Section Of Aortic Nerves Research Articles

Nitric oxide-dependent vasodilation and the regulation of arterial blood pressure.

Conflicting evidence has been reported on the hypothesis that vascular nitric oxide (NO) release is modulated by autonomic influences. Another controversial question is whether an insufficient degree of NO-dependent vasodilation may play a contributory role in the genesis of arterial hypertension. To address these questions we evaluated NO-dependent vasodilation in conscious rats subjected to various experimental manipulations that interfere with autonomic function: chronic chemical sympathectomy (CCSx), acute ganglionic blockade (AGx) and chronic sinoaortic denervation (CSAD). Experiments were also carried out on 6- and 12-week-old spontaneously hypertensive rats (SHR) (i.e. during the pre-hypertensive and the early established hypertensive stage) and in age-matched Wistar-Kyoto (WKY) rats. Nitric oxide-dependent vasodilation was quantified from the extent of blood pressure (BP) elevation in response to acute inhibition of NO synthesis by L-nitromonomethyl-L-arginine (L-NMMA). Chronic chemical sympathectomy was produced by repeated 6-hydroxydopamine injections; AGx was induced by hexamethonium infusion; and CSAD was obtained by aortic nerve section and carotid sinus wall stripping. Nitric oxide synthesis inhibition by L-NMMA was followed by a marked BP elevation in all groups. Rats with CCSx, Agx or CSAD never showed reduced BP responses to L-NMMA compared to intact, control rats. Neither 6- nor 12-week-old SHR had attenuated pressor responses to L-NMMA compared to age-matched WKY rats. In conclusion, the data indicate that (i) in unanaesthetized quietly-behaving rats there is no significant modulation of NO release by autonomic influences and (ii) young SHR have unimpaired NO-dependent vasodilation so it is unlikely that a deficit of vascular NO release plays any etiologic role in the BP elevation of this experimental model.

Prolonged apnea and impaired survival in piglets after sinus and aortic nerve section

We examined the effects of carotid body denervation (CX, n = 9), CX + aortic nerve section (CAX, n = 9), and sham surgery (SHAM, n = 7) on cardiorespiratory and metabolic function in young piglets (less than 9 days). For comparison, 1-mo-old pigs were also studied. Studies were performed 1 day after surgery, during which time ventilation (barometric plethysmography), heart rate, blood pressure, arterial blood gases, and electroencephalogram were recorded under normoxia. CX and CAX piglets hypoventilated (arterial PCO2 = 47.1 +/- 2.6 and 45.4 +/- 3.1 Torr, respectively) compared with SHAM piglets (arterial PCO2 = 36.4 +/- 1.5 Torr). CX piglets had an average of 8.0 +/- 3.0 apneas/h, lasting, on average, 26 +/- 3 s. CAX piglets averaged 17.2 +/- 7.9 apneas/h, lasting 30 +/- 5 s. Such long apneas were never observed in SHAM animals. Mean heart rate and blood pressure in denervated piglets were not significantly different from those in SHAM piglets. In animals followed up poststudy, significantly high mortality was observed in CX (5 of 9) and CAX (6 of 9) piglets by 7 days after surgery but not in SHAM animals (0 of 7) despite identical environmental and feed conditions (P less than 0.05; chi 2). One-month-old denervated animals showed periodic breathing and hypoventilation, but none died. These results suggest that in the newborn piglet 1) peripheral chemoreceptors have an active role in maintaining normal ventilation and avoidance of prolonged apnea and 2) survivability in early life is critically dependent on peripheral chemoreceptors.

Differential control of blood pressure and heart rate by carotid and aortic baroreceptors in unanaesthetized cats.

In unanaesthetized cats the most striking effects of sino-aortic denervation (SAD) consist of a marked increase in blood pressure variability and a concomitant marked reduction in heart rate variability. Because the relative contribution of carotid and aortic baroreceptors to these phenomena has never been assessed, blood pressure (intra-arterial catheter) and heart rate were measured in unanaesthetized, unrestrained cats for 8-10 h under three conditions: intact animals, 1 week after section of the carotid sinus or the aortic nerves and 1 week after SAD. Blood pressure and heart rate signals were analysed by a computer to provide mean values and variation coefficients of variation i.e. blood pressure and heart rate variabilities, for each recording period. In the intact cats the coefficient of variation was 6.6 +/- 0.6% (mean +/- s.e.) for mean blood pressure and 11.2 +/- 1.7% for heart rate. The coefficient of variation for mean blood pressure was not altered by either the aortic or the carotid sinus nerve section, a marked increase being observed only after SAD (11.5 +/- 1.3%, P less than 0.01). On the other hand, the coefficient of variation for heart rate was reduced either by the carotid or by the aortic nerve section. The reduction observed following the carotid baroreceptor denervation accounted for the greater fraction of the overall reduction (74 versus 26%) in coefficient of variation for heart rate observed after SAD (4.8 +/- 0.9%, P less than 0.01). These data show that the carotid sinus and aortic nerves are similarly involved in control of blood pressure variability.(ABSTRACT TRUNCATED AT 250 WORDS)

Maintained depressor responses evoked by continuous and intermittent stimulation of aortic nerve in the rabbit.

Stability of depressor responses evoked by long-lasting continuous and intermittent stimulation of the aortic nerve was studied in rabbits anaesthetized with urethane. Continuous stimulation produces blood pressure falls whose stability at low frequencies (1-10 cycles/sec) ranges from 91 to 86%. With rise of the stimulation frequency stability is decreased : at 500 cycles/sec, it amounts to 19%. Intermittent stimulation consisting in switching excitation on and off every 10 sec increases stability of depressor responses and at 500 cycles/sec, it is significantly higher than stability of effects produced by continuous stimulation. Following transection of aortic nerves, stability is increased at all frequencies of continuous stimulation and at all but the lowest frequency of intermittent stimulation. Vagotomy performed after section of the aortic nerves does not significantly affect the changes in stability observed after severing the aortic afferents. It is suggested that at high frequencies of stimulation, stability of depressor responses is reduced by homosynaptic depression. During intermittent stimulation, its effect is counteracted by post-tetanic changes occurring at intervals when the stimulation is switched off. The increase in stability after section of aortic nerves is probably related to its effect on excitability of the vasomotor centres.

Relative contributions of aortic and carotid sinus baroreceptors to the baroreceptor-heart rate reflex of the conscious rabbit

Conscious rabbits with previously implanted perivascular balloons for altering blood pressure were studied before and 6 days after: (i) sham-operation (n = 6); (ii) section of carotid sinus nerves alone (n = 7); (iii) section of aortic nerves alone (n = 5); and (iv) combined sino-aortic denervation (n = 5). Sigmoid mean arterial pressure (MAP)-heart period (HP) baroreflex curves were derived and were characterized by: (i) the HP range (HPR) between upper and lower plateau levels; (ii) the median blood pressure (BP 50); and (iii) the average gain ( G ). Resting MAP and HP and the 3 baroreflex parameters were not altered significantly 6 days after sham-operation. After section of the carotid sinus nerves alone resting MAP and BP 50 rose by 18 ± 2.6 mm Hg, resting HP fell by 31 ± 4.2 msec, whilst HPR and G fell to about 45% and 20% respectively of initial preoperative control. After cutting the aortic nerves alone there was a similar fall in resting HP as after carotid denervation. However, the rises in resting MAP and BP 50 were only about half of those observed after carotid denervation ( P < 0.05) and the changes in HPR and G to 65% and 58% of control respectively were also less marked ( P <0.01). The aortic baroreceptor zone also exerted smaller effects on the sympathetic efferent component of the baroreflex HP response. Despite the different effects exerted by each zone on the reflex parameters there was little difference in threshold pressure for producing cardiac slowing. After combined sino-aortic denervation there was a similar rise in resting MAP (19 mm Hg) as after carotid sinus denervation alone, but there was more marked tachycardia, with a fall in resting HP of 82 msec ( P < 0.001) and both resting and baroreflex-mediated vagal tones were completely abolished. The small residual pressure-determined HP changes of about 8 msec were entirely sympathetic and probably mediated through cardiopulmonary baroreceptors.

Interaction between the baroreceptor and Bezold-Jarisch reflexes.

The interaction between the carotid baroreflex and Bezold-Jarisch (BJ) reflex (intravenously administered veratridine) was studied in anesthetized rabbits after aortic nerve section. The carotid sinuses were vascularly isolated to regulate the intrasinus pressure (ISP). The extent of BJ reflex bradycardia and hypotension was progressively diminished as the ISP was elevated stepwise. When the carotid baroreflex was not operative by holding the ISP constant at control, the BJ reflex changes in heart rate (HR) and systemic arterial pressure (SAP) were not significantly different from those induced at the normal condition. Thus the calculated baroreflex static loop gain was greatly decreased during the BJ reflex. However, sinus denervation, analogous to keeping ISP below 50 mmHg, significantly enhanced the BJ reflex effects. A steady-state infusion of veratridine remarkably reduced the slope of the baroreflex function ISP-SAP and ISP-HR curves. The results indicate that the BJ reflex effects are affected by the prevailing arterial baroreceptor input, varying inversely with the ISP level. An attenuation in the baroreflex sinsitivity, in terms of the loop gain or slope of the transfer function curve, was observed during the BJ reflex. The presence of tonic cardiovascular inhibitions exerted by the arterial baroreceptors tends to reduce the BJ reflex bradycardia and hypotension, but the baroreceptors do not function adequately in buffering the cardiovascular inhibition produced by the cardiogenic reflex.

Hypertension following denervation of aortic baroreceptors in unanesthetized dogs.

After cervical aortic nerve section, mean arterial pressure in the unanesthetized dog increased by an average of 7.4 mm Hg. Following a more extensive denervation of aortic arch receptors by section of intrathoracic vagal branches, arterial pressure increased by 16.7 mm Hg. The above changes were seen in the stable state after the effects of surgery had disappeared. In both cases carotid baroreceptors were functional. After administration of nitroglycerin and phenylephrine subsequent to either denervation procedure, blood pressure changes were larger and heart rate responses were smaller than in the control state. The unanesthetized dog regulates mean arterial pressure at a higher-than-normal pressure after aortic baroreceptor denervation. Reflexes from the aortic baroreceptors continuously participate in the normal control of mean arterial pressure. Section of the cervical aortic nerves only partially denervates aortic baroreceptors. Our findings may be relevant to human essential hypertension.

Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog.

The purpose of this study was to determine the relative magnitudes of the reflex effects mediated by cardiac receptors during anterior as opposed to inferoposterior ischemia of the left ventricle of the dog. Cessation of perfusion (coronary "occlusion") of the circumflex coronary artery (Cx) in 29 chloralose-anesthetized dogs with common carotids ligated (group I) resulted in significant bradycardia and hypotension, but in no significant change in perfusion pressure in the gracilis muscle perfused at constant flow. Occlusion of the left anterior descending coronary artery (LAD) produced less hypotension, no change in heart rate, and vasoconstriction in the gracilis. After vagotomy and aortic nerve section, no significant change in heart rate or gracilis perfusion pressure was observed during lad or Cx occlusion, and the blood pressure responses to LAD and Cx occlusion were not different. In nine dogs with sinoaortic denervation (group II), brief Cx occlusion resulted in bradycardia, hypotension, and vasodilation in the gracilis muscle. LAD occlusion in group II dogs caused less hypotension and no change in heart rate or gracilis perfusion pressure. After vagotomy, the bradycardia and vasodilation resulting from Cx occlusion were abolished and the blood pressure responses to LAD and Cx occlusion were not different. The weights of left ventricle perfused by each occluded vessel were not different. These data show that left ventricular receptors with vagal afferents which are activated during coronary occlusion and which mediate cardioinhibitory and vasodepressor responses are located mainly in the inferoposterior left ventricle of the dog heart.

Mechanism of alteration in baroreflex cardiovascular responses due to volume loading.

The effect and mechanism of volume loading (VL) on the baroreflex sensitivity, in terms of the changes in arterial pressure (AP) and heart rate (HR) to a given change in carotid sinus pressure (CSP), were studied in rabbits anesthetized with chloralose and urethan. The carotid sinuses were vascularly isolated in order to regulate the CSP independently from the systemic arterial pressure. VL was accomplished by intravenous infusion of dextran solution or whole blood to raise the right atrial pressure from 0.4 to 10 cm water. When the CSP was lowered from 90 to 40 mmHg, VL reduced the baroreflex pressor response by 10.1 mmHg (42%) and 19.9 mmHg (46%) before and after aortic nerves section, respectively. The attenuation effect of VL on the carotid pressor response was abolished after cervical vagotomy. VL also reduced the extent of bradycardia and hypotension upon an elevation of CSP from 90 to 140 mmHg. Before aortic nerve section, the reduction by VL was 19.7 beats/min (41%) for the bradycardic response, and 15.1 mmHg (43%) for the depressor response. These attenuation effects of VL were absent after aortic denervation. The results suggest that VL alters the carotid baroreflex pressor response via the vagal afferents subserving the cardiopulmonary receptors, whereas it reduces the depressor and bradycardic responses through the aortic baroreceptor.

Reduction in baroreflex cardiovascular responses due to venous infusion in the rabbit.

We studied reflex bradycardia and depression of mean arterial blood pressure (MAP) during left aortic nerve (LAN) stimulation before and after volume infusion in the anesthetized rabbit. Step increases in mean right atrial pressure (MRAP) to 10 mm Hg did not result in a significant change in heart rate or MAP. After volume loading, responses to LAN stimulation were not as great and the degree of attenuation was propoetional to the level of increased MRAP. A change in responsiveness was observed after elevation of MRAP by only 1 mm Hg, corresponding to less than a 10% increase in average calculated blood volume. after an increase in MRAP of 10 mm Hg, peak responses were attenuated by 44% (heart rate) and 52% (MAP), and the initial slopes (rate of change) were reduced by 46% (heart rate) and 66% (MAP). Comparison of the responses after infusion with blood and dextran solutions indicated that hemodilution was an unlikely explanation for the attenuation of the reflex responses. Total arterial baroreceptor denervation (ABD) abolished the volume-related attenuation was still present following bilateral aortic nerve section or vagotomy. It thus appears that the carotid sinus responds to changes inblood volume and influences the reflex cardiovascular responses to afferent stimulation of the LAN. On the other hand, cardiopulmonary receptors subserved by vagal afferents do not appear to be involved.

The role of afferent barosensory neurons in respiratory and bronchomotor control

Ventilatory and bronchomotor responses to baroreceptor afferent stimulation were studied in anaesthetized rabbits breathing spontaneously. The stimuli used were either the increase in carotid sinus pressure or the electrical stimulation of the cut central end of the aortic nerve. Respiratory effects of aortic barodenervation were also studied. Normoxic, normocapnic steady state was verified by repeated measurement of PO2, PCO2 and pH in arterial blood. Stimulation of both aortic and carotid baroreceptors provoked an early decrease of tidal volume and total pulmonary resistances without change in respiratory frequency. Aortic nerve stimulation induced an important and slowly adapting ventilatory and bronchomotor effect, whereas changes in carotid sinus pressure produced slight variation in respiratory parameters. Aortic nerve section resulted in an early and prolonged increase of total pulmonary resistances. Surgical or chemical (atropine) vagotomy did not change the bronchodilation observed under stimulation of the carotid sinus; however this effect was suppressed by intravenous injection of propranolol. This observation shows the importance of the sympathetic outflow in the genesis of bronchomotor responses following baroreceptor stimulation. In conclusion the baroreceptor stimulation provokes simultaneous decrease of both ventilation and total pulmonary resistances; aortic nerves seemed to exert permanent control on bronchomotor tone.

The effect of section of aortic nerves on the relationship between the resting blood pressure and magnitude of pressure responses in the rabbit.

The effect of section of aortic nerves on the relationship between the resting blood pressure and magnitude of pressure responses in the rabbit.

Comparison of the averaged nervous activities of aortic and carotid sinus nerves.

ARTICLESComparison of the averaged nervous activities of aortic and carotid sinus nervesH Irisawa, and I NinomiyaH Irisawa, and I NinomiyaPublished Online:01 Aug 1967https://doi.org/10.1152/ajplegacy.1967.213.2.504MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByDischarges of aortic and carotid sinus baroreceptors during spontaneous motor activity and pharmacologically evoked pressor interventions11 May 2014 | The Journal of Physiological Sciences, Vol. 64, No. 4Signal transduction of aortic and carotid sinus baroreceptors is not modified by central command during spontaneous motor activity in decerebrate catsKanji Matsukawa, Kei Ishii, Akito Kadowaki, Tomoko Ishida, Mitsuhiro Idesako, and Nan Liang15 May 2014 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 306, No. 10Modulation of emetic response by carotid baro- and chemoreceptor activationsAutonomic Neuroscience, Vol. 128, No. 1-2Effects of the Head-Down Tilt Posture on Postnatal Development of the Aortic Baroreflex in the Rabbit.The Japanese Journal of Physiology, Vol. 52, No. 2Comparison of aortic and carotid baroreflex stimulus–response characteristics in humansAutonomic Neuroscience, Vol. 88, No. 1-2Cardiovascular responses to time delays of electrocardiogram-coupled electrical stimulation of carotid sinus nerves in dogsJournal of the Autonomic Nervous System, Vol. 25, No. 2-3An Analyzer for Autonomic Nerve Activities in Acute and Chronic AnimalsIEEE Transactions on Biomedical Engineering, Vol. BME-33, No. 1Baroreflex Control of Systemic Arterial Pressure and Vascular Bed1 January 2011Chronic localized hypotension and resetting of carotid sinus baroreceptors. Electrophysiological and histological studies in the dog.Circulation Research, Vol. 49, No. 3Coarctation of the aorta and baroreceptor resetting. A study of carotid baroreceptor stimulus-response characteristics before and after surgical repair in the dog.Circulation Research, Vol. 48, No. 3Cardiovascular neurography: Cardiac-rhythm based neurosignal distribution displayMedical & Biological Engineering & Computing, Vol. 18, No. 1Hypertension following denervation of aortic baroreceptors in unanesthetized dogs.Circulation Research, Vol. 45, No. 1Effect of Changing the Frequency of Conditioning Tetanus on Depressor Responses Evoked by Stimulation of the Aortic Nerve26 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 86, No. 4Response Characteristics of Carotid Baroreceptors to Steady PressureAn inexpensive technique for analysis of aortic-nerve activityMedical & Biological Engineering, Vol. 11, No. 5Comparison of Afferent Activity of Canine Aortic and Sinus NervesCirculation Research, Vol. 31, No. 4Reflex Effects of Stimulation of Carotid Sinus and Aortic Baroreceptors on Hindlimb Vascular Resistance in DogsCirculation Research, Vol. 29, No. 2The Effect of Section of Aortic nerves on the Relationship Between the Resting Blood Pressure and Magnitude of Pressure Responses in the Rabbit27 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 78, No. 1 More from this issue > Volume 213Issue 2August 1967Pages 504-510 Copyright & PermissionsCopyright © 1967 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1967.213.2.504PubMed6036338History Published online 1 August 1967 Published in print 1 August 1967 Metrics

The relative roles of the aortic and carotid sinus nerves in the rabbit in the control of respiration and circulation during arterial hypoxia and hypercapnia.

1. The respiratory and circulatory effects of graded arterial hypoxia, alone or with superadded hypercapnia, were studied in four groups of unanaesthetized rabbits including normal animals and those with selective section of the aortic nerves, selective section of the carotid sinus nerves and section of both sets of nerves.2. When measured 2-4 days after selective section of the carotid sinus nerves the resting respiratory minute volume and arterial P(O2) were lower and the P(CO2) higher than normal. These effects were not observed after selective section of the aortic nerves. Selective aortic nerve section, and selective carotid sinus nerve section each produced a similar increase in the resting arterial pressure and heart rate, but were without effect on the resting cardiac output.3. During arterial hypoxia reflex respiratory and circulatory effects ascribable to arterial chemoreceptor stimulation (hyperventilation, bradycardia, vasoconstriction) were mediated for the most part through the carotid sinus nerve. In animals with only the aortic nerves intact the circulatory response was determined largely by the opposing effects of aortic baroreceptor reflexes and the local peripheral dilator action of hypoxia.4. The circulatory effects of hyperventilation induced by hypercapnia during arterial hypoxia, in animals with both aortic and carotid sinus nerves cut were small.5. The results suggest that relatively few chemoreceptor fibres originate from the aortic region in the rabbit, though the carotid sinus and aortic nerves both contain baroreceptor fibres.