正常人动脉压力感受器反射开环增益的计算方法

为在闭环条件下测得正常人的动脉压力感受器反射的开环增益(G),利用三个不同特点的血压调节模型,导出了G的计算表达式及G与血液动力学变量间的关系。用所导出的公式,通过适当的实验设计,便可近似地分别计算出颈动脉窦和主动脉弓压力感受器反射的开环增益。文中给出了计算的例子。此外,还利用导出的关系式分析了心率、外周阻力的调节变化对系统开环增益的相对贡献及输入压力水平对增益效果的影响。     

Enhanced open-loop but not closed-loop cardiac baroreflex sensitivity during orthostatic stress in humans

The neural interaction between the cardiopulmonary and arterial baroreflex may be critical for the regulation of blood pressure during orthostatic stress. However, studies have reported conflicting results: some indicate increases and others decreases in cardiac baroreflex sensitivity (i.e., gain) with cardiopulmonary unloading. Thus the effect of orthostatic stress-induced central hypovolemia on regulation of heart rate via the arterial baroreflex remains unclear. We sought to comprehensively assess baroreflex function during orthostatic stress by identifying and comparing open- and closed-loop dynamic cardiac baroreflex gains at supine rest and during 60° head-up tilt (HUT) in 10 healthy men. Closed-loop dynamic "spontaneous" cardiac baroreflex sensitivities were calculated by the sequence technique and transfer function and compared with two open-loop carotid-cardiac baroreflex measures using the neck chamber system: 1) a binary white-noise method and 2) a rapid-pulse neck pressure-neck suction technique. The gain from the sequence technique was decreased from -1.19 ± 0.14 beats·min(-1)·mmHg(-1) at rest to -0.78 ± 0.10 beats·min(-1)·mmHg(-1) during HUT (P = 0.005). Similarly, closed-loop low-frequency baroreflex transfer function gain was reduced during HUT (P = 0.033). In contrast, open-loop low-frequency transfer function gain between estimated carotid sinus pressure and heart rate during white-noise stimulation was augmented during HUT (P = 0.01). This result was consistent with the maximal gain of the carotid-cardiac baroreflex stimulus-response curve (from 0.47 ± 0.15 beats·min(-1)·mmHg(-1) at rest to 0.60 ± 0.20 beats·min(-1)·mmHg(-1) at HUT, P = 0.037). These findings suggest that open-loop cardiac baroreflex gain was enhanced during HUT. Moreover, under closed-loop conditions, spontaneous baroreflex analyses without external stimulation may not represent open-loop cardiac baroreflex characteristics during orthostatic stress.     

Resonance in a mathematical model of baroreflex control: arterial blood pressure waves accompanying postural stress

A mathematical model of the arterial baroreflex was developed and used to assess the stability of the reflex and its potential role in producing the low-frequency arterial blood pressure oscillations called Mayer waves that are commonly seen in humans and animals in response to decreased central blood volume. The model consists of an arrangement of discrete-time filters derived from published physiological studies, which is reduced to a numerical expression for the baroreflex open-loop frequency response. Model stability was assessed for two states: normal and decreased central blood volume. The state of decreased central blood volume was simulated by decreasing baroreflex parasympathetic heart rate gain and by increasing baroreflex sympathetic vaso/venomotor gains as occurs with the unloading of cardiopulmonary baroreceptors. For the normal state, the feedback system was stable by the Nyquist criterion (gain margin = 0.6), but in the hypovolemic state, the gain margin was small (0.07), and the closed-loop frequency response exhibited a sharp peak (gain of 11) at 0.07 Hz, the same frequency as that observed for arterial pressure fluctuations in a group of healthy standing subjects. These findings support the theory that stresses affecting central blood volume, including upright posture, can reduce the stability of the normally stable arterial baroreflex feedback, leading to resonance and low-frequency blood pressure waves.     

Evaluation of muscle metaboreflex function through graded reduction in forearm blood flow during rhythmic handgrip exercise in humans

Hypoperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex. Our aim was to determine the muscle metaboreflex threshold and gain in humans by creating an open-loop relationship between active muscle blood flow and hemodynamic responses during a rhythmic handgrip exercise. Eleven healthy subjects performed the exercise at 5 or 15% of maximal voluntary contraction (MVC) in random order. During the exercise, forearm blood flow (FBF), which was continuously measured using Doppler ultrasound, was reduced in five steps by manipulating the inner pressure of an occlusion cuff on the upper arm. The FBF at each level was maintained for 3 min. The initial reductions in FBF elicited no hemodynamic changes, but once FBF fell below a threshold, mean arterial blood pressure (MAP) and heart rate (HR) increased and total vascular conductance (TVC) decreased in a linear manner. The threshold FBF during the 15% MVC trial was significantly higher than during the 5% MVC trial. The gain was then estimated as the slope of the relationship between the hemodynamic responses and FBFs below the threshold. The gains for the MAP and TVC responses did not differ between workloads, but the gain for the HR response was greater in the 15% MVC trial. Our findings thus indicate that increasing the workload shifts the threshold for the muscle metaboreflex to higher blood flows without changing the gain of the reflex for the MAP and TVC responses, whereas it enhances the gain for the HR response.     

Estimation of arterial and cardiopulmonary total peripheral resistance baroreflex gain values: validation by chronic arterial baroreceptor denervation

Feedback control of total peripheral resistance (TPR) by the arterial and cardiopulmonary baroreflex systems is an important mechanism for short-term blood pressure regulation. Existing methods for measuring this TPR baroreflex mechanism typically aim to quantify only the gain value of one baroreflex system as it operates in open-loop conditions. As a result, the normal, integrated functioning of the arterial and cardiopulmonary baroreflex control of TPR remains to be fully elucidated. To this end, the laboratory of Mukkamala et al. (Mukkamala R, Toska K, and Cohen RJ. Am J Physiol Heart Circ Physiol 284: H947-H959, 2003) previously proposed a potentially noninvasive technique for estimating the closed-loop (dimensionless) gain values of the arterial TPR baroreflex (GA) and the cardiopulmonary TPR baroreflex (GC) by mathematical analysis of the subtle, beat-to-beat fluctuations in arterial blood pressure, cardiac output, and stroke volume. Here, we review the technique with additional details and describe its experimental evaluation with respect to spontaneous hemodynamic variability measured from seven conscious dogs, before and after chronic arterial baroreceptor denervation. The technique was able to correctly predict the group-average changes in GA and GC that have previously been shown to occur following chronic arterial baroreceptor denervation. That is, reflex control by the arterial TPR baroreflex was virtually abolished (GA = -2.1 +/- 0.6 to 0.3 +/- 0.2; P < 0.05), while reflex control by the cardiopulmonary TPR baroreflex more than doubled (GC = -0.7 +/- 0.4 to -1.8 +/- 0.2; P < 0.05). With further successful experimental testing, the technique may ultimately be employed to advance the basic understanding of TPR baroreflex functioning in both humans and animals in health and disease.     

High-cut characteristics of the baroreflex neural arc preserve baroreflex gain against pulsatile pressure

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.     

Dynamic baroreflex control of blood pressure: influence of the heart vs. peripheral resistance

The aim in the present experiments was to assess the dynamic baroreflex control of blood pressure, to develop an accurate mathematical model that represented this relationship, and to assess the role of dynamic changes in heart rate and stroke volume in giving rise to components of this response. Patterned electrical stimulation [pseudo-random binary sequence (PRBS)] was applied to the aortic depressor nerve (ADN) to produce changes in blood pressure under open-loop conditions in anesthetized rabbits. The stimulus provided constant power over the frequency range 0-0.5 Hz and revealed that the composite systems represented by the central nervous system, sympathetic activity, and vascular resistance responded as a second-order low-pass filter (corner frequency approximately 0.047 Hz) with a time delay (1.01 s). The gain between ADN and mean arterial pressure was reasonably constant before the corner frequency and then decreased with increasing frequency of stimulus. Although the heart rate was altered in response to the PRBS stimuli, we found that removal of the heart's ability to contribute to blood pressure variability by vagotomy and beta(1)-receptor blockade did not significantly alter the frequency response. We conclude that the contribution of the heart to the dynamic regulation of blood pressure is negligible in the rabbit. The consequences of this finding are examined with respect to low-frequency oscillations in blood pressure.     

Dynamic characteristics of baroreflex neural and peripheral arcs are preserved in spontaneously hypertensive rats

Although baroreceptors are known to reset to operate in a higher pressure range in spontaneously hypertensive rats (SHR), the total profile of dynamic arterial pressure (AP) regulation remains to be clarified. We estimated open-loop transfer functions of the carotid sinus baroreflex in SHR and Wistar Kyoto (WKY) rats. Mean input pressures were set at 120 (WKY??? and SHR???) and 160 mmHg (SHR???). The neural arc transfer function from carotid sinus pressure to efferent splanchnic sympathetic nerve activity (SNA) revealed derivative characteristics in both WKY and SHR. The slope of dynamic gain (in decibels per decade) between 0.1 and 1 Hz was not different between WKY??? (10.1 ± 1.0) and SHR??? (10.4 ± 1.1) but was significantly greater in SHR??? (13.2 ± 0.8, P < 0.05 with Bonferroni correction) than in SHR???. The peripheral arc transfer function from SNA to AP showed low-pass characteristics. The slope of dynamic gain (in decibels per decade) did not differ between WKY??? (-34.0 ± 1.2) and SHR??? (-31.4 ± 1.0) or between SHR??? and SHR??? (-32.8 ± 1.3). The total baroreflex showed low-pass characteristics and the dynamic gain at 0.01 Hz did not differ between WKY??? (0.91 ± 0.08) and SHR??? (0.84 ± 0.13) or between SHR??? and SHR??? (0.83 ± 0.11). In both WKY and SHR, the declining slope of dynamic gain was significantly gentler for the total baroreflex than for the peripheral arc, suggesting improved dynamic AP response in the total baroreflex. In conclusion, the dynamic characteristics of AP regulation by the carotid sinus baroreflex were well preserved in SHR despite significantly higher mean AP.     

Time-dependent change in baroreflex control capacity of arterial pressure by pentobarbital anesthesia in rabbits.

The present study is designed to investigate the time-dependent effect of pentobarbital anesthesia on the baroreflex arterial pressure (AP) control system in rabbits. The overall AP control capacity of the baroreflex system was assessed with mean arterial pressure (MAP) responses to the rapid mild hemorrhage (2 ml/kg body weight) and an overall open-loop gain (G) of the system. The G value was determined by means of the following formula: G = delta API/delta APS-1, where delta APl is an immediate MAP fall and delta APS a steady-state fall after the rapid hemorrhage. Prior to the experiment, two catheters for AP measurement and hemorrhage were chronically in-dwelt in the aortic arch via the left subclavian and left common carotid arteries, respectively. Control mean arterial pressure averaged for 30 sec before the rapid hemorrhage (CMAP), delta API and delta APS significantly increased and reached the maximal value at 14 min (CAMP: p < 0.01) and 28 min (delta API: p < 0.01 and delta APS: p < 0.01) after the intravenous injection of sodium pentobarbital in a 25.0 mg/kg dose, respectively. These values gradually decreased in the course of time and tended to recover to near the preanesthetic level at 77-98 min after the anesthesia. The G value significantly decreased from 7.3 in the conscious state to 1.5 at 28 min after the anesthesia (p < 0.001), gradually increased with lapse of time and recovered to near the preanesthetic level at 77-98 min after the anesthesia. No significant difference in G was observed between in the conscious and anesthetized states beyond 70 min after the anesthesia (p > 0.05). These findings suggest that pentobarbital sodium exerts a time-dependent inhibitory effect on the baroreflex system but does not significantly affect the overall AP control capacity of the baroreflex system itself at least 70 min after the intravenous administration at a dose of 25.0 mg/kg.     

Dynamics of sympathetic baroreflex control of arterial pressure in rats

By a white noise approach, we characterized the dynamics of the sympathetic baroreflex system in 11 halothane-anesthetized rats. We measured sympathetic nerve activity (SNA) and systemic arterial pressure (SAP), while carotid sinus baroreceptor pressure (BRP) was altered randomly. We estimated the transfer functions from BRP to SNA (mechanoneural arc), from SNA to SAP (neuromechanical arc), and from BRP to SAP (total arc). The gain of the mechanoneural arc gradually increased about threefold as the frequency of BRP change increased from 0.01 to 0.8 Hz. In contrast, the gain of the neuromechanical arc rapidly decreased to 0.4% of the steady-state gain as the frequency increased from 0.01 to 1 Hz. Although the total arc also had low-pass characteristics, the rate of attenuation in its gain was significantly slower than that of the neuromechanical arc, reflecting the compensatory effect of the mechanoneural arc for the sluggish response of the neuromechanical arc. We conclude that the quantitative estimation of the baroreflex dynamics is vital for an integrative understanding of baroreflex function in rats.     

The neural basis of catalepsy in the stick insect cuniculina impigra

Catalepsy in the femur-tibia joint can be characterized as follows: When the joint is passively bent and then released, the joint first extends rapidly by 10°–30° and then returns to its starting position with extremely low speed.Catalepsy is a characteristic of the femur-tibia control system. This system is quantitatively described in the open-loop configuration (input: stimulation of the femoral chordotonal organ; output: movement of the tibia). The output shows a predominant dynamic portion which only responds to movement and a weak static portion which responds to position. The dynamic portion can be described by a high-pass and a low-pass filter in series. The time constant of the high-pass filter in series. The time constant of the high-pass filter depends on input slope. The system possesses a large phase reserve and is therefore very stable in the closed loop configuration.The results confirm the hypothesis that the high gain of the phasmid control system evolved only under a selection pressure towards catalepsy.Supported by DFG Ba 578     

Blood pressure regulation in the three-toed sloth, Bradypus variegatus

The aim of this study was to elucidate the role of the baroreflex in blood pressure control in sloths, Bradypus variegatus, since these animals show labile levels in this parameter. Unanesthetized cannulated sloths were positioned in an experimental chair and the arterial catheter was coupled to a strain gauge pressure transducer. Blood pressure was monitored before, during and after the administration of phenylephrine (0.0625 to 4 microg/kg) and sodium nitroprusside (0.0625 to 2 microg/kg), bringing about changes in mean blood pressure from +/-30 mmHg in relation to control values. The relation between heart rate changes due to blood pressure variation was estimated by linear regression analysis. The slope was considered the reflex baroreceptor gain. The results (means+/-SD) showed that the reflex baroreceptor gain was -0.3+/-0.1 bpm/mmHg (r=0.88) to phenylephrine and -0.5+/-0.1 bpm/mmHg (r=0.92) to sodium nitroprusside, denoting a reduced reflex baroreceptor gain when compared with other mammals, suggesting that in sloths the baroreceptors are minimally involved in the buffering reflex response to these drugs. These findings suggest that the labile blood pressure could be influenced or be a result of this lowering in the reflex baroreceptor gain.     

Difference of arterial pressure regulatory mechanism between awake and anesthetized human subjects

This experiment was conducted to clarify difference of arterial pressure regulatory mechanism between awake and anesthetized human subjects. In 18 subjects who were scheduled for surgical operations, passive tilting test was performed both in awake and anesthetized conditions. Arterial pressure and heart rate were measured during four types of tilting test, i.e., 1. supine-10 degrees head down tilt 2. 10 degrees head down tilt-supine 3. supine-10 degrees head up tilt 4. 10 degrees head up tilt-supine. Relative changes in arterial pressure and heart rate in response to these four tilting tests were compared. After postural changes, all anesthetized subjects showed significant arterial pressure changes followed by restoration of arterial pressure towards control level with opposite changes of heart rate. This initial arterial pressure changes were mainly induced by shift of blood due to gravity and subsequent arterial pressure and heart rate changes were mainly by baro-receptor reflex. On the other hand, awake subjects showed transient increase of heart rate immediately after tilting followed by arterial pressure rise 2 to 3 seconds later in all four tilting tests. However, arterial pressure did not change so remarkably as in anesthetized condition and remained almost constant during tilting test. In awake subjects, their arterial pressure was regulated rapidly and reflex control of arterial pressure was masked. This rapid regulation of arterial pressure may be induced directly by higher central nervous system.     

Insulin-exacerbated hypertension in captopril-treated spontaneously hypertensive rats: role of sympathoexcitation

Insulin excess exacerbates hypertension in spontaneously hypertensive rats (SHR). This study examined the relative contribution of the renin-angiotensin system and the sympathetic nervous system in this phenomenon. In SHR, daily subcutaneous injections of insulin were initiated either before short-term angiotensin-converting enzyme inhibition with captopril or after lifetime captopril treatment. Insulin treatment resulted in significant increases in mean arterial pressure and heart rate and captopril treatment lowered arterial pressure, but captopril did not lower arterial pressure more in the insulin-treated compared with control rats. To test the contribution of the sympathetic nervous system to this form of hypertension, each rat was intravenously infused with either a ganglionic blocker (i.e., hexamethonium) or a centrally acting alpha2-adrenergic receptor agonist (i.e., clonidine). Administration of either agent largely eliminated the differences in mean arterial pressure and heart rate between the insulin-treated and saline-treated SHR, irrespective of captopril treatment. These data indicate that in SHR, the ability of insulin to increase blood pressure is closely related to sympathoexcitation, which is unresponsive to blockade of angiotensin-converting enzyme.     

Static handgrip exercise modifies arterial baroreflex control of vascular sympathetic outflow in humans

To examine effects of static exercise on the arterial baroreflex control of vascular sympathetic nerve activity, 22 healthy male volunteers performed 2 min of static handgrip exercise at 30% of maximal voluntary force, followed by postexercise circulatory arrest (PE-CA). Microneurographic recording of muscle sympathetic nerve activity (MSNA) was made with simultaneous recording of arterial pressure (Portapres). The relationship between MSNA and diastolic arterial pressure was calculated for each condition and was defined as the arterial baroreflex function. There was a close relationship between MSNA and diastolic arterial pressure in each subject at rest and during static exercise and PE-CA. The slope of the relationship significantly increased by >300% during static exercise (P < 0.001), and the x-axis intercept (diastolic arterial pressure level) increased by 13 mmHg during exercise (P < 0.001). These alterations in the baroreflex relationship were completely maintained during PE-CA. It is concluded that static handgrip exercise is associated with a resetting of the operating range and an increase in the reflex gain of the arterial barorelex control of MSNA.     

Carotid and aortic baroreflexes of the rat: II. Open-loop frequency response and the blood pressure spectrum

To determine the relationship between blood pressure (BP) variability and the open-loop frequency domain transfer function (TF) of the baroreflexes, we measured the pre- and postsinoaortic denervation (SAD) spectra and the effects of periodic and step inputs to the aortic depressor nerve and isolated carotid sinus of central nervous system-intact, neuromuscular-blocked (NMB) rats. Similar to previous results in freely moving rats, SAD greatly increased very low frequency (VLF) (0.01-0.2 Hz) systolic blood pressure (SBP) noise power. Step response-frequency measurements for SBP; interbeat interval (IBI); venous pressure; mesenteric, femoral, and skin blood flow; and direct modulation analyses of SBP showed that only VLF variability could be substantially attenuated by an intact baroreflex. The -3-dB frequency for SBP is 0.035-0.056 Hz; femoral vascular conductance is similar to SBP, but mesenteric vascular conductance has a reliably lower and IBI has a reliably higher -3-dB point. The overall open-loop transportation lag, of which 相似文献   

Fetal blood volume responses to fetal haemorrhage: autonomic nervous contribution

The purpose of this study was to determine whether the autonomic nervous system contributes to short-term fetal blood volume restitution following fetal haemorrhage. Unanaesthetized, chronically catheterized fetal sheep averaging 130 days gestation (term = 145-150 days) were studied 5 days after catheter implantation. Blockade of the autonomic nervous system was produced with a bolus intravenous injection of hexamethonium. In 7 blocked fetuses, an average of 17.6% of the initial blood volume was removed over 5 min and this was not different from the 16.5% blood volume removed in 7 control fetuses. However, blood volume restoration averaged 44.6% after 30 min in the blocked fetuses and this was significantly less than the 60.2% volume restoration in the control fetuses (P less than 0.05). Thus blood volume restoration averaged 74% of control in the blocked fetuses. Following blood reinfusion over 5 min, blood volume was transiently elevated in the control group, but averaged 3.4, 4.7, and 5.3% below normal (P less than 0.05) at 10, 20 and 30 min post reinfusion in the blocked group. In addition, arterial pressure was lower after haemorrhage in the blocked group and increased twice that in the control group during reinfusion. Thus, the present data suggest that the fetal autonomic nervous system plays a significant role in mediating the short-term changes in fetal blood volume and vascular pressures following fetal haemorrhage and reinfusion.     

Regulation of middle cerebral artery blood velocity during recovery from dynamic exercise in humans.

We sought to examine the regulation of cerebral blood flow during 10 min of recovery from mild, moderate, and heavy cycling exercise by measuring middle cerebral artery blood velocity (MCA V). Transfer function analyses between changes in arterial blood pressure and MCA V were used to assess the frequency components of dynamic cerebral autoregulation (CA). After mild and moderate exercise, the decreases in mean arterial pressure (MAP) and mean MCA V (MCA Vm) were small. However, following heavy exercise, MAP was rapidly and markedly reduced, whereas MCA Vm decreased slowly (-23 +/- 4 mmHg and -4 +/- 1 cm/s after 1 min for MAP and MCA Vm, respectively; means +/- SE). Importantly, for each workload, the normalized low-frequency transfer function gain between MAP and MCA Vm remained unchanged from rest to exercise and during recovery, indicating a maintained dynamic CA. Similar results were found for the systolic blood pressure and systolic MCA V relationship. In contrast, the normalized low-frequency transfer function gain between diastolic blood pressure and diastolic MCA V (MCA Vd) increased from rest to exercise and remained elevated in the recovery period (P < 0.05). However, MCA Vd was quite stable on the cessation of exercise. These findings suggest that MCA V is well maintained following mild to heavy dynamic exercise. However, the increased transfer function gain between diastolic blood pressure and MCA Vd suggests that dynamic CA becomes less effective in response to rapid decreases in blood pressure during the initial 10 min of recovery from dynamic exercise.     

Counteraction of aortic baroreflex to carotid sinus baroreflex in a neck suction model.

Although neck suction has been widely used in the evaluation of carotid sinus baroreflex function in humans, counteraction of the aortic baroreflex tends to complicate any interpretation of observed arterial pressure (AP) response. To determine whether a simple linear model can account for the AP response during neck suction, we developed an animal model of the neck suction procedure in which changes in carotid distension pressure during neck suction were directly imposed on the isolated carotid sinus. In six anesthetized rabbits, a 50-mmHg pressure perturbation on the carotid sinus decreased AP by -27.4+/-4.8 mmHg when the aortic baroreflex was disabled. Enabling the aortic baroreflex significantly attenuated the AP response (-21.5+/-3.8 mmHg, P<0.01). The observed closed-loop gain during simulated neck suction was well predicted by the open-loop gains of the carotid sinus and aortic baroreflexes using the linear model (-0.43+/-0.13 predicted vs. -0.41 +/-0.10 measured). We conclude that the linear model can be used as the first approximation to interpret AP response during neck suction.     

Baroreceptors, alpha1-adrenergic receptors, and regulation of mesenteric blood flow

In the mesenteric circulation of the rat a myogenic autoregulatory system operates at 0.1-0.15 Hz. Negative admittance phase in the region above 0.2 Hz suggested operation of an arterial baroreflex. The present study was designed to test this interpretation and to identify the neurotransmitter involved. In rats anesthetized with isoflurane, blood pressure and mesenteric blood flow (transit time ultrasound) were measured with central mechanisms intact, after sinoaortic denervation, and after denervation of the mesenteric bed. Sinoaortic denervation abrogated the negative phase in the band from 0.3 to 0.6 Hz and increased admittance gain in this region. Subsequent mesenteric denervation had no further effect on the pressure-flow transfer function. In a separate experiment, alpha1-adrenergic blockade reduced, but did not remove, the negative admittance phase in the 0.2- to 0.5-Hz band without altering admittance gain. It is concluded that the baroreflex acting on the mesenteric circulation can be identified by admittance phase, but that admittance gain is uninformative. Part of the response is mediated by alpha1-adrenergic transmission.