Sensitization of cardiac receptors (vagal afferents) by intracoronary acetylstrophanthidin.

The purpose of this study was to determine if sensitization of cardiac receptors with acetylstrophanthidin augments the inhibition of renal nerve activity resulting from expansion of the blood volume or from coronary artery occlusion. Ten chloralose-anesthetized dogs with sinoaortic baroreceptor denervation were subjected to volume expansion with dextran in saline. Under control conditions, volume expansion resulted in decreases in renal nerve activity (% or control) that were inversely related to left atrial pressure (-13.0%/mmHg left atrial pressure). After intracoronary acetylstrophanthidin, volume expansion resulted in a significantly greater suppression of renal nerve activity (-20.6%/mmHg). Occlusion of the circumflex coronary artery in 19 dogs with carotid baroreceptor denervation resulted in a 29 +/- 5% (SE) reduction in renal nerve activity. After intracoronary acetylstrophanthidin, circumflex occlusion resulted in a significantly greater decrease in renal nerve activity (45 +/- 4%). Vagotomy abolished the decreases in renal nerve activity, which resulted from volume expansion and from circumflex coronary occlusion. These data show that volume expansion and coronary occlusion reflexly decrease renal nerve activity via cardiac afferent vagal endings. These reflex inhibitory influences are augmented after intracoronary acetylstrophanthidin. The results are consistent with the view that intracoronary acetylstrophanthidin sensitizes cardiac afferent vagal endings.