Quantification of mechanical and neural components of vagal baroreflex in humans

Traditionally, arterial baroreflex control of vagal neural outflow is quant ified by heart period responses to falling and/or rising arterial pressures (ms/mm Hg). However, it is arterial pressure-dependent stretch of barosens ory vessels that determines afferent baroreceptor responses, which, in turn , generate appropriate efferent cardiac vagal outflow. Thus, mechanical tra nsduction of pressure into barosensory vessel stretch and neural transducti on of stretch into vagal outflow are key steps in baroreflex regulation tha t determine the conventional integrated input-output relation. We developed a novel technique for direct estimation of gain in both mechanical and neu ral components of integrated cardiac vagal baroreflex control. Concurrent, beat-by-beat measures of arterial pressures (Finapres), carotid diameters ( B-mode ultrasonography), and R-R intervals (ECG lead II) were made during b olus vasoactive drug infusions (modified Oxford technique) in 16 healthy hu mans. The systolic carotid diameter/pressure relationship (r(2)=0.79 +/-0.0 08, mean +/- SEM) provided a gain estimate of dynamic mechanical transducti on of pressure into a baroreflex stimulus. The R-R interval/systolic diamet er relationship (r(2)=0.77 +/-0.009) provided a gain estimate of efferent-e fferent neural transduction of baroreflex stimulus into a vagal response. V ariance between repeated measures for both estimates was no different than that for standard gain (P <0.40). Moreover, in these subjects, the simple p roduct of the 2 estimates almost equaled standard baroreflex gain (ms/mm Hg =0.98x+2.27; r(2)=0.93, P=0.001). This technique provides reliable informat ion on key baroreflex components not distinguished by standard assessments and gives insight to dynamic mechanical and neural events during acute chan ges in arterial pressure.