Adrenergic and pressure-induced modulation of carotid sinus baroreceptors in rabbit

The sympathetic control of the carotid sinus baroreceptor activity was studied in rabbits. Stimulation of the cervical sympathetic trunk (10 Hz, 1 ms, 4–12 V) elicited an increase in discharge frequency of the non-medullated baroreceptor afferents but not of the medullated fibers. An isolated carotid sinus area preparation was used to examine the influence of noradrenaline perfusion on baroreceptor activity. Non-medullated baroreceptor afferents, but not the medullated afferents, responded to noradrenaline perfusion (10^-6 g/ml) with a significant increase in firing rate. Short-term resetting of the baroreceptors was also studied with the same preparation. After perfusing the sinus at a hypertensive level for 30 min the pressure-response curves of both the non-medullated and the medullated baroreceptor afferents shifted to the right with increased thresholds and decreased maximal discharge frequencies. The extent of the short-term resetting was greater in non-medullated afferents than in medullated ones. It is concluded that the carotid sinus baroreceptors with non-medullated afferents are under the sympathetic control. The physiological significance of this is discussed.     

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 influence of cardiopulmonary receptors on long-term blood pressure control and plasma renin activity in conscious dogs

The isolated and combined influence of cardiopulmonary and arterial baroreceptor denervation on long-term blood pressure (MAP), heart rate (HR), plasma volume (PV) and plasma renin activity (PRA) was studied in 10 conscious, chronically instrumented foxhounds receiving a normal sodium diet. Cardiopulmonary denervation was achieved by surgically stripping both thoracic vagi. Near complete arterial baroreceptor denervation, leaving most cardiopulmonary fibres intact, was made by left vagal deafferentiation which has been shown to eliminate most aortic baroreceptor afferents, and a carotid sinus denervation. Five groups were studied: (I) control (n = 9), (II) cardiopulmonary denervation (n = 5), (III) aortic baroreceptor denervation (n = 5), (IV) arterial baroreceptor denervation (n = 4) and (V) total denervation (n = 6). No changes in PV were observed. Only group V revealed significantly higher levels of MAP (119.5 +/- 5.4 vs. 100.1 +/- 1.6 mmHg; P less than 0.05), HR (118.1 +/- 4.4 vs. 87.8 +/- 3.7 beats min-1; P less than 0.001) and PRA (3.0 +/- 0.8 vs. 0.9 +/- 0.2 ng AI m-1 h-1; P less than 0.05). It is suggested that the isolated function of either cardiopulmonary or arterial baroreceptors is sufficient to maintain these variables at a normal level. Contrary to the results of other reports the cardiopulmonary receptors do not seem to regulate MAP at a level about which the arterial baroreceptors operate. When both groups of afferents were interrupted MAP, HR and PRA rose to significantly higher levels, implying that cardiopulmonary and arterial baroreceptor afferents interact in a sense of a non-additive attenuation.     

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.     

Resetting of cardiac C-fiber endings in the spontaneously hypertensive rat

The characteristics of 11 left atrial receptors in 9 adult male spontaneously hypertensive rats (SHR) were investigated. All the receptor afferents were non-medullated with conduction velocities from 0.5 to 1.5 m/s. Elevation of left atrial pressure during graded aortic occlusion always induced a marked increase in receptor discharge with maximal frequencies ranging from 29 to 70 Hz. The threshold for activation was from 7.5 to 13 mmHg in mean left atrial pressure (mean +/- S.E., 10.2 +/- 0.6 mmHg). Upon atrial distension all the receptors displayed a clear rhythmicity and the discharge correlated mainly with the v-wave, indicating distension as the cause of receptor activation. The relationship between the mean left atrial pressure and the frequency of discharge was constructed for all the receptors and compared with similar data obtained from normotensive control rats (NCR) (Thorén et al. 1979). It was then obvious that the left atrial receptors are reset in SHR probably secondarily to a decreased distensibility of the left atrium.     

Effects of calcium channel blockers on isolated carotid baroreceptors and baroreflex

Our study determined the effects of the calcium antagonists, nifedipine and verapamil, on the carotid sinus baroreceptors and baroreflex. The left carotid sinus region in dogs was vascularly isolated and filled with oxygenated physiological salt solution. Steady-state multiunit activity was recorded from the carotid sinus nerve for sinus pressures of 50-200 mmHg after bathing the carotid sinus region in a solution containing no drug, 10 micrograms/ml nifedipine (n = 6), or 5 micrograms/ml verapamil (n = 5). The slopes of the curves relating carotid sinus nerve activity (% of maximum control) to carotid sinus pressure were control, 0.81 +/- 0.06; nifedipine, 1.29 +/- 0.14; and verapamil, 0.48 +/- 0.06%/mmHg, indicating that nifedipine increased and verapamil decreased the sensitivity of the carotid sinus baroreceptors. Additional studies with bilateral carotid sinus isolation (carotid sinus nerves intact) indicated that nifedipine enhanced and verapamil attenuated carotid baroreflex control of renal sympathetic nerve activity. Pressure-volume curves generated in the isolated carotid sinus showed that effects on smooth muscle do not account for the opposing effects of the two Ca2+ antagonists. Omitting Ca2+ from the physiological solution resulted in increased carotid sinus nerve activity, an effect blocked by verapamil but not nifedipine. Verapamil, but not nifedipine, inhibited veratrine-induced (Na+-dependent) excitation of carotid baroreceptors. Thus the excitatory effects of nifedipine on the carotid sinus baroreceptors are dependent on Ca2+ mechanisms, whereas the inhibitory effects of verapamil may be due mainly to interference with the inward Na+ current.     

Neural control of sympathetic nerve response to cardiogenic hypotension in anesthetized cat

The present study was designed to determine effect of the preganglionic splanchnic nerve activity (SNA) on the brief hypotension accompanied with the occlusion of left circumflex coronary artery (CxCAO) in chloralose anesthetized cats. Following CxCAO in animals with neuraxis intact, no significant alterations of SNA occurred despite the significant fall in mean blood pressure (MBP). A significant fall in MBP also occurred in vagotomized animals with arterial baroreceptors intact, but SNA was significantly augmented from 12.9 +/- 2.7 impulses/sec before CxCAO to 24.4 +/- 4.3 impulses/sec 60 sec after the occlusion. In vagotomized animals, in which their carotid sinuses were isolated and perfused with the constant pressure at a level equal to systemic blood pressure (112 +/- 6 mmHg) and with higher pressure (167 +/- 7 mmHg), SNA was not altered significantly during the hypotension due to CxCAO. When the carotid sinuses were perfused with lower pressure (53 +/- 8 mmHg), a significant increase in SNA occurred simultaneously with the decrease in MBP after CxCAO. The peak decreases in blood pressure during the coronary occlusion were significantly greater in the vagotomized group (-46 +/- 5 mmHg) and in the Low-CSP group (-50 +/- 5 mmHg) than in other groups. Onset of this excitatory efferent sympathetic response to the hypotension due to the coronary occlusion in the vagotomized and Low-CSP groups was delayed significantly despite a significant fall in arterial blood pressure. These results show that vagal afferents from the heart may play a role of inhibiting the sympathetic augmentation mediated by arterial baroreceptors during cardiogenic hypotension. An excessive activation of cardiac receptors with sympathetic afferents may be induced by the profound fall in blood pressure, resulting in further impairment of cardiac function due to progressive myocardial ischemia under the condition of high sympathetic tone activated by baroreceptor reflex.     

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.     

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 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.     

Cardiac receptors with non-medullated vagal afferents in the rat.

The characteristics of 22 atrial receptors in 15 normotensive adult male Wistar rats were investigated. All the receptor afferents were included in the C-fibre group with conduction velocities from 0.4 to 1.2 m/sec. No atrial medullated receptors or ventricular C-fibre endings were found. Two receptors were located in right atrium and 2 receptors throughout left atrium. Upon elevation of the left atrial pressure the receptor discharge was markedly elevated with thresholds from 2.5 to 9 mmHg in mean left atrial pressure. Ten of the atrial receptors displayed a clear cardiac rhythmicity upon activation and the discharge correlated with the v-wave, indicating distension as the cause of receptor activation. The maximal firing rate in most receptors was very high (up to 70 Hz), but 8 receptors had maximal firing rates below 25 Hz. These low frequency receptors had higher threshold and showed a more irregular firing. Thus, there is a substantial population of atrial receptors with vagal non-medullated afferents in the rat heart and the thresholds for many of these receptors are so low that they are likely to be active during normal conditions.     

Cardiac receptors with non-medullated vagal afferents in the rat

The characteristics of 22 atrial receptors in 15 normotensive adult male Wistar rats were investigated. AH the receptor afferents were included in the C-fibre group with conduction velocities from 0.4 to 1.2 m/sec. No atrial medullated receptors or ventricular C-fibre endings were found. Two receptors were located in right atrium and 2 receptors throughout left atrium. Upon elevation of the left atrial pressure the receptor discharge was markedly elevated with thresholds from 2.5 to 9 mmHg in mean left atrial pressure. Ten of the atrial receptors displayed a clear cardiac rhythmicity upon activation and the discharge correlated with the v-wave, indicating distension as the cause of receptor activation. The maximal firing rate in most receptors was very high (up to 70 Hz), but 8 receptors had maximal firing rates below 25 Hz. These low frequency receptors had higher threshold and showed a more irregular firing. Thus, there is a substantial population of atrial receptors with vagal non-medullated afferents in the rat heart and the thresholds for many of these receptors are so low that they are likely to be active during normal conditions.     

Reflex responses on blood pressure and renal nerve activity to local intra-arterial injection of capsaicin in anesthetized dogs

The present study was performed to examine effects of intra-arterial and intravenous injection of capsaicin on efferent renal sympathetic nerve activity (RNA) in pentobarbital anesthetized dogs. In animals with intact baroreceptors, intra-arterial injection of capsaicin (4 +/- 1 microgram) produced significant increases in mean blood pressure (MBP) and heart rate (HR) by +43 +/- 8 mmHg and +33 +/- 15 beats/min at 20 s after the injection, respectively. There followed a recovery toward the control so that 60 s after the intra-arterial injection changes in MBP and HR were +8 +/- 5 mmHg and +18 +/- 8 beats/min, respectively. RNA showed a biphasic response, comprising of an initial increase (+52 +/- 28% of the control at 20 s) followed by a decrease by -30 +/- 8% of the control 60 s after the injection. Following bilateral cervical vagotomy the initial increase in RNA did not differ significantly from the value of RNA in animals with intact baroreceptors. However, the later decrease in RNA reversed above the control so that 60 s after the injection change in RNA was +5 +/- 10% of the control. Complete baroreceptor denervation showed a similar response on RNA in the vagotomized animals (+49 +/- 9 and +14 +/- 10% of the control at 20 and 60 s after the injection, respectively). In contrast, intravenous injection of capsaicin (6 +/- 1 microgram/kg) resulted in significant decreases in MBP (-19 +/- 11 mmHg) and HR (-9 +/- 4 beats/min). RNA at 20 s after the injection showed a unidirectional decrease by -16 +/- 7% of the control in animals with intact baroreceptors. These responses reversed above the control after cervical vagotomy. Thus, these data indicate that activation of C-fiber afferents in skeletal muscles by intra-arterial injection of capsaicin results in renal sympathoexcitation, and that the later sympathoinhibition is mediated by combined activation of systemic baroreceptors.     

Differential sensitivity to bradykinin of esophageal distension-sensitive mechanoreceptors in vagal and sympathetic afferents of the opossum.

1. Single-unit activity was recorded from afferent fibers in the cervical vagus and thoracic sympathetic nerves in the opossum. Seventy-six fibers that responded to balloon distension (100 mmHg for 10 s) of the smooth muscle portion of the esophagus were selected for further study. 2. Forty-nine distension-sensitive afferents were identified in the vagus nerve. The stimulus response function (SRF) of 41 fibers behaved as "low-threshold mechanoreceptors" (LTM), with mean threshold value of 0.29 +/- 0.17 mmHg and saturation pressure of 50-70 mmHg. All fibers demonstrated background activity, with a mean rate of 8.83 +/- 0.93 imp/s (range 0.5-31.25). 3. Twenty-seven distension-sensitive afferents were identified in the thoracic sympathetic chain (T6-T8) and splanchnic nerve. The SRF study revealed two types of fibers: 1) a wide-dynamic-range mechanonociceptor (WDRMN) with a mean response threshold of 3.43 +/- 0.90 mmHg (n = 15) and 2) a "high-threshold mechanonociceptor" (HTMN) with a mean response threshold of 34.93 +/- 2.70 mmHg (n = 12). The mean background activities of WDRMN and HTMN fibers were 0.5 +/- 0.13 and 0.20 +/- 0.08 imp/s, respectively. Both of these fibers had saturation pressures of > 120 mmHg. 4. The conduction velocities were measured in 14 LTM, 10 WDRMN, and seven HTMN fibers. The mean conduction velocity of LTM fibers was 5.03 +/- 1.35 m/s (range 0.97-18.00), with five unmyelinated "C"-fibers (< 2.5 m/s) and nine A-delta fibers (> 2.5 m/s). The mean conduction velocity of WDRMN fibers was 3.64 +/- 0.84 m/s (range 1.10-8.25), consisting of five C-fibers and five A-delta fibers. The mean conduction velocity of HTMN fibers was 6.22 +/- 2.35 m/s (range 1.73-24.66); three fibers were unmyelinated C-fibers, and four fibers were A-delta fibers. 5. The sensitivity to bradykinin (BK) administered systemically (1-300 micrograms/kg) was tested in LTM (n = 34), WDRMN (n = 15), and HTMN (n = 8) fibers. Twenty-six (66%) LTM fibers responded to BK, and eight (34%) fibers were insensitive to BK. All 15 WDRMN and eight HTMN fibers tested responded to BK. 6. Tachyphylaxis to repeated application of BK was tested in all three classes of fibers. The vagal LTM fibers did not exhibit tachyphylaxis when BK was given at an intervals of 10 min. The sympathetic WDRMN and HTMN fibers demonstrated partial tachyphylaxis when BK was injected at 10-min intervals, but not when BK was injected at 20-min intervals.(ABSTRACT TRUNCATED AT 400 WORDS)     

Long-latency baroreceptor inhibition of supraoptic neurones in the cat

Experiments were done to determine the central delay to inhibition of supraoptic neurosecretory neurones by carotid baroreceptors in chloralose-anaesthetised, paralysed cats. Fourteen out of 18 neurosecretory cells (identified by antidromic activation from the pituitary neural lobe) were tested for their response to inflation of the ipsilateral carotid sinus (prepared as a blind sac). This stimulus inhibited the spontaneous activity of 10 neurones, which were thus identified as putative vasopressin cells. Repetitive, precisely timed pressure pulses were delivered to the carotid sinus and used to construct post-stimulus histograms of this inhibition. The latency measured from the baroreceptor afferent barrage (recorded from the sinus nerve) to the onset of inhibition in supraoptic neurones was 251 +/- 58 ms (range 152-328, n = 10). The significance of this long latency for the neural pathways involved is discussed.     

Characteristics of vagal esophageal tension-sensitive afferent fibers in the opossum

1. Single-unit vagal afferent activity was recorded from 35 fibers that demonstrated evoked response to distension in the smooth muscle portion of the esophagus in anesthetized opossums. 2. The conduction velocities, measured in 22 fibers, varied from 1.0 to 21.33 m/s. Eight fibers (36%) had conduction velocities in the range of C-fibers (less than 2.5 m/s), whereas 14 (64%) had velocities in the range of A delta-fibers (3.16-21.33 m/s). All fibers were spontaneously active with an average discharge rate of 7.3 +/- 1.0 imp/s (mean +/- SE; range, 1.2-23 imp/s). 3. Esophageal distension produced a reproducible increase in discharge rate that adapted slowly to sustained distension. The average threshold pressure of the endings was 10 mmHg. The saturation pressure was 70 mmHg with cumulative, stepwise distension and 56 mmHg with graded, discrete distensions, respectively. 4. The discharge rate at the saturation pressure was 46 +/- 7 imp/s with cumulative, stepwise distensions and was 59 +/- 4 imp/s with graded, discrete distensions. The difference in maximum discharge between these two modes of distension was not statistically significant (P greater than 0.05). 5. Esophageal peristaltic contraction was associated with bursts of spike discharge with an average rate of 53.6 +/- 4.7 imp/s. 6. Two types of fibers were identified based on their duration of spike discharge associated with peristaltic contraction. The short-activity fibers showed a short duration of response consisting of approximately 3 s of spike bursts in response to swallows. These short-activity fibers were not activated by either stretch or contraction of the longitudinal esophageal muscle. The long-activity fibers showed a long duration of response consisting of approximately 10 s of activity in response to swallows. These long-activity fibers could be activated by longitudinal muscle stretch or contraction. 7. It is concluded that esophageal tension-sensitive mechano-receptors associated with vagal afferents are activated by physiological peristalsis and are present "in series" with either circular or longitudinal muscle layers.     

Effect of cervical sympathetic nerve stimulation on canine carotid sinus reflex.

In the chloralose-anesthetized dog the carotid sinus on one side of the neck was isolated vascularly. Pressure in the isolated sinus [carotid sinus pressure (CSP)], electrocardiogram, and systemic arterial pressure were recorded. Both vagosympathetic trunks were cut and the contralateral common carotid artery was occluded or the contralateral sinus nerve was cut to reduce reflex buffering of arterial pressure changes. By varying CSP from 50 to 250 mmHg the full range of the reflex response was examined. Electrical stimulation of the peripheral end of the cut ipsilateral cervical sympathetic nerve brought about a rapid decrease in mean arterial pressure (MAP) and heart rate (HR) at lower CSPs, no change in these variables at midrange CSPs, and a gradual increase at higher CSPs, such that the gain of the reflex was reduced (1.89 +/- 0.19 to 1.33 +/- 0.15 mmHg/mmHg). The decrease in MAP and HR at lower CSPs implies an increase in baroreceptor activity whereas the converse would appear to occur at higher CSPs. These responses attained a maximum value at low stimulus frequencies (less than 10 Hz).     

Influence of low- and high-pressure baroreceptors on plasma renin activity in humans

We evaluated effects of the low- and high-pressure baroreceptors on plasma renin activity (immunoassay) using graded lower body suction (LBS) in six healthy men. LBS at -10 and -20 mmHg for 10 min decreased central venous pressure without changing arterial pressure and thereby presumably reduced low- but not high-pressure baroreceptor inhibition of renin release. LBS at these levels produced forearm vasoconstriction, but did not increase renin. LBS at -40 mmHg decreased central venous and arterial pulse pressure and thus reduced both low- and high-pressure baroreceptor inhibition. LBS at this level produced forearm vasoconstriction and tachycardia and increased renin from 2.1 +/- 0.4 (mean +/- SE to 7.4 +/- 1.4 ng.ml-1.h-1 (P less than 0.05). In summary, reduction in low-pressure baroreceptor inhibition in humans did not increase renin in the presence of physiological tonic inhibition from high-pressure baroreceptors. Increases in renin did not occur until there was combined reduction of high- and low-pressure baroreceptor inhibition on plasma renin activity.     

The Carotid Sinus Nerve—Structure,Function, and Clinical Implications

Interest has been renewed in the anatomy and physiology of the carotid sinus nerve (CSN) and its targets (carotid sinus and carotid body, CB), due to recent proposals of surgical procedures for a series of common pathologies, such as carotid sinus syndrome, hypertension, heart failure, and insulin resistance. The CSN originates from the glossopharyngeal nerve soon after its appearance from the jugular foramen. It shows frequent communications with the sympathetic trunk (usually at the level of the superior cervical ganglion) and the vagal nerve (main trunk, pharyngeal branches, or superior laryngeal nerve). It courses on the anterior aspect of the internal carotid artery to reach the carotid sinus, CB, and/or intercarotid plexus. In the carotid sinus, type I (dynamic) carotid baroreceptors have larger myelinated A-fibers; type II (tonic) baroreceptors show smaller A- and unmyelinated C-fibers. In the CB, afferent fibers are mainly stimulated by acetylcholine and ATP, released by type I cells. The neurons are located in the petrosal ganglion, and centripetal fibers project on to the solitary tract nucleus: chemosensory inputs to the commissural subnucleus, and baroreceptor inputs to the commissural, medial, dorsomedial, and dorsolateral subnuclei. The baroreceptor component of the CSN elicits sympatho-inhibition and the chemoreceptor component stimulates sympatho-activation. Thus, in refractory hypertension and heart failure (characterized by increased sympathetic activity), baroreceptor electrical stimulation, and CB removal have been proposed. Instead, denervation of the carotid sinus has been proposed for the “carotid sinus syndrome.” Anat Rec, 302:575–587, 2019. © 2018 Wiley Periodicals, Inc.     

Can human cardiovascular regulation during exercise be learnt from feedback from arterial baroreceptors?

During dynamic exercise, a large fall in systemic vascular resistance occurs. Arterial pressure (AP) is, however, maintained through a combination of central command and neural activity from muscle afferents that adjust the autonomic outflow to the circulation. How these signals are calibrated to provide accurate regulation of AP remains unclear. This study tests the hypothesis that the calibration can be 'learnt' through feedback from the arterial baroreceptors arising over multiple trials of exercise. Eight healthy subjects undertook three different protocols in random order. The test protocol consisted of 7 days' training, when subjects were exposed on 70 occasions to 4 min of exercise (50% of maximal oxygen uptake capacity) paired with neck suction (-40 mmHg) to mimic an excessive rise in AP at the carotid baroreceptors with exercise. Two control protocols involved training with either exercise or neck suction alone. No significant changes in mean AP, diastolic AP or heart rate during normal exercise were detected following training with any protocol. However, the rise in systolic AP with exercise was attenuated by an average of 7.3 +/- 2.0 mmHg (mean +/- s.e.m., P < 0.01) on the first and second days following training with the test protocol, but not with either control protocol (P < 0.05 for difference between protocols, ANOVA). In conclusion, this study failed to show that mean AP during normal exercise could be reduced through prior conditioning by overstimulation of the baroreceptors during exercise. However, a reduction in systolic AP was observed that suggests the presence of some plasticity within the autonomic response, consistent with our hypothesis.