The left ventricle increases contractility in response to baroreceptor unloading, which is sympathetically-mediated in the anesthetized rat

Contemporary discussion of the baroreflex includes the efferent vascular-sympathetic and cardio-vagal arms. Since sympathetic post-ganglionic neurons also innervate the left ventricle (LV), it is oft-assumed that the LV produces a sympathetically-mediated increase in contractility during baroreceptor unloading, but this has not been characterized using a load-independent index of contractility. We aimed to determine a) whether LV contractility increases in response to baroreceptor unloading, and b) whether such increases are mediated via the sympathetic or parasympathetic arm of the autonomic nervous system. Ten male Wistar rats were anesthetized (urethane) and instrumented with arterial and LV pressure-volume catheters to measure mean arterial pressure (MAP) and load-independent LV contractility [maximal rate of increase in pressure adjusted to end-diastolic volume (PAdP/dt )], respectively. Rats were placed in a servo-controlled lower-body negative pressure (LBNP) chamber to reduce MAP by 10% for 60s to mechanically unload baroreceptors under control conditions. LBNP was repeated in each animal following infusions of cardiac autonomic blockers using esmolol (sympathetic), atropine (parasympathetic), and esmolol+atropine. Under control conditions, PAdP/dt increased during baroreceptor unloading (26±6 vs. 31±9 mmHg·s ·μL , p=0.031). During esmolol, there was no increase in LV contractility during baroreceptor unloading (11±2 vs. 12±2, p=0.125); however, during atropine, there was an increase in LV contractility during baroreceptor unloading (26±6 vs. 31±9, p=0.019). During combined esmolol and atropine, there was a small increase in contractility vs control (13±3 vs. 15±4, p=0.046). Our results demonstrate that, in anesthetized rats, LV contractility increases in response to baroreceptor unloading, which is largely sympathetically mediated.