central administration of ghrelin (1 nmol), dialysate NE and ACh concentrations were measured as indices of NE and ACh release from nerve endings using high-performance liquid chromatography.
Results: After central administration of ghrelin, heart rate gradually decreased from 270 ± 4 bpm in control, reached 234 ± 9 bpm (P < 0.01) at 70 min after administration, and gradually recovered (271 ± 8 bpm at 170 min) (Fig. A). Dialysate ACh concentration gradually increased from 5.5 ± 0.8 nM in control, reached 8.8 ± 1.2 nM (P < 0.01) at 70 min after central administration of ghrelin. From 110 min after administration, dialysate ACh concentration gradually decreased and reached 5.6 ± 0.8 nM at 170 min (Fig. B). Central ghrelin did not change mean arterial pressure or dialysate NE concentration. Transection of cervical vagal nerves after central administration of ghrelin rapidly diminished this increase in ACh concentration.
Conclusions: Centrally administered ghrelin increases ACh release from cardiac vagal nerve endings.
- © 2010 by American Heart Association, Inc.