Chemical stimulation of cardiac receptors attenuates locomotion in mesencephalic cats.

The purpose of the present investigation was to determine whether chemical stimulation of cardiac receptors is sufficient to inhibit locomotion. Decerebrate, unanesthetized cats were induced to walk on a treadmill by electrically stimulating the mesencephalic locomotor region (MLR). Cardiac receptors were stimulated by injecting nicotine (62.3 +/- 8.6 microg/kg, mean +/- SE) into the pericardial sac. Cardiac nerve activity was reversibly blocked by injecting procaine (2%) into the pericardial sac. Locomotion was monitored by using bipolar needle electrodes inserted into the lateral gastrocnemius (LG) and tibialis anterior (TA) muscles. Integrated electromyographic (iEMG) activity from each muscle was quantified on a step-by-step basis. Intrapericardial (ipc) nicotine inhibited locomotion and evoked the coronary chemoreflex. Blood pressure and heart rate decreased significantly by 45.6 +/- 7.1 mmHg and 59.3 +/- 12.3 beats/min, respectively. Nicotine ipc significantly reduced iEMG activity by 24-28% in the LG muscles. The TA muscles were not affected consistently by ipc nicotine. The locomotor inhibition and the depressor reflex paralleled each other and occurred within 5 s of nicotine injection. Procaine ipc blocked the nicotine-induced locomotor inhibition and depressor reflex. The effects of procaine were largely reversible, because ipc nicotine reduced iEMG activity in the LG (25-46%) but not in the TA muscles after washing procaine from the pericardial sac. These results demonstrate that cardiac receptors sensitive to nicotine inhibit MLR-induced locomotion in the decerebrate cat. These findings indicate the presence of a neural pathway from the heart whereby endogenous stimuli could reflexly alter motor control.