Interaction between carotid baroreflex and exercise pressor reflex depends on baroreceptor afferent input.

Abstract

Because arterial baroreceptor and skeletal muscle receptor afferents project to cardiovascular regions in the lower brain stem such as the nucleus tractus solitarii (NTS), it is likely that the level of baroreceptor afferent input will modify the excitatory cardiovascular responses evoked by contraction-sensitive skeletal muscle afferents. The purpose of this study was to determine the effect of carotid sinus baroreceptor afferent input (CSA) on reflex heart rate (HR) and mean arterial pressure (MAP) responses evoked by activation of skeletal muscle receptor afferents (SMA). CSA input was servo controlled at three levels of carotid sinus pressure using the isolated carotid sinus preparation, and SMA input was varied by induced muscle contraction (L7-S1 ventral root stimulation) or passive muscle stretch. Experiments were performed in alpha-chloralose-anesthetized and vagotomized dogs (n = 9). When CSA input was low (106 +/- 35 mmHg), electrically induced muscle contraction increased HR and MAP (30 +/- 8 beats/min and 42 +/- 12 mmHg, respectively, P < 0.05). However, when CSA input was high (221 +/- 9 mmHg), the reflex changes in HR and MAP during muscle contraction were attenuated (6 +/- 4 beats/min and 18 +/- 4 mmHg, respectively, P < 0.05). Similarly, the sympathoexcitatory responses evoked by passive muscle stretch were attenuated in a baroreceptor-dependent manner. These results suggest that changing CSA input from low (106 mmHg) to high (221 mmHg) shifts the interaction from facilitation to inhibition. Therefore, it is concluded that the nature of the interaction (i.e., facilitation or inhibition) between the baroreflex and the exercise pressor reflex is dependent on the level of baroreceptor input. Moreover, our findings substantiate early studies showing that the level of afferent input from arterial baroreceptors is a powerful modulator of sympatho-excitation evoked by mechanically and metabolically sensitive skeletal muscle receptors.