The baroreflex loop consists of a fast neural arc and a slow mechanical arc. We hypothesized that the neural baroreflex arc compensates the slow mechanical response and thus improves the quality of blood pressure regulation. We estimated the open-loop transfer characteristics of the neural baroreflex arc (HP), i.e., from carotid sinus pressure to sympathetic nerve activity (SNA), and that of the effective peripheral baroreflex arc (Hp), i.e., from SNA to arterial pressure, in anesthetized rabbits. The gain of Hn was constant below 0.12 +/- 0.057 Hz and increased with a slope of 6.1 +/- 0.06 dB/octave above its frequency up to 1 Hz. In contrast, the gain of Hp was constant below 0.071 +/- 0.03 Hz and decreased with a slope of -11.0 +/- 1.48 dB/octave above the frequency. These data indicate that Hn accelerates slow peripheral responses in the frequency range of 0.1-1 Hz. Although too much acceleration in the high-frequency range could result in instability of the system, numerical analysis of the closed-loop baroreflex response indicated that the neural arc optimized arterial pressure regulation in achieving both stability and quickness.

Although the characteristics of the static interaction between the sympathetic and parasympathetic nervous systems in regulating heart rate (HR) have been well established, how the dynamic interaction modulates the HR response remains unknown. We therefore investigated dynamic interaction by estimating the transfer function from nerve stimulation to HR using a band-limited Gaussian white-noise technique. The transfer function relating dynamic sympathetic stimulation to HR had characteristics of a second-order low-pass filter. Simultaneous tonic vagal stimulation at 5 and 10 Hz increased gain of the transfer function by 55.0 +/- 40.1 and 80.7 +/- 50.5%, respectively (P < 0.05). The transfer function from dynamic vagal stimulation to HR had characteristics of a first-order low-pass filter. Simultaneous tonic sympathetic stimulation at 5 and 10 Hz increased the gain by 18.2 +/- 17.9 and 24.1 +/- 18.0%, respectively (P < 0.05). Thus interaction augmented dynamic gain bidirectionally, even though it affected mean HR antagonistically. By virtue of this interaction, the autonomic nervous system appears to extend its dynamic range of operation.

We developed new methods for isolating in situ baroreceptor regions of carotid sinus and aortic depressor nerves in halothane-anesthetized rats. After ligation of the root of the external carotid artery, the internal carotid and pterygopalatine arteries were embolized with two ball bearings of 0.8 mm in diameter. Bilateral carotid sinus pressures were changed between 60 and 180 mmHg in 20-mmHg steps lasting 1 min each. The sigmoidal steady-state relationship between aortic and carotid sinus pressures in 11 rats indicated the maximum gain of the carotid sinus baroreflex to be −2.99 ± 0.75 at 120 ± 5 mmHg. An in situ isolation of the baroreceptor area of the right aortic depressor nerve could be made by ligation of the innominate, common carotid, and subclavian arteries in 9 rats. Pressure imposed on the subclavian baroreceptor was altered between 40 and 180 mmHg in 20-mmHg steps lasting 1 min each. The sigmoidal steady-state relationship between the aortic depressor nerve activity and imposed pressure showed that the baroreceptor gain peaked at 118 ± 4 mmHg. We established an easy approach to the rat baroreflex and baroreceptor research.

In the circulatory system, a change in blood pressure operates through the baroreflex to alter sympathetic efferent nerve activity, which in turn affects blood pressure. Existence of this closed feedback loop makes it difficult to identify the baroreflex open-loop transfer characteristics by means of conventional frequency domain approaches. Although several investigators have demonstrated the advantages of the time domain approach using parametric models such as the autoregressive moving average model, specification of the model structure critically affects their results. Thus we investigated the applicability of a nonparametric closed-loop identification technique to the carotid sinus baroreflex system by using an exogenous perturbation according to a binary white-noise sequence. To validate the identification method, we compared the transfer functions estimated by the closed-loop identification with those estimated by open-loop identification. The transfer functions determined by the two identification methods did not differ statistically in their fitted parameters. We conclude that exogenous perturbation to the baroreflex system enables us to estimate the open-loop baroreflex transfer characteristics under closed-loop conditions.

We evaluated dynamic effects of the carotid sinus baroreflex on ventriculoarterial coupling. In seven anesthetized, vagotomized dogs, we bilaterally isolated carotid sinuses and randomly changed carotid sinus pressure while measuring aortic pressure, aortic flow, and left ventricular pressure. Estimating left ventricular end-systolic elastance (E.) and effective arterial elastance (Ea) on a beat-to-beat basis, we determined transfer functions from the carotid sinus pressure to Ees (HE,,) Figure 1 illustrates the basic framework of the ventriculoarterial coupling in the pressure-volume plane. End-systolic elastance (Ees), which represents contractility of the left ventricle, is the slope of the end-systolic pressure-volume relation (line A in Figure 1). Effective arterial elastance (Ea), which in the steady state approximates arterial resistance divided by the cardiac cycle length, is the slope of the end-systolic pressure-stroke volume relation (line B in Figure 1). Increases in Ea reflect increases in arterial resistance or heart rate. The end-systolic equilibrium point that re-