Pressure Baroreceptor Research Articles

Threshold and saturation pressures of baroreflex-mediated myocardial interstitial acetylcholine release in rats.

Cardiac microdialysis allows the assessment of cardiac efferent vagal nerve activity from myocardial interstitial acetylcholine (ACh) levels with minimal influence on the neural control of the heart; however, a total picture of the baroreflex-mediated myocardial interstitial ACh release including the threshold and saturation pressures has yet to be quantified. In eight anesthetized Wistar-Kyoto rats, we implanted microdialysis probes in the left ventricular free wall and measured the myocardial interstitial ACh release simultaneously with efferent sympathetic nerve activity (SNA) during a carotid sinus baroreceptor pressure input between 60 and 180mmHg. The baroreflex-mediated ACh release approximated a positive sigmoid curve, and its threshold and saturation pressures were not significantly different from those of an inverse sigmoid curve associated with the baroreflex-mediated SNA response (threshold: 94.3±8.6 vs. 99.3±6.0mmHg; saturation: 150.0±10.3 vs. 158.8±5.8mmHg). The sympathetic and vagal systems have certain levels of activities across most of the normal pressure range.

Contrasting open-loop dynamic characteristics of sympathetic and vagal systems during baroreflex-mediated heart rate control in rats.

Although heart rate (HR) is governed by the sympathetic and parasympathetic nervous systems, a head-to-head comparison of the open-loop dynamic characteristics of the total arc from a baroreceptor pressure input to the HR response has yet to be performed. We estimated the transfer function from carotid sinus pressure input to the HR response (HCSP→HR) before and after bilateral vagotomy (n = 7) as well as before and after the administration of a β-blocker propranolol (n = 8) in anesthetized male Wistar-Kyoto rats. The carotid sinus pressure was perturbed according to a Gaussian white noise signal so that the input power spectra were relatively flat between 0.01 and 1 Hz. The gain plot of HCSP→HR was V-shaped. Vagotomy reduced the dynamic gain at 1 Hz (0.0598 ± 0.0065 to 0.0025 ± 0.0004 beats·min-1·mmHg-1, P < 0.001) but not at 0.01 or 0.1 Hz. β-Blockade reduced the dynamic gain at 0.01 Hz (0.247 ± 0.069 to 0.077 ± 0.017 beats·min-1·mmHg-1, P = 0.020) but not at 0.1 or 1 Hz. We also estimated the efferent limb transfer function from electrical vagal efferent stimulation to the HR response (HVN→HR) under β-blockade conditions. We associated the model parameters of HVN→HR with the mean HR and the standard deviation of HR so that HVN→HR could be estimated based only on the HR data. We finally estimated the neural arc transfer function from a pressure input to efferent vagal nerve activity by dividing HCSP→HR by HVN→HR. The mathematically determined vagal neural arc showed derivative characteristics with its phase near zero radians at the lowest frequency.

Static magnetic field reduces blood pressure short-term variability and enhances baro-receptor reflex sensitivity in spontaneously hypertensive rats

Purpose: It has been shown that chronic exposure of young spontaneously hypertensive rats (SHR) to static magnetic field (SMF) delays the development of overt hypertension. Therefore the aim of the present work was to investigate the effects of SMF on autonomic cardiovascular control in adult spontaneously hypertensive rats.Materials and methods: Experiments were performed in freely moving spontaneously hypertensive rats equipped with femoral arterial catheter for blood pressure recording. Spontaneously hypertensive rats were exposed for 30 days to upward-oriented SMF (n = 17) or downward-oriented SMF (n = 17) of 16 mT intensity. A control group of spontaneously hypertensive rats (n = 17) was not exposed to SMF. Neurogenic cardiovascular control was evaluated by spectral analysis of arterial blood pressure and heart rate short-term variability and baro-receptor reflex sensitivity using the sequence method.Results: Exposure of spontaneously hypertensive rats to both upward- and downward-oriented SMF significantly reduced arterial blood pressure and enhanced baro-receptor reflex sensitivity. Downward-oriented SMF reduced heart rate, too. SMF of either orientation reduced systolic blood pressure variability in very low frequency domain while downward-oriented SMF also reduced low-frequency and increased high frequency domains.Conclusion: It follows that prolonged exposure to SMF is beneficial for neurogenic cardiovascular control in hypertension.

Acute arterial baroreflex-mediated changes in plasma catecholamine concentrations in a chronic rat model of myocardial infarction.

While it may be predictable that plasma norepinephrine (NE) concentration changes with efferent sympathetic nerve activity (SNA) in response to baroreceptor pressure inputs, an exact relationship between SNA and plasma NE concentration remains to be quantified in heart failure. We examined acute baroreflex‐mediated changes in plasma NE and epinephrine (Epi) concentrations in normal control (NC) rats and rats with myocardial infarction (MI) (n = 6 each). Plasma NE concentration correlated linearly with SNA in the NC group (slope: 2.17 ± 0.26 pg mL−1 %−1, intercept: 20.0 ± 18.2 pg mL−1) and also in the MI group (slope: 19.20 ± 6.45 pg mL−1 %−1, intercept: −239.6 ± 200.0 pg mL−1). The slope was approximately nine times higher in the MI than in the NC group (P < 0.01). Plasma Epi concentration positively correlated with SNA in the NC group (slope: 1.65 ± 0.79 pg mL−1 %−1, intercept: 115.0 ± 69.5 pg mL−1) and also in the MI group (slope: 7.74 ± 2.20 pg mL−1 %−1, intercept: 24.7 ± 120.1 pg mL−1). The slope was approximately 4.5 times higher in the MI than in the NC group (P < 0.05). Intravenous administration of desipramine (1 mg kg−1) significantly increased plasma NE concentration but decreased plasma Epi concentration in both groups, suggesting that neuronal NE uptake had contributed to the reduction in plasma NE concentration. These results indicate that high levels of plasma catecholamine in MI rats were still under the influence of baroreflex‐mediated changes in SNA, and may provide additional rationale for applying baroreflex activation therapy in patients with chronic heart failure.

Systematic understanding of acute effects of intravenous guanfacine on rat carotid sinus baroreflex-mediated sympathetic arterial pressure regulation

AimsTo assess the acute effects of intravenous guanfacine, an α2A-adrenergic agonist, on sympathetic outflow from the central nervous system and on sympathetic arterial pressure (AP) response. Main methodsIn anesthetized Wistar Kyoto rats, carotid sinus baroreceptor regions were isolated. Changes in electrical sympathetic nerve activity (SNA) and AP in response to a baroreceptor pressure input were examined before and after an intravenous administration of a high dose (100μg/kg, n=7) or a low dose (20μg/kg, n=5) of guanfacine. Key findingsThe higher dose of guanfacine significantly narrowed the range of the AP response (86.8±6.4 to 38.4±12.9mmHg, P<0.01) but increased the minimum AP (79.3±7.5 to 93.2±8.7mmHg, P<0.05). In the neural arc, guanfacine reduced both the response range (90.4±2.3 to 33.4±10.7%, P<0.01) and the minimum SNA (11.4±1.9 to 2.6±1.5%, P<0.01). In the peripheral arc, guanfacine increased the intercept (67.6±7.1 to 92.8±8.5mmHg, P<0.01) without a significant effect on the slope. The lower dose of guanfacine weakened the effects on both the neural and peripheral arcs. SignificanceGuanfacine suppressed SNA without a significant reduction of AP, which may be attributable to the peripheral vasoconstrictive effect. Reducing the dose of acutely administered intravenous guanfacine does not aid in separating the central sympathoinhibitory effect from the peripheral vasoconstrictive effect on AP in anesthetized rats in vivo.

Influence of Age on Blood Pressure Variability and Baroreceptor Sensitivity in Response to Acute Exercise

Aging and depressed spontaneous baroreceptor sensitivity (sBRS) and blood pressure variability (BPV) have been linked to negative cardiovascular outcomes. Understanding the interaction between agin...

Acute effects of intravenous nifedipine or azelnidipine on open-loop baroreflex static characteristics in rats.

To assess the acute effects of intravenous azelnidipine, a third-generation L-type calcium channel blocker, on sympathetic outflow from the central nervous system and to compare the effects of intravenous azelnidipine with those of intravenous nifedipine. In anesthetized Wistar Kyoto rats, carotid sinus baroreceptor regions were isolated. Changes in sympathetic nerve activity (SNA) and arterial pressure (AP) in response to a stepwise baroreceptor pressure input were examined before and during intravenous nifedipine or azelnidipine (for each: 100 μg/kg bolus followed by 300 μg/kg/h infusion, n = 6). Nifedipine significantly reduced the range of the AP response from 76.8 ± 7.4 to 45.4 ± 7.0 mmHg (P < 0.01) but did not affect the range of the SNA response (from 84.4 ± 5.1 to 85.9 ± 10.2%) or the SNA maximum gain (from 2.26 ± 0.28 to 2.35 ± 0.55%/mmHg). Similarly, azelnidipine significantly reduced the range of the AP response from 62.4 ± 3.9 to 31.4 ± 4.1 mmHg (P<0.01) but did not affect the range of the SNA response (from 71.2 ± 5.5 to 74.9 ± 7.2%) or the SNA maximum gain (from 1.64 ± 0.17 to 2.08 ± 0.26%/mmHg). A depressor dose of nifedipine or azelnidipine does not have an acute sympathoinhibitory effect in normotensive Wistar Kyoto rats even when the level of SNA was varied over the entire operating range of the carotid sinus baroreflex.

Systems physiology of the baroreflex during orthostatic stress: from animals to humans.

The baroreflex is a key mechanism involved in the control of arterial pressure (AP) during orthostasis in humans. However, the baroreflex is a closed-loop feedback system, from baroreceptor pressure input to systemic AP, and therefore requires open-loop experiments to identify its system characteristics. The requirement limits our ability to identify baroreflex system characteristics in humans. Open-loop research in animals has revealed dynamic and static characteristics of the two baroreflex subsystems: the neural and peripheral arcs. The neural arc, from baroreceptor pressure input to sympathetic nerve activity (SNA), has high-pass dynamic characteristics, indicating that more rapid change in input AP causes greater response in SNA. In contrast, the peripheral arc, from SNA input to systemic AP, has low-pass characteristics. Orthostasis increases the gain of the neural arc, which compensates for the lower transfer gain of the peripheral arc and in turn maintains total baroreflex function. Here, I discuss the possibility that baroreflex subsystem characteristics identified in animals can be applicable to the human sympathetic response to orthostasis, with a focus on loading speed-dependence of orthostatic sympathetic activation.

Cardiovascular function alterations induced by acute paradoxical sleep deprivation in rats

Sleep loss has been implicated in triggering the hypertension. The goal of the present study was investigated the possible mechanisms underlying cardiovascular alterations after acute paradoxical sleep deprivation (PSD). Male Wistar rats were assigned in two experimental groups: (1) control and (2) PSD for 24 h using the modified single platform method. Paradoxical sleep deprived rats exhibited higher blood pressure, heart rate (HR) and impaired baroreceptor sensitivity. After pharmacological autonomic double blockade (propranolol and methylatropine administration), intrinsic heart rate was decreased after PSD. The PSD rats showed a reduction in the vagal tone without affecting sympathetic tone. Isoproterenol administration (0.001, 0.01 and 1 µg/kg) induced an increase in ΔHR responses in PSD group. Electrocardiographic analysis in response to β-adrenergic stimulation indicated that PSD contributed to ventricular cardiac arrhythmias. Our findings suggest that acute paradoxical sleep loss induce cardiovascular alterations, autonomic imbalance accompanied by impaired baroreflex sensitivity and increased arrhythmia susceptibility.

Reflexes from pulmonary arterial baroreceptors in dogs: interaction with carotid sinus baroreceptors

In contrast to the reflex vasodilatation occurring in response to stimulation of baroreceptors in the aortic arch, carotid sinuses and coronary arteries, stimulation of receptors in the wall of pulmonary arteries results in reflex systemic vasoconstriction. It is rare for interventions to activate only one reflexogenic region, therefore we investigated how these two types of reflexes interact. In anaesthetized dogs connected to cardiopulmonary bypass, reflexogenic areas of the carotid sinuses, aortic arch and coronary arteries and the pulmonary artery were subjected to independently controlled pressures. Systemic perfusion pressure (SPP) measured in the descending aorta (constant flow) provided an index of systemic vascular resistance. In other experiments, sympathetic efferent neural activity was recorded in fibres dissected from the renal nerve (RSNA). Physiological increases in pulmonary arterial pressure (PAP) induced significant increases in SPP (+39.1 ± 10.4 mmHg) and RSNA (+17.6 ± 2.2 impulses s(−1)) whereas increases in carotid sinus pressure (CSP) induced significant decreases in SPP (−42.6 ± 10.8 mmHg) and RSNA (−42.8 ± 18.2 impulses s(−1)) (P < 0.05 for each comparison; paired t test). To examine possible interactions, PAP was changed at different levels of CSP in both studies. With CSP controlled at 124 ± 2 mmHg, the threshold, 'set point' and saturation pressures of the PAP–SPP relationship were higher than those with CSP at 60 ± 1 mmHg; this rightward shift was associated with a significant decrease in the reflex gain. Similarly, increasing CSP produced a rightward shift of the PAP–RSNA relationship, although the effect on reflex gain was inconsistent. Furthermore, the responses to changes in CSP were influenced by setting PAP at different levels; increasing the level of PAP from 5 ± 1 to 33 ± 3 mmHg significantly increased the set point and threshold pressures of the CSP–SPP relationship; the reflex gain was not affected. These results indicate the existence of interaction between pulmonary arterial and carotid sinus baroreceptor reflexes; physiological and pathological states that alter the stimulus to one may alter the reflex responses from the other.

Cellular and molecular biomechanics

Cells exist in a mechanical environment and must be able to elicit an appropriate response to strains evoked by fluid flow, compression, pressure and stretch. The ability to detect a range of forces (from 10−4 through to 104 N m−2, reflecting a faint sound and aortic pressure, respectively) is vital in order to elicit the appropriate cascade of molecular events that facilitate the physiological processing of sensory information. The detection of mechanical strain is mediated by mechano-sensitive components of cells and is a property of a wide range of tissue types. Mechanosensors in the cells of the skin and ear are critical for processing information about touch and hearing, while other mechanosensors respond to blood pressure (baroreceptors), muscle stretch (spindle receptors) and limb positions (proprioceptors). Bone tissue detects mechanical stress, and this informs the bone remodeling process, while endothelial cells lining blood vessels respond to shear stress evoked by fluid flow to initiate vascular remodeling. The ability to respond to mechanical stimuli also regulates fundamental cellular events such as proliferation, cell spreading, differentiation, motility and the maintenance of cell shape. The precise cellular mechanisms underlying mechanosensation remain to be fully resolved, but in recent years a number of surface proteins have been identified that serve a role as mechanoreceptors. Biological systems have evolved a complex array of mechanoreceptors to transduce force into an electrical and/or intracellular biochemical cascade. Such signaling pathways are intricately linked with cellular responsiveness and adaptation to mechanical stimulation.

Neural Reflex Hypotension Induced by Very Small Dose of Hypertonic NaCl Solution in Rats

Although the precise mechanisms of transient hypotension after intravenous infusion of hypertonic saline (HTS) are not yet clarified, a rapid infusion of HTS is widely used as the initial therapy of hypovolemia. We investigated the effect of the intravenous infusion of a small dose of 0.97-9.7% NaCl solutions in anesthetized rats. Intravenous infusion of HTS at a rate of 0.3 ml/kg/min for 1 min produced the transient hypotension lasting for several minutes. The depressor response to HTS was not abolished by bilateral cervical vagotomy. The HTS infusion into the femoral vein evoked the depressor response with a larger magnitude and a shorter latency than that into the aortic arch. While the arterial baroreceptor pressure was kept constant at the baseline level of systemic arterial pressure, HTS-induced hypotension was significantly augmented. The gain factor of the arterial baroreflex was reduced by intravenous HTS. Pretreatment with bretylium tosylate completely abolished the depressor response without affecting the baseline level of arterial pressure. These results suggest that the depressor response to the very small dose of intravenous HTS is the sympathosympathetic neural reflex with cardiopulmonary afferents and vasomotor efferents.

Muscle Sympathetic Nerve Activity Averaged Over 1 Minute Parallels Renal and Cardiac Sympathetic Nerve Activity in Response to a Forced Baroreceptor Pressure Change

Despite the accumulated knowledge of human muscle sympathetic nerve activity (SNA) as measured by microneurography, whether muscle SNA parallels renal and cardiac SNAs remains unknown. In experiment 1, muscle (microneurography, tibial nerve), renal, and cardiac SNAs were recorded in anesthetized rabbits (n=6) while arterial pressure was changed by intravenous bolus injections of nitroprusside (3 microg/kg) followed by phenylephrine (3 microg/kg). In experiment 2, the carotid sinus region was vascularly isolated in anesthetized, vagotomized, and aorta-denervated rabbits (n=10). The 3 SNAs were recorded while intracarotid sinus pressure was increased stepwise from 40 to 160 mm Hg in 20-mm Hg increments maintained for 60 seconds each. Muscle SNA averaged over 1 minute was well correlated with renal (r=0.96+/-0.01, mean+/-SE) and cardiac (r=0.96+/-0.01) SNAs in experiment 1 (baroreflex closed-loop condition) and also with renal (r=0.97+/-0.01) and cardiac (r=0.97+/-0.01) SNAs in experiment 2 (baroreflex open-loop condition). Muscle SNA averaged over 1 minute parallels renal and cardiac SNAs in response to a forced baroreceptor pressure change.

A derivative-sigmoidal model reproduces operating point-dependent baroreflex neural arc transfer characteristics.

A cascade model comprised of a derivative filter followed by a nonlinear sigmoidal component reproduces the input size dependence of transfer gain in the baroreflex neural arc from baroreceptor pressure input to efferent sympathetic nerve activity (SNA). We examined whether the same model could predict the operating point dependence of the baroreflex neural arc transfer characteristics estimated by a binary white noise input. In eight anesthetized rabbits, we isolated bilateral carotid sinuses from the systemic circulation and controlled intracarotid sinus pressure (CSP). We estimated the linear transfer function from CSP to SNA while varying mean CSP among 70, 100, 130, and 160 mmHg (P(70), P(100), P(130), and P(160), respectively). The transfer gain at 0.01 Hz was significantly smaller at P(70) (0.61 +/- 0.26) and P(160) (0.60 +/- 0.25) than at P(100) (1.32 +/- 0.42) and P(130) (1.36 +/- 0.45) (in arbitrary units/mmHg; means +/- SD; P < 0.05). In contrast, transfer gain values above 0.5 Hz were similar among the protocols. As a result, the slope of increasing gain between 0.1 and 0.5 Hz was significantly steeper at P(70) (17.6 +/- 3.6) and P(160) (14.1 +/- 4.3) than at P(100) (8.1 +/- 4.4) and P(130) (7.4 +/- 6.6) (in dB/decade; means +/- SD; P < 0.05). These results were consistent with those predicted by the derivative-sigmoidal model, where the deviation of mean input pressure from the center of the sigmoidal nonlinearity reduced the transfer gain mainly in the low-frequency range. The derivative-sigmoidal model functionally reproduces the dynamic SNA regulation by the arterial baroreflex over a wide operating range.

Bezold-Jarisch Reflex Blunts Arterial Baroreflex via the Shift of Neural Arc toward Lower Sympathetic Nerve Activity

Although the Bezold-Jarisch (BJ) reflex is potentially evoked during acute myocardial ischemia or infarction, its effects on the static characteristics of the arterial baroreflex remain to be analyzed in terms of an equilibrium diagram between the neural and peripheral arcs. The neural arc represents the static input-output relationship between baroreceptor pressure input and efferent sympathetic nerve activity (SNA), whereas the peripheral arc represents that between SNA and arterial pressure (AP). In 8 anesthetized rabbits, we increased carotid sinus pressure stepwise from 40 to 160 mmHg in increments of 20 mmHg at one-minute intervals while measuring renal SNA and AP under control conditions and during the activation of the BJ reflex by intravenous administration of phenylbiguanide (PBG, 100 microg.kg(-1).min(-1)). The neural arc approximated a sigmoid curve whereas the peripheral arc approximated a straight line. PBG decreased AP at the operating point from -91.3 +/- 2.4 to -71.7 +/- 3.1 mmHg (P < 0.01), and attenuated the total loop gain at the operating point from -1.31 +/- 0.44 to -0.51 +/- 0.14 (P < 0.05). The equilibrium diagram indicated that PBG caused a parallel shift of the neural arc toward lower SNA such that the maximum SNA was reduced to approximately 60% of control. PBG decreased neural and peripheral arc gains at the operating point to approximately 43% and 77%, respectively. In conclusion, the BJ reflex blunts arterial baroreflex via the shift of the neural arc toward lower SNA.

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.

Carotid-sinus baroreflex modulation of core and skin temperatures in rats: an open-loop approach.

The neural mechanisms of the thermoregulatory control of core and skin temperatures in response to heat and cold stresses have been well clarified. However, it has been unclear whether baroreceptor reflexes are involved in the control of core and skin temperatures. To investigate how the arterial baroreceptor reflex modulates the body temperatures, we examined the effect of pressure changes of carotid sinus baroreceptors on core and skin temperatures in halothane-anesthetized rats. To open the baroreflex loop and control arterial baroreceptor pressure (BRP), we cut vagal and aortic depressor nerves and isolated carotid sinuses. We sequentially altered BRP in 20-mmHg increments from 60 to 180 mmHg and then in 20-mmHg decrements from 180 to 60 mmHg while measuring systemic arterial pressure (SAP), heart rate (HR), and core blood temperature (T(core)) at the aortic arch and skin temperature (T(skin)) at the tail. In response to the incremental change in BRP by 120 mmHg, SAP, HR, and T(core) fell by 90.3 +/- 5.1 mmHg, 60.3 +/- 10.5 beats min(-1), and 0.18 +/- 0.01 degrees C, respectively. T(skin) rose by 0.84 +/- 0.10 degrees C. The maximum rate of change per unit BRP change was -2.1 +/- 0.2 for SAP, -1.5 +/- 0.4 beats min(-1) mmHg(-1) for HR, -0.003 +/- 0.001 degrees C mmHg(-1) for T(core), and 0.011 +/- 0.002 degrees C mmHg(-1) for T(skin). After the administration of hexamethonium or bretylium, these baroreflexogenic responses were completely abolished. We concluded that T(core) and T(skin) are modulated by the arterial baroreceptor reflex.

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.

Estimation of baroreflex gain using a baroreflex equilibrium diagram.

Two types of closed-loop perturbations can be applied to the arterial baroreflex system. The first (P(D1)) is introduced into the baroreceptors without a direct effect on arterial pressure (AP), whereas the second (P(D2)) initially affects AP. Neck suction and hemorrhage are examples of P(D1) and P(D2), respectively. To estimate the baroreflex open-loop gain (G(Baro)) without knowing the absolute magnitudes of P(D1) and P(D2), we explored a new strategy to estimate G(Baro) by combining P(D1) and P(D2) in a baroreflex equilibrium diagram. In this diagram, the neural arc presents the input-output relationship between baroreceptor pressure input and sympathetic nerve activity (SNA). The peripheral arc presents the input-output relationship between SNA and AP. In 8 anesthetized rabbits, we estimated G(Baro) by multiplying the slopes of the peripheral arc determined from P(D1) and the neural arc determined from P(D2). We also estimated G(Baro) by a conventional open-loop analysis. The G(Baro) values estimated by the equilibrium diagram and the open-loop analysis showed a positive correlation (y = 0.80x + 0.22, r(2) = 0.95) and a standard error of estimate of 0.21 across the animals. We conclude that G(Baro) was estimated well by combining P(D1) and P(D2) in the equilibrium diagram.

Absence of early resetting of coronary baroreceptors in anaesthetized dogs.

1. Both carotid and aortic arch baroreceptors have been shown to reset after as little as 20 min exposure to a different conditioning pressure; the mid-point of the stimulus-response curve is displaced towards the conditioning pressure. 2. Coronary baroreceptors operate over much lower pressures and induce slower reflex vasoconstriction than the other baroreceptors and this investigation was designed to determine whether their resetting characteristics are also different. 3. In chloralose anaesthetized dogs, a perfusion circuit allowed independent control of pressures distending carotid, aortic and coronary baroreceptors. Stimulus-response curves were obtained for carotid and coronary baroreceptors after maintaining the distending pressure at 60 or 180 mmHg for 20 min. 4. Neither the magnitude of the responses nor the baroreceptor pressure corresponding to 50 % of the response (BP50) of the coronary curves was changed by the conditioning regime. In contrast, conditioning carotid baroreceptors with the same regime produced significant shifts in the BP50 towards the conditioning pressure. 5. No changes were obtained after conditioning the coronary baroreceptors at 60 or 120 mmHg for 40 min. 6. These results confirm early resetting of carotid baroreceptors but show that coronary baroreceptors do not reset over a period of at least 40 min.