Although regional difference in sympathetic efferent nerve activity has been well investigated, whether this regional difference exists in the dynamic baroreflex regulation of sympathetic nerve activity remains uncertain. In anesthetized, vagotomized, and aortic-denervated rabbits, we isolated carotid sinuses and randomly perturbed intracarotid sinus pressure (CSP) while simultaneously recording cardiac (CSNA) and renal sympathetic nerve activities (RSNA). The neural arc transfer function from CSP to CSNA and that from CSP to RSNA revealed high-pass characteristics. The increasing slope of the transfer gain in the frequencies between 0.03 and 0.3 Hz was significantly greater for CSNA than for RSNA (2.96 +/- 0.72 vs. 1.64 +/- 0.73 dB/octave, P < 0.01, n = 9). The difference was hardly explained by the difference in static nonlinear characteristics of CSP-CSNA and CSP-RSNA relationships or by the difference in conduction velocities in the multifiber recording. These results indicate that the central processing in the brain stem differs between CSNA and RSNA. The neural arc of the baroreflex may exert differential effects on the heart and kidney in response to dynamic baroreflex activation.

A transfer function from baroreceptor pressure input to sympathetic nerve activity (SNA) shows derivative characteristics in the frequency range below 0.8 Hz in rabbits. These derivative characteristics contribute to a quick and stable arterial pressure (AP) regulation. However, if the derivative characteristics hold up to heart rate frequency, the pulsatile pressure input will yield a markedly augmented SNA signal. Such a signal would saturate the baroreflex signal transduction, thereby disabling the baroreflex regulation of AP. We hypothesized that the transfer gain at heart rate frequency would be much smaller than that predicted from extrapolating the derivative characteristics. In anesthetized rabbits (n = 6), we estimated the neural arc transfer function in the frequency range up to 10 Hz. The transfer gain was lost at a rate of -20 dB/decade when the input frequency exceeded 0.8 Hz. A numerical simulation indicated that the high-cut characteristics above 0.8 Hz were effective to attenuate the pulsatile signal and preserve the open-loop gain when the baroreflex dynamic range was finite.

Static characteristics of the baroreflex neural arc from pressure input to sympathetic nerve activity (SNA) show sigmoidal nonlinearity, whereas its dynamic characteristics approximate a derivative filter where the magnitude of SNA response becomes greater as the input frequency increases. To reconcile the static nonlinear and dynamic linear components, we examined the effects of input amplitude on the apparent linear transfer function of the neural arc. In nine anesthetized rabbits, we perturbed isolated carotid sinus pressure by using binary white noise while varying the input amplitude among 5, 10, 20, and 40 mmHg. With increasing input amplitude, the transfer gain at 0.01 Hz decreased from 1.21 +/- 0.27 to 0.49 +/- 0.28 arbitrary units/mmHg (P < 0.01). Moreover, the slope of the transfer gain between 0.03 and 0.3 Hz decreased from 14.3 +/- 3.7 to 6.5 +/- 2.5 dB/decade (P < 0.01). We conclude that the model consisting of a sigmoidal component following rather than preceding a derivative component explains the observed results and thus can be used as a first approximation of the overall neural arc transfer characteristics.

The chemoreflex system controlling ventilation consists of two subsystems, i.e., the central controller (controlling element), and peripheral plant (controlled element). We developed an integral framework to quantitatively characterize individual ventilatory regulation by experimental determination of an equilibrium diagram using a modified metabolic hyperbola and the CO2 response curve. In 13 healthy males, the steady-state arterial CO2 pressure (P(a)CO2) and minute ventilation (V(E)) were measured. To characterize the central controller, we changed fraction of inspired CO2 (0, 3.5, 5 and 6% CO2 in 80% oxygen with nitrogen balance) and measured the P(a)CO2-V(E) relation. To characterize the peripheral plant, we altered V(E) by hyper- or hypoventilation using a visual feedback method, which made it possible to control both tidal volume and breathing frequency, and measured the VE-P(a)CO2 relation. The intersection between the two relationship lines gives the operating point. The relationship between P(a)CO2 and V(E) for the central controller was reasonably linear in each subject (r2 = 0.808-0.995). The peripheral plant approximated a modified metabolic hyperbolic curve (r = 0.962-0.996). The operating points of the system estimated from the two relationship lines were in good agreement with those measured under the closed-loop condition. The gain of the central controller was 1.9 (1.0) l min(-1) mmHg(-1) and that of the peripheral plant was 3.0 (0.5) mmHg l(-1) min(-1). The total loop gain, the product of the two gains, was 5.3 (2.5). We conclude that human ventilatory regulation by the respiratory chemoreflex system can be quantitatively characterized using an equilibrium diagram. This framework should be useful for understanding the mechanisms responsible for abnormal ventilation under various pathophysiological conditions.

No abstract