Aortic Depressor Nerve Stimulation Research Articles

Central effect of captopril on baroreflex.

To clarify effect of converting enzyme inhibitors (CEI) on heart rate regulation, captopril (2 mg/kg) was injected intravenously (i.v.) with or without pretreatment of atropine and also responses to intracisternal (i.c.) injections were examined. Captopril induced bradycardia with lowering blood pressure, and this bradycardia was abolished by pretreatment of atropine. Reduction of heart rate by i.c. injection of captopril was significantly larger than those of i.v. injection. Furthermore, to determine whether CEI can modify baroreflexes centrally, the aortic depressor nerve (ADN) was stimulated electrically in captopril treated rats. Vasodepressor and sympatho-inhibitory responses induced by ADN stimulation were significantly attenuated by captopril, while the bradycardiac response was not changed. These findings suggest that captopril attenuated centrally vasodepressor and sympatho-inhibitory responses of the baroreflex and activated centrally cardiac vagal efferent activity.

Impaired central mediation of the arterial baroreflex in chronic renal hypertension.

After 6 wk of renal hypertension in rabbits, the arterial baroreflex control of heart rate (HR) is impaired but the baroreflex control of lumbar sympathetic nerve activity ( LSNA ) is preserved. This selective impairment may reflect a predominant abnormality in the baroreceptors. In this study, we tested the hypothesis that renal hypertension of longer duration may impair baroreflex control of LSNA through a defect in the central nervous system mediation of the reflex. Four months after induction of renal hypertension, baroreflex responses were determined during increases in arterial pressure with intravenous phenylephrine or decreases in pressure with vena caval occlusion under chloralose-urethan anesthesia. Reflex control of LSNA and HR was impaired markedly in hypertensive rabbits. Reflex inhibition of LSNA and HR in response to afferent electrical stimulation of the left aortic depressor nerve (all arterial baroreceptor afferents cut) was attenuated in hypertensive in contrast to normotensive rabbits. This attenuation was noted when the medullated fibers only were stimulated or when both medullated and nonmedullated fibers were stimulated. We conclude that baroreflex control of LSNA that is preserved after 6 wk of hypertension is impaired after 4 mo of hypertension. The impairment reflects an abnormality in the central nervous system mediation of the reflex.

Parabrachial units responding to stimulation of buffer nerves and forebrain in the cat.

Spontaneously firing units in the region of parabrachial nuclei (PB) and Kölliker-Fuse nuclei (KF) of 19 chloralose-anesthetized cats were monitored for changes in firing frequency during electrical stimulation of carotid sinus (CSN) and aortic depressor (ADN) nerves, of central nucleus of the amygdala (ACE), and of paraventricular nuclei of the hypothalamus (PVH). In the ipsilateral PB 64 of 189 and in the contralateral PB 9 of 103 units responded to CSN stimulation; 18 of 185 ipsilaterally and 7 of 97 contralaterally responded to ADN stimulation. Responses were primarily excitatory, and units were located primarily in the ventrolateral portion of the PB. Only 9 of 267 units responded to stimulation of both CSN and ADN. Stimulation of the ACE and PVH antidromically activated 9 and 7 units, respectively, in PB and approximately half of these also responded to buffer nerve stimulation. In the ipsilateral PB 56 of 207 and in the contralateral PB 11 of 103 units responded orthodromically to ACE stimulation, and 23 of 177 ipsilaterally and 2 of 103 contralaterally responded orthodromically to PVH stimulation with primarily excitatory responses and were located primarily in the ventrolateral portion of the PB and KF. Of these units approximately half also responded to buffer nerve stimulation. These results suggest an important role for PB-KF in mediating ascending and descending cardiovascular and respiratory control signals.

Abnormal baroreflex control in renal hypertension is due to abnormal baroreceptors.

We determined if baroreflex control (BC) of lumbar sympathetic nerve activity (LSNA) is preserved despite impaired control of heart rate (HR) in rabbits with 6 wk of renal hypertension (HT). Baroreflex responses were determined during transient or steady-state increases (phenylephrine, PE) or decreases (nitroglycerin or caval occlusion) in arterial pressure. Impaired BC of HR was confirmed in conscious and anesthetized HT rabbits with all baroreflexes intact. In contrast, BC of LSNA was preserved in anesthetized HT rabbits. We further determined whether this selective impairment of BC of HR but not of LSNA could be due to an abnormality in the central nervous system (CNS) or in the afferent limb of the baroreflex. With only the left aortic depressor nerve (ADN) intact (other arterial baroreceptor afferents cut), BC of both HR and LSNA in HT was significantly impaired during infusion of PE. However, responses of HR and LSNA to afferent electrical stimulation of the left ADN (all arterial baroreceptor afferents cut) were similar in HT and normotensive controls. We conclude that 1) BC of LSNA is preserved in renal HT even though control of HR is impaired; 2) selective impairment of BC of HR in HT results from an abnormality in the afferent limb of baroreflex and not in CNS; 3) this abnormality in the afferent limb is not sufficient to impair BC of LSNA when all baroreflexes are intact but is sufficient after partial arterial baroreceptor denervation.

Evidence for central reorganization of ventilatory chemoreflex pathways in the cat during regeneration of visceral afferents in the carotid sinus nerve

There are two sets of peripheral arterial chemoreceptors in the cat, the carotid bodies innervated by the carotid sinus nerve and the aortic bodies with afferents in the aortic depressor nerves. Reflex stimulation of ventilation in response to hypoxia is abolished acutely after interrupting the sensory pathway from the carotid body chemoreceptors in the cat even though the reflex pathway from the aortic body chemoreceptors is intact. However, in chronically maintained preparations, there is a restoration of the hypoxic response which is mediated by the aortic chemoreflex pathway. It was proposed that restoration was due to a ‘central reorganization’ of chemoreflex pathways which followed interruption of the sensory pathway from the carotid bodies and that the reorganization enhanced the efficacy of the aortic ventilation chemoreflex. This proposal was tested in the present experiments by measuring reflex ventilatory and cardiovascular responses to electrical stimulation of the sensory nerves containing aortic and carotid chemoreceptor afferents following bilateral interruption of carotid sinus nerves and carotid body resection. Responses measured acutely (1–6 h) after interruption were compared with those measured 60–80 and 110–140 days later. At 60–80 days, a chemoreflex response (increase in tidal volume of ventilation) to stimulation of the interrupted carotid sinus sensory pathway was markedly attenuated while the response to stimulation of the uninterrupted pathway in aortic depressor nerves was enhanced. At 110–140 days, the tidal volume response to carotid sinus nerve stimulation was greatly enhanced while the aortic depressor nerve response declined from the elevated level. There were significant but less pronounced changes in the response of other ventilatory and cardiovascular variables to aortic depressor nerve and carotid sinus nerve stimulation. The results support the idea that there is a ‘central reorganization’ of chemoreflex pathways which is reflected functionally by changes in the efficacy of reflexes evoked from aortic depressor nerve and carotid sinus nerve. The changes are analagous to those occurring in somatic reflexes during regeneration of sensory nerves. It is suggested that the changes in efficacy of carotid sinus nerve reflexes are due to a degenerative loss of synapses of the central projections of interrupted carotid sinus nerve sensory axons (degenerative atrophy) and subsequent regenerative like changes (regenerative proliferation) in the central projections. The changes in the efficacy of aortic depressor nerve reflexes may be attributed to formation of new synapses by converging central projections of this uninterrupted pathway (reactive synaptogenesis) and subsequent regression of the newly formed synapses.

Projections to the hypothalamus from buffer nerves and nucleus tractus solitarius in the cat.

In 18 cats anesthetized with chloralose, electrical activity of spontaneously active hypothalamic units was monitored for changes in firing frequency during electrical stimulation of carotid sinus (CSN) and aortic depressor (ADN) nerves and the nucleus tractus solitarius (NTS). Stimulation of the CSN altered the activity of 55% (381/691) of the tested. These responsive units were widely distributed in the ipsi- and contralateral hypothalamus. Of the units tested during stimulation of the ADN only 6% (17/274) changed their firing frequency. Responsive units were located only on the ipsilateral side and primarily in the paraventricular and supraoptic nuclei, Electrical stimulation of the NTS altered the firing frequency of all 84 hypothalamic units previously identified by stimulation of the CSN. NTS stimulation elicited responses that had a significantly shorter latency and followed significantly higher frequencies of stimulation when compared to stimulation of the CSN. These results demonstrate that the two buffer nerves have distinctly different central projections to the hypothalamus and suggest different functional roles for the ADN and CSN in homeostatic regulatory mechanisms mediated by the hypothalamus.

Cardiac Sympathetic Nerves in Rats: Anatomical and Functional Features

Anatomical pathways and natures of reflex as well as spontaneous activities of cardiac sympathetic nerves (CNs) were investigated in rats.2. Anatomically, the stellate CNs on both sides provide a major sympathetic supply to the rat heart with additional contribution of the thoracic CNs on the left side.3. Functions of these CNs were studied in chloralose-urethane anesthetized and artificially ventilated rats. Electrical stimulation of these CNs produced an increase in heart rate and a rise in blood pressure. The increase in heart rate was more potent on the right-side stimulation, while the rise in blood pressure was greater on the left-side stimulation.4. Stimulation of the aortic depressor nerve (ADN) inhibited spontaneous discharges of the CN for a longer period as compared with those of the cervical postganglionic sympathetic nerve (CSN). On the other hand, stimulation of the sural nerve produced a longer lasting reflex increase in discharges of the CN as compared with that of the CSN. These findings suggest that cardioregulatory sympathetic outflow is more affected by visceral and somatosensory input than is the other sympathetic outflows.5. Spontaneous discharges of both nerves showed a rhythmicity associated with heart beats. Although the magnitude of this rhythmicity was not clearly different between these two nerves, the time from bottom to peak firing level of the phasic discharges of the CN was significantly longer than that of the CSN. This finding is consistent with the longer lasting effect of the ADN stimulation on the CN discharges.