The effects of changes of extramural, `intrathoracic', pressure on aortic arch baroreceptors

1. The isolated aortic arch was perfused by a method enabling the mean pressure, pulse pressure and pulse frequency to be varied independently. The preparation was also subjected to phasic and non-phasic changes of extramural pressure.2. The aortic arch baroreceptor impulse activity in single or few-fibre preparations was increased by raising the intra-aortic pressure and by applying a negative extramural pressure at constant intra-aortic pressure.3. Curves relating impulse frequency and negative extramural pressure were similar to those relating impulse frequency to intra-aortic pressure. The effective stimulus to the aortic arch baroreceptors is the transmural pressure resulting from the algebraic difference of the intra-aortic and extramural pressures.4. Rhythmical alterations in extramural pressure caused phasic changes in baroreceptor impulse activity. As the pressure became more negative, the impulse frequency increased and other baroreceptors were recruited.5. During pulsatile perfusion of the aortic arch the maximum impulse activity occurred when the negative phase of extramural pressure coincided with the systolic phase of the perfusion pressure.6. These findings are discussed in relation to the effects of changes of intrathoracic pressure on aortic baroreceptor activity in vivo     

The effects of altering mean pressure, pulse pressure and pulse frequency on the impulse activity in baroreceptor fibres from the aortic arch and right subclavian artery in the rabbit

1. A method is described for perfusing an isolated preparation of the rabbit aortic arch with independently controlled mean pressure, pulse pressure and pulse frequency.

2. Recordings made from single or few-fibre preparations from the aortic arch and right subclavian baroreceptor regions show that the number of impulses per second or per cycle in a single fibre is the same during pulsatile perfusion as during non-pulsatile perfusion if the pressure is above the threshold pressure to non-pulsatile perfusion during all phases of the pressure cycle.

3. In multi-fibre recordings the total number of impulses is greater during pulsatile perfusion than during non-pulsatile perfusion due largely to recruitment of fibres during systole.

4. The relationship between instantaneous impulse frequency and aortic arch pressure during one pressure cycle forms an elliptiform curve.

5. Increasing the pulse pressure increases the ellipse and causes additional recruitment of other fibres during systole, thus augmenting the total impulse activity.

6. Increasing the pulse frequency reduces the number of impulses per cycle for single fibres but produces a small increase in the total impulse frequency in one second period due to recruitment.

7. Increasing the rate of change of pressure by increasing the pulse pressure or pulse frequency produced a small reduction or no change of the threshold pressure. Similarly the `cut off' pressure was elevated in some fibres.

8. At low initial mean pressures, an increment of pressure, at constant pulse pressure and pulse frequency, increases the total impulse activity by increasing the frequency of impulses in single fibres already active during systole and diastole and by additional recruitment of other fibres. At higher mean pressures there is little increase in impulse activity as the maximum frequency of fibres is attained or superseded and there is little recruitment.

     

Comparison of the reflex vasomotor responses to separate and combined stimulation of the carotid sinus and aortic arch baroreceptors by pulsatile and non-pulsatile pressures in the dog

1. In the anaesthetized dog the carotid sinuses and aortic arch were isolated from the circulation and separately perfused with blood by a method which enabled the mean pressure, pulse pressure and pulse frequency to be varied independently in each vasosensory area. The systemic circulation was perfused at constant blood flow by means of a pump and the systemic venous blood was oxygenated by an extracorporeal isolated pump-perfused donor lung preparation.2. When the vasosensory areas were perfused at non-pulsatile pressures within the normal physiological range of mean pressures, the reflex reduction in systemic vascular resistance produced by a given rise in mean carotid sinus pressure was significantly greater than that resulting from the same rise of aortic arch pressure.3. On the other hand, when the vasosensory areas were perfused at normal pulsatile pressures and within the normal physiological range of mean pressures, there was no difference in the size of the reflex vascular responses elicited by the same rise in mean pressure in the carotid sinuses and in the aortic arch.4. Whereas the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in pulse pressure, those evoked by the aortic arch baroreceptors through changes of mean pressure are only weakly affected by modifications in pulse pressure. Evidence for this was obtained from single stepwise changes of mean pressure in each vasosensory area during pulsatile and non-pulsatile perfusion, and from curves relating the mean pressure in the carotid sinuses or aortic arch and systemic arterial perfusion pressure.5. The vasomotor response elicited by combined stimulation of the carotid sinus and aortic arch baroreceptors was greater than either response resulting from their separate stimulation.6. When the mean perfusion pressures in the two vasosensory areas are changed together, the curve relating mean pressure to systemic arterial pressure during pulsatile perfusion of the areas is considerably flatter than that for non-pulsatile perfusion.7. Increasing the pulse pressure in the carotid sinuses or aortic arch caused a decrease in systemic vascular resistance, the response elicited from the carotid sinuses being the larger.8. Altering the phase angle between the pulse pressure waves in the carotid sinuses and aortic arch had no effect on systemic vascular resistance.9. In both vasosensory areas, increasing the pulse frequency caused a reduction in systemic vascular resistance.     

Reflex discharge patterns of cardiac vagal efferent fibres

1. Unit activity was recorded from single and few fibre preparations in a cardiac branch of the right vagus nerve of the cat.2. Increases in blood pressure mediated solely by the right carotid sinus nerve produced bradycardia when all other nerves to the heart had been cut. Myelinated fibres in the cardiac branch of the right vagus nerve were reflexly activated by the same procedure.3. The fibres were silent when blood pressure was below 140-150 mm Hg. As the pressure began to rise, they discharged phasically with the cardiac cycle. At pressures greater than 180 mm Hg, the discharge was continuous attaining maximum rates of 40/sec.4. Stimulation of carotid body chemoreceptors also reflexly excited these fibres, as did stimulation of baroreceptors in both the left carotid sinus and aortic arch. Afferent fibres in the left vagus discharging in response to changes in blood pressure reflexly excited the cardiac efferent fibres. Increases in phrenic motoneurone discharge coincided with inhibition of these fibres. Electrical stimulation of the glossopharyngeal nerve also produced inhibition.     

Inotropic responses of the left ventricle to changes in aortic arch pressure in anaesthetized dogs

1. Inotropic changes in the left ventricle in chloralose anaesthetized dogs were determined in response to changes in non-pulsatile pressure perfusing the vascularly isolated aortic arch.2. Inotropic responses were assessed by measuring the maximum rate of change of left ventricular pressure (dP/dt max) in preparations in which heart rate, mean ascending aortic pressure and brachiocephalic (i.e. carotid sinus and cerebral) perfusion pressure were held constant.3. dP/dt max increased (average +43%) when aortic pressure was reduced from a level above that which produced maximum depression of the myocardium to a level below which no further responses could be obtained; responses occurred as aortic arch pressure was changed between 250 and 90 mm Hg.5. In the same preparations changes in the brachiocephalic artery perfusion pressure with aortic arch pressure held constant resulted in similar inotropic responses.6. It is suggested that aortic arch baroreceptors may be of importance in the control of the inotropic state of the heart.     

The influence of heart rate on baroreceptor fibre activity in the carotid sinus and aortic depressor nerves of the rabbit

The arterial baroreceptors and their afferent fibres provide the sensory arm of the reflex that regulates systemic arterial pressure. We have examined whether the relationship between mean baroreceptor discharge and mean arterial pressure is altered when heart rate changes. Experiments were performed on pentobarbitone-anaesthetized rabbits. We recorded the activity of single and multifibre preparations of the carotid sinus (CSN) and aortic depressor nerves (ADN). Data were collected under control conditions and while heart rate was increased by approximately 30-35% by right atrial pacing. Baroreceptor regions were exposed to ramps of pressure (from approximately 25 to 140 mmHg, at approximately 0.5-1 mmHg s(-1)), generated by inflation and deflation of cuffs placed around the inferior vena cava and descending thoracic aorta. Response curves relating baroreceptor discharge to mean pressure were constructed and fitted with third-order polynomial expressions. To provide a measure of an effect of an increase in heart rate on the response curve in the region of the normal operating pressure, we calculated the position of the test response curve relative to the position of the control curve at 90 mmHg (deltaBP(90)). For the ADN, the activity of single fibres (presumptive myelinated fibres) was unaffected by increasing heart rate (deltaBP(90) = +0.1 +/- 1.0 mmHg), while single fibres in the CSN showed a small increase in activity (deltaBP(90) = -1.5 +/- 0.3 mmHg). In multifibre preparations there was a small increase in activity that may be attributable to additional activity in unmyelinated fibres (ADN, deltaBP(90) = -3.4 +/- 1.2 mmHg; CSN, deltaBP(90) = -5.2 +/- 0.9 mmHg). We conclude that the mean discharge of arterial baroreceptors remains a reliable index of mean arterial pressure in the presence of substantial changes in heart rate.     

The KCNQ/M-current modulates arterial baroreceptor function at the sensory terminal in rats

The ion channels responsible for the pattern and frequency of discharge in arterial baroreceptor terminals are, with few exceptions, unknown. In this study we examined the contribution of KCNQ potassium channels that underlie the M-current to the function of the arterial baroreceptors. Labelled aortic baroreceptor neurons, immunohistochemistry and an isolated aortic arch preparation were used to demonstrate the presence and function of KCNQ2, KCNQ3 and KCNQ5 channels in aortic baroreceptors. An activator (retigabine) and an inhibitor (XE991) of the M-current were used to establish a role for these channels in setting the resting membrane potential and in regulating the response to ramp increases in arterial pressure. Retigabine raised the threshold for activation of arterial baroreceptors and shifted the pressure–response curve to higher aortic pressures. XE991, on the other hand, produced an increase in excitability as shown by an increase in discharge at elevated pressures as compared to control. We propose that KCNQ2, KCNQ3 and KCNQ5 channels provide a hyperpolarizing influence to offset the previously described depolarizing influence of the HCN channels in baroreceptor neurons and their terminals.     

Reflex vascular responses to changes in left ventricular pressures, heart rate and inotropic state in dogs.

Dogs were anaesthetized with chloralose, artificially ventilated and the chests widely opened. Left ventricular mechanoreceptors, including those in or near the coronary arteries, were stimulated by changing the pressure in the aortic root. The pressures distending the left atrium and the aortic and carotid baroreceptors were controlled. Reflex vascular responses were assessed from changes in perfusion pressures to a hind limb and to the rest of the systemic circulation, which were perfused independently at constant flows. Physiological increases in peak left ventricular and coronary arterial pressures resulted in vasodilatation in both regions. These responses were not influenced by changes in the heart rate. Stimulation of the left cardiac sympathetic nerves resulted in increases in peak ventricular pressure and in the maximal rate of change of pressure (dP/dtmax). This also resulted in increases in perfusion pressures (vasoconstriction) at all levels of peak ventricular pressure although there was little effect on the responses to changes in ventricular pressure. Sympathetic stimulation had little effect on the relationship between perfusion pressures and aortic root pressure. Increases in ventricular filling also resulted in vasoconstriction at all levels of peak ventricular pressure. Increases in filling, however, did not affect the relationship between either perfusion pressure and aortic root pressure. Conversely, decreases in left ventricular filling, by bypassing some of the left atrial blood, resulted in vasodilatation at all levels of peak ventricular pressures but had no effect on the perfusion pressures at any aortic root pressure. The combination of sympathetic stimulation with decreased ventricular filling resulted in little effect on perfusion pressures or on their responses to changes in either aortic root or ventricular systolic pressures. We conclude that the vascular responses to stimulation of left ventricular mechanoreceptors are not enhanced by sympathetic stimulation, decreases in ventricular filling or the combination of the two. The apparent effects of each of these interventions alone on the relationships between perfusion pressures and ventricular, but not aortic root, pressure, could be explained if the receptors responsible were sensitive more to changes in aortic root and coronary arterial pressures than to pressure changes in the ventricle itself.     

Effects of graded pulsatile pressure on the reflex vasomotor responses elicited by changes of mean pressure in the perfused carotid sinus-aortic arch regions of the dog

1. In the anaesthetized dog, the carotid sinuses and aortic arch were isolated from the circulation and separately perfused with blood by a method which enabled the mean pressure, pulse pressure and pulse frequency to be varied independently in each vasosensory area. The systemic circulation was perfused at constant blood flow by means of a pump and the systemic venous blood was oxygenated by an extracorporeal isolated pump-perfused donor lung preparation.2. We have confirmed our previous observations that under steadystate conditions the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in carotid sinus pulse pressure, whereas those evoked by changes of mean aortic arch pressure are only weakly affected by modifications of aortic pulse pressure.3. When the carotid sinus and aortic arch regions are perfused in combination at constant pulse frequency (110 c/min), the relationship between mean carotid sinus-aortic arch pressure and systemic arterial perfusion pressure is dependent on the size of the pulse pressure.4. Increasing the pulse pressure alters the curve relating the mean carotid sinus-aortic arch pressure to systemic arterial perfusion pressure in such a way that the perfusion pressure is lower at a given carotid sinus-aortic arch pressure within the range 80-150 mm Hg. The larger the pulse pressure, up to about 60 mm Hg, the greater the fall in systemic arterial perfusion pressure. Above a mean carotid sinus-aortic arch pressure of about 150 mm Hg, alterations of pulse pressure have little effect.5. There is a family of curves representing the relation between mean carotid sinus-aortic arch pressure and systemic vascular resistance, depending on the pulse pressure.     

Resetting of aortic baroreceptors with non-myelinated afferent fibers in spontaneously hypertensive rats

The phenomenon of resetting and the possible mechanisms responsible for it were investigated in aortic baroreceptors having unmyelinated axons. Recordings were obtained from 31 aortic baroreceptor C-fibers in 20 normotensive Wistar Kyoto rats (WKY) and 37 baroreceptor C-fibers in 11 spontaneously hypertensive rats (SHR). The recordings were obtained from the left aortic nerve of an in vitro aortic nerve-aortic arch preparation. The thresholds for activation of baroreceptor C-fibers were not different between SHR's and WKY's at 16 weeks of age (139±7 and 133±5 mmHg, respectively). However, the thresholds for activation in SHR at 36 weeks of age were considerably higher (163±4 mmHg) indicating resetting of the receptors in the older rats. The pressure-discharge curves were not different between SHR's and WKY's at 16 weeks of age and WKY's at 35 weeks of age, but were shifted to the right for SHR's at 36 weeks of age. The receptors showed greater responses to pulsatile pressures than to steady state pressures at the same mean level of pressure. We found that aortic C-fibers were not reset during the early established phase of hypertension in SHR's because of enhanced receptor strain sensitivity. This is likely to be of importance for tonic vasomotor control at this time. In later stages of hypertension and despite enhanced strain sensitivity the endings were reset to higher pressures probably due to an increased collagen content in the aortic wall.     

Influence of intravenous saline infusion on the aortic baroreceptor and left atrial B-type receptor activity in dogs

Influence of i.v. saline infusion on aortic arch pressure, left atrial mean pressure, heart rate, and the time-related characteristics of aortic arch baroreceptor and left atrial B-type receptor activities were studied in 20 beagle dogs. Saline infusion induced tachycardia in 10 dogs and bradycardia in 10. Aortic arch and left atrial pressures increased in both HR response groups. The average discharge rate of baroreceptors increased in both HR response groups, while the duration of baroreceptor burst, the number of baroreceptor action potentials/heart cycle and the average burst frequency did not increase significantly in the group that responded with tachycardia but increased significantly in the group that responded with bradycardia. The number of left atrial B-type action potentials/heart cycle, the average discharge rate and average burst frequency increased in both HR response groups. We conclude that the duration of baroreceptor burst, baroreceptor average burst frequency and the number of baroreceptor impulses/cardiac cycle are the important parameters eliciting baroreceptor reflex to i.v. saline infusion.     

A comparison of the stimulus-response curves of aortic and carotid sinus baroreceptors in decerebrated cats

Recordings of total nerve activity suggested differences in the sensitivities and working ranges between aortic and carotid sinus baroreceptors. This result however, conflicts with single fibre studies from isolated receptor zones. Thus it appeared of some interest to compare the function curves of aortic and carotid sinus baroreceptors in the intact animal.This was achieved by comparing the response characteristics of two groups of aortic and carotid sinus baroreceptors in decerebrated cats. One smaller group consisted of 11 receptor pairs, each member of the pair being studied simultaneneously in the same cat, and a larger group consisting of 98 aortic and 49 carotid sinus baroreceptors studied independently of each other.The response of each receptor to wide pressure variations was recorded by inflating and deflating an intraaortic catheter tip balloon. Function curves were derived by plotting receptor discharge in terms of spikes per second against mean aortic pressure. No significant differences were found either in the slope of the function curves or their mean pressures at minimum activity, the latter appearing to be set by the working blood pressure level.Thus it was concluded that aortic and carotid sinus baroreceptors differ neither in their sensitivities nor in their working ranges when in their physiological environment.The support of the Deutsche Forschungsgemeinschaft through the Sonderforschungsbereich 30, Kardiologie Düsseldorf is gratefully acknowledged     

Mechanisms for activation of aortic baroreceptor C-fibres in rabbits and rats.

In an earlier study, we examined the pressure-response characteristics of rat aortic baroreceptors with C-fibre (non-medullated) afferents. Compared with aortic baroreceptor fibres with A-fibre (medullated) afferents, the C-fibres were activated at higher pressures and discharged more irregularly when stimulated with a steady level of pressure. Here we examine the relationship between discharge and the aortic diameter in these two types of afferents in rats and rabbits. An in vitro aortic arch/aortic nerve preparation was used to record single-fibre activity simultaneously with aortic arch pressure and diameter. Diameter was measured using a highly sensitive non-contact photoelectric device. Baroreceptor discharge was characterized by stimulating the nerve endings with either slow pressure ramps from subthreshold to 200-250 mmHg, at a rate of rise of 2 mmHg s-1, or pressure steps from subthreshold to suprathreshold levels, at amplitudes of 110-180 mmHg. In response to these inputs, C-fibres in rabbits (conduction velocities= 0.8-2.2 m s-1) behaved much like those in rats. The C-fibres had significantly higher pressure thresholds (95 +/- 3 mmHg vs. 53 +/- 2 mmHg; mean +/- SEM), lower threshold frequencies (2.4 +/- 0.5 vs. 27.7 +/- 1.8 spikes s-1), lower maximum discharge frequencies (22.7 +/- 2.3 vs. 65 +/- 5.8 spikes s-1) and more irregular discharge in response to a pressure step when compared with A-fibres (conduction velocities of 8-16 m s-1). When plotted against diameter, C-fibre ramp-evoked discharge increased gradually at first, and then rose steeply at increasingly higher ramp pressures where aortic diameter became relatively constant. In contrast, A-fibre discharge was linearly related to diameter over a wide range of pressure. These results suggest two interpretations: (1) The relation between stretch and C-fibre discharge is highly non-linear, with a marked increase in sensitivity at large diameters. (2) C-fibres are stimulated by changes in intramural stress rather than stretch.     

The relationship between aortic baroreceptor activity and arterial pressure is not monotonic

Previous reports indicate that when aortic pressure (AP) falls below the threshold (P _th) for baroreceptor sensitivity, activity in the aortic depressor nerve (ADN) may increase. To quantify and explain this anomalous behaviour, we analysed curves describing the relationship of baroreceptor fibre activity in rabbit left ADN to AP. Data were obtained in anaesthetised New Zealand White rabbits. Occlusion and release of cuffs around the inferior vena cava and descending aorta generated AP ramps (25–140 mmHg). Response curves were obtained for 173 fibres in 26 animals. Thirty percent of curves had a nadir (J-shaped curve), and in 40% activity was always present. In fibres showing activity below P _th, firing was predominantly diastolic, switching to systolic firing at P _th. The unusual behaviour of a substantial fraction of aortic baroreceptors below P _th accounts for the J-shaped response curve of the whole ADN. We suggest that fibres that fire during diastole at pressures below P _th may have sensory endings close to the origin of the left subclavian artery. As a consequence of this anatomical location, low pressures can impose strain on these receptors, which is then relieved by the systolic pulse.     

Characteristics of aortic baroreceptors with non-medullated afferents arising from the aortic arch of rabbits with chronic renovascular hypertension

The characteristics of 47 non-medullated and 54 medullated fibres arising from aortic arches of 6 hypertensive rabbits have been investigated. The threshold for activation of the aortic C-fibres lay between 78 and 190 (mean 122) mmHg. The threshold for activation of 54 medullated aortic baroreceptors in the same animals was from 70 to 140 (mean 109) mmHg. At the awake mean arterial blood pressure (MABP) of these hypertensive rabbits (143 mmHg) all the medullated fibres were active as were 78% of the C-fibres. In contrast in a group of normotensive animals 91% of the medullated and only 28% of the non-medullated fibres were active. Pressure response curves were constructed for 19 C-fibres and 12 medullated fibres from the hypertensive animals. At a MABP of 110 mmHg the firing in the non-medullated fibres was 2.0 Hz as compared with 19.0 Hz in the medullated fibres and at the awake MABP mean firing was 9.0 Hz in the non-medullated fibres and 48.0 Hz in the medullated fibres. The firing at awake MABP was considerably higher in the hypertensives (9.0 Hz) as compared with the normotensives (1.1 Hz). Thus these data indicate that although the aortic C-fibres are reset in chronic hypertension, they are reset less than the medullated aortic baroreceptors from the same animal. It is suggested that arterial baroreceptor C-fibres may have an important role in the tonic control of the circulation in hypertension.     

The aortic arch baroreceptor response to static and dynamic stretches in an isolated aorta-depressor nerve preparation of cats in vitro.

1. The aortic arch baroreceptors of cats were studied in an isolated aortic arch-depressor nerve preparation in vitro to analyse their transmission properties. 2. Sinusoidal length changes of varying amplitudes (0-34-1-2 mm) and frequencies (1-10 Hz) at a given pre-stretch were imposed on the isolated receptor zone to quantitate the velocity sensitivity of these receptors and to test the linearity of the system. 3. The receptor response was evaluated from the spike activity of single fibres of the depressor nerve in number of spikes per stimulus period, average discharge rate, instantaneous frequency, and phase angle between forcing function and instantaneous frequency. 4. The static response is characterized by a threshold, saturation range, and a relatively large linear part between these two non-linearities. 5. The aortic receptors exhibit rate sensitivity. Depending on the stimulus amplitude and frequency the phase angles between the forcing function and the instantaneous frequency ranged from -14 to -68 degrees. 6. The average discharge rate (spikes/sec) is sensitive to stimulus amplitude but not to stimulus frequency at near-threshold operation; in the linear part of the static response curve, the receptor response becomes independent of the stimulus mode. 7. The baroreceptors of the aorta share many properties with other mechanoreceptors of different species and organ systems, particularly with those of the rest of the circulation. They exhibit static and to some degree rate sensitivity and operate physiologically near their thresholds, i.e. the afferent arc of the baroreflexes is highly non-linear.     

经皮穿刺主动脉弓法灌注尸体的解剖学研究

目的研究经皮穿刺主动脉弓法灌注尸体,为尸体防腐灌注提供一种新途径。方法对30具经10%福尔马林防腐固定成尸标本,用穿刺针从胸骨柄上缘点,经皮胸骨后方穿刺到主动脉管弓腔内,测量进针角度和进针深度。结果主动脉弓上下径为(29.5±2.9)mm,前后径(24.0±3.1)mm,主动脉弓长(68.0±12.6)mm。主动脉弓的体表位置:下界平胸骨角中点,上界相当于胸骨柄中部,胸骨柄上缘点向下(26.0±2.0)mm,右侧界约平右第二肋软骨上缘的胸骨柄右缘,左界第二肋软骨上缘,距胸骨柄左缘(15.7±6.8)mm。进针点位于胸骨柄上缘中点,进针角度以胸骨柄中点垂直线为准,穿刺针向后下(39.0±35),至主动脉弓管腔内进针深度为(56.9±6.3)mm。结论经皮穿刺为从胸骨柄上缘中点进针,针尖穿入主动脉弓管腔内,注入尸体防腐固定液固定尸体。     

The function of baroreceptor C fibres in the rabbit's aortic nerve

The participation of aortic nerve C fibers in the baroreflex was investigated by recording changes in renal nerve activity in response to acute increases in arterial pressure, in two experimental situations: with the A and C fibres of the aortic nerve intact, and with the A fibres temporarily blocked by a hyperpolarizing current (anodal block). Pressure was increased by manual inflation of an intra-aortic balloon, and interference from other barorecptor areas was avoided by carotid occlusion and sectioning of the right aortic nerve. Rises in mean arterial pressure exceeding 20 mmHg, to levels above 110 mmHg, were needed to trigger sympathetic inhibition via C fibres. A rise of 45 mmHg caused 50% reduction in sympathetic activity, equal to that obtained by stimulation of aortic nerve C fibres at about 3 Hz. In contrast, a rise of 20-30 mmHg evoked more than 60% reduction in sympathetic activity when the A fibres were operative. Judged by these studies of peak reflex responses to brief pressure rises, baroreceptors with C fibres in the aortic nerve have a much higher threshold to pressure than their myelinated counterpart; the C fibres contribute to the baroreflex inhibition sympathetic discharge only when pressure is increased well above normal resting levels.     

Mechanisms for activation of aortic baroreceptor C-fibres in rabbits and rats

In an earlier study, we examined the pressure–response characteristics of rat aortic baroreceptors with C-fibre (non-medullated) afferents. Compared with aortic baroreceptor fibres with A-fibre (medullated) afferents, the C-fibres were activated at higher pressures and discharged more irregularly when stimulated with a steady level of pressure. Here we examine the relationship between discharge and the aortic diameter in these two types of afferents in rats and rabbits. An in vitro aortic arch/aortic nerve preparation was used to record single-fibre activity simultaneously with aortic arch pressure and diameter. Diameter was measured using a highly sensitive non-contact photoelectric device. Baroreceptor discharge was characterized by stimulating the nerve endings with either slow pressure ramps from subthreshold to 200–250 mmHg, at a rate of rise of 2 mmHg s^?1, or pressure steps from subthreshold to suprathreshold levels, at amplitudes of 110–180 mmHg. In response to these inputs, C-fibres in rabbits (conduction velocities= 0.8–2.2 m s^?1) behaved much like those in rats. The C-fibres had significantly higher pressure thresholds (95 ± 3 mmHg vs. 53 ± 2 mmHg; mean ± SEM), lower threshold frequencies (2.4 ± 0.5 vs. 27.7 ± 1.8 spikes s^?1), lower maximum discharge frequencies (22.7 ± 2.3 vs. 65 ± 5.8 spikes s^?1) and more irregular discharge in response to a pressure step when compared with A-fibres (conduction velocities of 8–16 m s^?1). When plotted against diameter, C-fibre ramp-evoked discharge increased gradually at first, and then rose steeply at increasingly higher ramp pressures where aortic diameter became relatively constant. In contrast, A-fibre discharge was linearly related to diameter over a wide range of pressure. These results suggest two interpretations: (1) The relation between stretch and C-fibre discharge is highly non-linear, with a marked increase in sensitivity at large diameters. (2) C-fibres are stimulated by changes in intramural stress rather than stretch.     

The effect of baroreceptors on the latency of evoked responses in sympathetic nerves during the cardiac cycle

1. A rapid increase in pressure in a vascularly isolated perfused carotid sinus has been shown to inhibit a reflex response in efferent sympathetic nerves of the dog evoked by electrical stimulation of the radial nerve.2. In intact preparations with the carotid baroreceptors innervated, the mean latency and the variance of the latency of reflex sympathetic nerve responses was reduced when the stimuli evoking the responses were applied at one point of both cardiac and respiratory cycles. When the baroreceptors were denervated there were no significant differences in the responses to random and synchronized stimuli.3. In intact preparations the latency of evoked responses in sympathetic nerves was found to vary progressively during a cardiac cycle; the maximum increase in latency was observed with the responses that occurred at that phase of the cardiac cycle when the baroreceptors exert maximal inhibition on spontaneous sympathetic activity. After denervation of the carotid sinuses a much smaller change during the cardiac cycle was still present, possibly due to effects produced by baroreceptors of the aortic arch and elsewhere.4. It was concluded that changes in baroreceptor activity, due to beat to beat fluctuations of the systemic arterial pressure are a major factor causing variations in the latency of responses in sympathetic nerves evoked by stimuli applied to a cutaneous nerve.