Baroreceptor Reflex Arc Research Articles

Evaluation of efficacy of Valsalva maneuver for attenuating propofol injection pain: a prospective, randomized, single blind, placebo controlled study.

BackgroundPain on injection is a limitation with propofol use. The effect of the Valsalva maneuver on pain during propofol injection has not been studied. This maneuver reduces pain through the sinoaortic baroreceptor reflex arc and by distraction. We aimed to assess the efficacy of the Valsalva maneuver in reducing pain during propofol injection.MethodsEighty American Society of Anesthesiologists class I adult patients undergoing general anesthesia were enrolled and divided into two groups of 40 each. Group I (Valsalva) patients blew into a sphygmomanometer tube raising the mercury column up to 30 mmHg for 20 seconds, while Group II (Control) patients did not. Anesthesia was induced with 1% propofol immediately afterwards. Pain was assessed on a 10-point visual analog scale (VAS), where 0 represented no pain, and 10, the worst imaginable pain, and a 4-point withdrawal response score, where 0 represented no pain, and 3, the worst imaginable pain. Scores were presented as median (interquartile range).ResultsWe analyzed the data of 70 patients. The incidence of pain was significantly lower in the Valsalva than in the control group (53% vs 78%, P = 0.029). The withdrawal response score was significantly lower in the Valsalva group (1.00 [0.00-1.00] vs 2.00 [2.00-3.00], P < 0.001). The VAS score was significantly lower in the Valsalva group (1.00 [0.00-4.00] vs 7.00 [6.25-8.00], P < 0.001).ConclusionsA prior Valsalva maneuver is effective in attenuating injection pain due to propofol; it is advantageous in being a non-pharmacological, safe, easy, and time-effective technique.

The effect of Valsalva maneuver in attenuating skin puncture pain during spinal anesthesia: a randomized controlled trial.

BackgroundValsalva maneuver reduces pain by activating sinoaortic baroreceptor reflex arc. We planned this study to evaluate the role of valsalva in attenuating spinal needle-puncture pain.MethodsNinety American Society of Anesthesiologists (ASA) grade I and II enrolled patients undergoing elective surgery were randomized into 3 groups of 30 each. Group I (Control): didn't blow; group II (Distraction): patients blew into rubber tube; Group III (Valsalva): blew into sphygmomanometer tube and raise mercury column up to 30 mmHg for at least 20 seconds. During above procedures, spinal puncture was performed with 25-gauge spinal needle.ResultsEighty-two patient data were analyzed. Incidence of spinal puncture pain was reduced to 10% (3 of 27) in Valsalva group as compared to 100% (28 of 28 in control group and 27 of 27 in Distraction group) observed in other two groups (P < 0.05). Severity of lumbar puncture pain as assessed by visual analog scale (0−10; where 0 is no pain and 10 is the worst imaginable pain) presented as Median (Interquartile range) were significantly reduced in the Valsalva group (0.0 [0.0] as compared to other 2 groups 2.0 [0.0] in the Distraction group and 3.0 [0.8] in Control group) (P < 0.05). Regarding time taken by CSF to fill spinal needle hub, there was no difference among the three groups (P > 0.05). None patient of all groups had post dural puncture headache (P > 0.05).ConclusionsValsalva can be performed routinely in ASA I and II patients undergoing spinal anesthesia as it is safe, painless and non-pharmacological method of pain attenuation.

Medial prefrontal cortex TRPV1 channels modulate the baroreflex cardiac activity in rats.

The ventral portion of the medial prefrontal cortex (vMPFC) comprises the infralimbic (IL), prelimbic (PL) and dorsopenducular (DP) cortices. The IL and PL regions facilitate the baroreceptor reflex arc. This facilitatory effect on the baroreflex is thought to be mediated by vMPFC glutamatergic transmission, through NMDA receptors. The glutamatergic transmission can be modulated by other neurotransmitters, such as the endocannabinoids, which are agonists of the TRPV1 receptor. TRPV1 channels facilitate glutamatergic transmission in the brain. Thus, we hypothesized that TRPV1 receptors in the vMPFC enhance the cardiac baroreflex response. Stainless steel guide cannulae were bilaterally implanted into the vMPFC of male Wistar rats. Afterwards, a catheter was inserted into the femoral artery, for recording MAP and HR, and into the femoral vein for assessing baroreflex activation. Microinjections of the TRPV1 receptor antagonists capsazepine and 6-iodo-nordihydrocapsaicin (6-IODO) into the vMPFC reduced the cardiac baroreflex activity in unanaesthetized rats. Capsaicin microinjected into the vMPFC increased the cardiac baroreflex activity in unanaesthetized rats. When an ineffective dose of the TRPV1 receptor antagonist 6-IODO was used, the capsaicin-induced increase in the cardiac baroreflex response was abolished. The higher doses of capsaicin administered into the vMPFC after the ineffective dose of 6-IODO displaced the dose-response curve of the baroreflex parameters to the right, with no alteration in the maximum effect of capsaicin. The results of the present study show that stimulation of the TRPV1 receptors in the vMPFC increases the cardiac baroreceptor reflex response.

Vasculocentricity Versus Cerebrocentricity: What Stroke-Related Baroreceptor Reflex Sensitivity Changes Might Be Telling Us

Vasculocentricity Versus Cerebrocentricity: What Stroke-Related Baroreceptor Reflex Sensitivity Changes Might Be Telling Us

Cardiac Baroreceptor Sensitivity Predicts Long-Term Outcome After Acute Ischemic Stroke

The baroreceptor reflex arc is important in the short-term regulation of the cardiovascular system, and small studies have reported impaired cardiac baroreceptor sensitivity (BRS) after acute stroke. However, the prognostic significance of impaired BRS is uncertain. One hundred twenty-four patients underwent simultaneous ECG and noninvasive beat-to-beat blood pressure (BP) monitoring within 72 hours of neuroradiologically confirmed acute ischemic stroke. Cardiac BRS was assessed from the combined alpha-index by means of power spectral analysis techniques. Baseline data for acute stroke patients were compared with those of a control group matched for age, sex, and casual BP. Patients were followed up for a median of 1508 days (range, 9 to 2656 days), and outcome was compared between patients with and without impaired BRS. Median BRS values were significantly lower in stroke patients than in controls (5 [interquartile range, 3.5 to 7.4] versus 6.2 [interquartile range, 4.5 to 8.3] ms/mm Hg; P=0.04). Sixty-one (33 male) patients (mean age, 70.2 [SD 10.5] years) had impaired BRS (< or =5.0 ms/mm Hg) compared with 63 (35 male) patients (mean age, 70.6 [SD 11.7] years) without impaired BRS (>5.0 ms/mm Hg). Stroke patients with impaired BRS values had a significantly poorer prognosis (28% versus 8% mortality rate during the follow-up period) although there were no differences in age, stroke severity, stroke type, or casual or 24-hour BP parameters between the 2 groups. Impaired cardiac BRS is associated with increased long-term mortality after acute ischemic stroke, irrespective of age, sex, stroke type, and BP. This may reflect cardiac arrhythmias, but the mechanisms underlying this association are unknown, although therapies that improve cardiac BRS after stroke warrant further investigation.

Serotonin2 receptors in the nucleus tractus solitarius: characterization and role in the baroreceptor reflex arc.

1. There is a general agreement concerning the key role of the baroreceptor reflex in blood pressure homeostasis. It is also well accepted that baroreceptor afferent messages are first integrated within the nucleus tractus solitarius (NTS) and that an excitatory amino acid, probably glutamate, is the principal neurotransmitter of corresponding afferents fibers. However, important points concerning the processing of baroreceptor messages within the NTS remain to be clarified, in particular the possible modulatory role of other neuroactive substances at this particular level in the medulla oblongata. 2. In this context, the present review focuses on serotonin, and the possible facilitatory influence of NTS serotonergic afferents and receptors on the baroreceptor reflex arc. Relevant pharmacological, electrophysiological, immunohistochemical, and biochemical data, are presented and discussed. They can be summarized as follows. 3. The selective destruction of the nodose ganglion-NTS serotonergic pathway produces a long-term increase in blood pressure variability, similar to that caused by baroreceptor denervation. 4. Microinjection of picomolar doses of 5-HT into the NTS elicits the typical responses of baroreceptor activation. 5. The cardiovascular effects elicited by local microinjections of specific agonists and antagonists into the NTS of intact rats and of animals that underwent nodose ganglionectomy indicate that the baroreceptor-like effects of locally administered 5-HT are mediated by the activation of postsynaptic 5-HT2 receptors. 6. The medullary pathways which mediate NTS 5-HT2 receptor-evoked responses are similar to those involved in the baroreceptor reflex arc. 7. Pharmacological and electrophysiological studies suggest that the cardiovascular effects of intra-NTS 5-HT involve the 5-HT2A receptor subtype expressed by NTS barosensitive neurons that receive polysynaptic vagal afferents 8. Intra-NTS microinjection of a subthreshold dose of DOI, a 5-HT2 receptor agonist, which, on its own, does not produce any cardiovascular changes, significantly enhances the bradycardiac component of the baroreflex. 9. Altogether, the data summarized above show that, in the NTS, 5-HT acting at 5-HT2A receptors exerts a facilitatory influence on the baroreceptor reflex, especially on the cardiac component of this reflex. 10. Convergent pharmacological and electrophysiological data indicate that, in the NTS, functional interactions between NMDA- and 5-HT2A-receptors coexpressed by the same neurons probably underlie the facilitatory influence of 5-HT upon the baroreceptor reflex. 11. Under physiological conditions, the 5-HT2A receptor-mediated facilitatory modulation of the cardiovagal component of the baroreflex might be triggered by 5-HT released from nodose ganglion-NTS serotoninergic afferent neurons and/or for serotoninergic projections originating in raphe nuclei. The latter possibility might notably occur during recovery after physical exercise and/or during the "freezing" reaction in stressed animals.

Spontaneous baroreflex modulation of heart rate and heart rate variability during orthostatic stress in tetraplegics and healthy subjects.

This study was addressed to investigate the contribution of vagal and sympathetic mechanisms to the genesis of low-frequency (LF) oscillations of RR-interval. To this aim, we utilized the pathophysiological model of tetraplegics, who have intact vagal afferent and efferent pathways of the baroreceptor reflex arc but interrupted medullary-spinal sympathetic pathways. We studied nine complete, traumatic, tetraplegics (C4-C7, TET) and 10 normally healthy subjects (NR) at rest and during physiological baroreceptors unloading induced by 70 degrees head-up tilt. Autoregressive power spectral analysis was used to investigate RR-interval and systolic arterial pressure (SAP) variabilities. Baroreflex modulation of sinus node was assessed by the spontaneous baroreflex sequences method. Both at-rest and during-tilt LF and high frequency (HF) components were detected in RR-interval of NR, whereas in TET only the HF component was observed in both conditions (with one exception). Baroreflex sensitivity (BRS) did not significantly differ between TET and NR at rest, and underwent a significant and similar decrease during tilt in both groups, being accompanied in NR by a significant increase in LF relative power. Spectral analysis of SAP provided results similar to RR-interval. Tilt also slowed the centre frequency of the LF components of RR-interval and SAP. During unperturbed physiological conditions, a change in efferent vagal activity to the heart from baroreflex stimulation by spontaneous arterial pressure changes, is unlikely to contribute on its own to the genesis of LF heart period oscillations in humans who lack the ability to modulate sympathetic nerve traffic to the heart. However, the possibility that a baroreflex modulation of LF oscillations require an intact sympathetic control should be carefully considered.

Group differences in pain modulation: pain-free women compared to pain-free men and to women with TMD

Previously reported differences in sensitivity to experimental pain stimuli between the sexes, as well as between temporomandibular disorder (TMD) patients and healthy control subjects, may be attributable in part to group differences in two pain modulatory mechanisms: the baroreceptor reflex arc and the endogenous opioid system. Twenty-two pain-free (PF) men, 20 PF women and 20 women with TMD underwent two testing sessions in which heat pain and ischemic arm pain threshold and tolerance were measured during both sessions, but followed relaxation during one session and laboratory stress tasks during the other. Blood pressure (BP) and plasma β-endorphin (βE) concentration were measured during a baseline rest and during the stress or relaxation periods. PF men's threshold and tolerance for heat pain, but not for ischemic pain, exceeded that of PF women's during both sessions. PF women and TMD women did not differ in sensitivity to either pain modality; however, significantly lower ischemic pain threshold (IPTh) was linked to oral contraceptive use in PF women but not TMD patients. In the men alone, higher baseline systolic BP (SBP) was correlated with higher heat pain threshold on both days and heat pain tolerance on the stress day. Conversely, in TMD women, higher baseline SBP was correlated with lower ischemic pain tolerance (IPTol) on both days; BP and pain sensitivity were not related in PF women. In men, but not in PF or TMD women, stress systolic and diastolic BP were positively correlated with heat pain threshold and tolerance and higher diastolic reactivity to stress were correlated with higher heat pain and IPTh and tolerance. On the stress day, higher baseline βE level was strongly associated with higher IPTol in PF women but marginally associated with lower IPTol in TMD women. Thus, it appears that a BP-related analgesic mechanism (probably baroreceptor-mediated) predominates in PF men, while an endogenous opioid mechanism predominates in PF women. Stress enhances the expression of these central mechanisms. Female TMDs appear unable to effectively engage normal pain-inhibitory systems; opioid receptor desensitization and/or downregulation are probably implicated, because TMDs' production of βE appears normal.

Failure of acute hyperinsulinemia to alter blood pressure is not due to baroreceptor feedback

It is well documented that acute insulin administration stimulates the sympathetic nervous system in both humans and animals. Despite marked sympathetic activation during acute hyperinsulinemia, blood pressure is generally not increased because it is overridden by the vasodilator action of insulin. The maintenance of blood pressure in the face of sympathetic activation is unknown. A possible mechanism includes feedback regulation by the baroreceptor reflex arc. In normotensive states, hyperinsulinemic-induced sympathetic activation may tend to elevate blood pressure, but this change is rapidly sensed by the baroreceptors in the carotid arteries (and aortic arch), and a counterbalancing increase in vasodilation could return blood pressure to normal. Thus, it can be speculated that, in the event of diminished baroreceptor sensitivity and suppressed vasodilator actions of insulin, common abnormalities in hypertension, acute insulin infusion would be expected to increase blood pressure. We undertook the present study to determine whether the baroreceptor reflex arc modulated the blood pressure response to acute hyperinsulinemia. To this end, six normotensive dogs underwent saline or insulin infusions before and after deactivation of the carotid and aortic baroreceptors. Baroreceptor dysfunction was documented after denervation in all cases by an abnormal response to phenylephrine injections. Before denervation, insulin infusions caused a slight but nonsignificant rise in mean arterial pressure (MAP; 110 ± 5 to 120 ± 5 mm Hg; P = 0.13). Baroreceptor denervation caused a marked variability in blood pressure. However, basal mean arterial pressure was not significantly altered. Neither saline nor insulin infusions (105 ± 10 v 105 ± 8 mm Hg, basal v steady state) caused a significant change in MAP in denervated dogs. Likewise, insulin and saline did not change heart rates significantly in intact or denervated animals. Furthermore, glucose metabolism was similar in both groups of animals. This study demonstrates that the baroreceptor reflex arc does not mediate the blood pressure response to acute hyperinsulinemia.

Failure of acute hyperinsulinemia to alter blood pressure is not due to baroreceptor feedback

It is well documented that acute insulin administration stimulates the sympathetic nervous system in both humans and animals. Despite marked sympathetic activation during acute hyperinsulinemia, blood pressure is generally not increased because it is overridden by the vasodilator action of insulin. The maintenance of blood pressure in the face of sympathetic activation is unknown. A possible mechanism includes feedback regulation by the baroreceptor reflex arc. In normotensive states, hyperinsulinemic-induced sympathetic activation may tend to elevate blood pressure, but this change is rapidly sensed by the baroreceptors in the carotid arteries (and aortic arch), and a counterbalancing increase in vasodilation could return blood pressure to normal. Thus, it can be speculated that, in the event of diminished baroreceptor sensitivity and suppressed vasodilator actions of insulin, common abnormalities in hypertension, acute insulin infusion would be expected to increase blood pressure. We undertook the present study to determine whether the baroreceptor reflex arc modulated the blood pressure response to acute hyperinsulinemia. To this end, six normotensive dogs underwent saline or insulin infusions before and after deactivation of the carotid and aortic baroreceptors. Baroreceptor dysfunction was documented after denervation in all cases by an abnormal response to phenylephrine injections. Before denervation, insulin infusions caused a slight but nonsignificant rise in mean arterial pressure (MAP; 110 ± 5 to 120 ± 5 mm Hg; P = 0.13). Baroreceptor denervation caused a marked variability in blood pressure. However, basal mean arterial pressure was not significantly altered. Neither saline nor insulin infusions (105 ± 10 v 105 ± 8 mm Hg, basal v steady state) caused a significant change in MAP in denervated dogs. Likewise, insulin and saline did not change heart rates significantly in intact or denervated animals. Furthermore, glucose metabolism was similar in both groups of animals. This study demonstrates that the baroreceptor reflex arc does not mediate the blood pressure response to acute hyperinsulinemia. Am J Hypertens 1999;12:405–413 © 1999 American Journal of Hypertension, Ltd.

Cardiac baroreceptor sensitivity is impaired after acute stroke.

The blood pressure (BP) fall and increased BP variability after acute stroke have been previously described. The underlying pathophysiological mechanisms producing these findings are unclear but may include abnormalities of cardiac baroreceptor reflex arc and/or changes in sympathetic nervous system activity. To date, evidence of impaired cardiac baroreceptor sensitivity (BRS) after stroke is limited to patients with chronic disease as determined by invasive methodology. Therefore, it was proposed to assess cardiac BRS and sympathovagal balance with the use of novel noninvasive techniques after acute stroke. Thirty-seven acute stroke patients underwent simultaneous surface electrocardiographic and noninvasive beat-to-beat BP recording. Cardiac BRS was assessed by power spectral analysis techniques, and sympathovagal balance was determined from the ratio of the low- to high-frequency powers for pulse interval variability. The responses were compared with a control group matched for age, sex, and BP. Median cardiac BRS was significantly lower in stroke patients than in control subjects (high-frequency alpha-index, 4.89 versus 6.50 ms/mm Hg; P = .007; combined alpha-index, 4.65 versus 5.46 ms/mm Hg; P = .02). Median normalized high- but not low-frequency power of systolic BP variability was significantly greater in stroke patients (11.0 versus 6.7 normalized units; P < .001), probably reflecting differences in the mechanical effects of respiration on BP in stroke patients. No significant differences were observed in the power spectrum of pulse interval variability between stroke patients and control subjects. Patients with tight hemisphere strokes, however, had a significant reduction in median high-frequency pulse interval power compared with patients with left hemisphere strokes (8 versus 20 normalized units; P = .03), which may reflect a change in sympathovagal balance in favor of increased sympathetic tone in this group. The impairment of cardiac BRS may be important in explaining the increased BP variability after stroke. There was no significant difference in surrogate measures of sympathovagal activity between acute stroke patients and control subjects, but right hemisphere stroke patients had a significant alteration in the sympathovagal balance of pulse interval variability compared with left hemisphere stroke patients. This sympathetic predominance in right hemisphere strokes may be important in the development of cardiac arrhythmias after stroke. The prognostic implications of these findings need to be further explored.

Absence of evidence for a powerful tonic baroreflex-mediated inhibition on catechol activity in the rat rostral ventrolateral medulla: in vivo voltammetric evidence during sino-aortic deafferentation.

To test in a catechol-specific and dynamic manner for the existence of a powerful long-lasting inhibition arising from barosensitive afferents that depresses the activity of adrenergic neurons in the rostral ventrolateral medulla (RVLM), in vivo voltammetry was used before and after acute sino-aortic deafferentation. Rats were anaesthetized with pentobarbital or halothane and ventilated with a mixture of air and oxygen. Snares were inserted around the vagus, the glossopharyngeal and the superior laryngeal nerves. After placing the animal prone in the stereotaxic frame and stabilization at a high mean arterial pressure (MAP approximately 120 mmHg), the snares were rapidly closed to produce complete barodeafferentation, assessed by loss of heart rate responses and changes in renal nerve sympathetic activity in response to vasoactive agents. Recording of a catechol signal was maintained in the RVLM during deafferentation. Under pentobarbital-induced anaesthesia (n = 5), deafferentation did not lead to a significant change in the catechol signal within the deafferented group. Under halothane-induced anaesthesia and phenylephrine-induced high baseline pressure (n = 5), no changes in the catechol signal were observed upon deafferentation (not significant vs. sham animals: n = 5). This failure to demonstrate a major increase in catechol activity upon deafferentation does not fit with the hypothesis that a powerful tonic baroreflex-mediated inhibition depresses the activity of adrenergic RVLM barosensitive bulbospinal neurons, even when the baseline MAP is high. Rather, these data are compatible with weak or no inhibition of catechol activity by the baroreceptors and a nonessential role of adrenergic neurons within the baroreceptor reflex arc itself: the adrenergic neurons may not be in series within this arc but in parallel with the arc. This interpretation is in keeping with newer schemas of autonomic core circuitry that are devoid of adrenergic neurons.

Increased sympathetic nerve discharge without alteration in the sympathetic baroreflex response by serotonin 3 receptor stimulation in the nucleus tractus solitarius of the rat

Previous studies have shown that serotonin3 receptor activation in the nucleus tractus solitarius (NTS) increased mean arterial pressure (MAP) and inhibited the cardiac component of the baroreceptor reflex [9]. We have examined the effects of such stimulation upon spontaneous and evoked sympathetic nerve activity. Microinjection of serotonin (10 nmol) into the NTS of halothaneanaesthetized, paralyzed and artificially ventilated rats produced an increase in MAP and lumbar sympathetic nerve discharge which could be completely prevented by prior local microinjection of zacopride, a potent serotonin3 antagonist (200 pmol). In addition, 1-( m-chlorophenyl)-biguanide, a selective serotonin 3 receptor agonist, mimicked the sympathoexcitatory effect of serotonin. Since the gain of the sympathetic component of the baroreflex was unaltered after intra-NTS microinjection of serotonin, it could be concluded that serotonin 3 receptors activation in the NTS induces a sympathetic activation which is not mediated through an inhibition of the sympathetic baroreceptor reflex arc.

Neurotransmitters and neuropeptides in the baroreceptor reflex arc: connections between the nucleus of the solitary tract and the ventrolateral medulla oblongata in the rat.

The primary baroreceptor area (nucleus of the solitary tract-NTS) is anatomically interconnected with the rostral ("vasomotor area") and the caudal ("vasodepressor area") ventrolateral medulla by a well-defined arc of neuronal pathways. The chemical character and the direction of these pathways have been investigated with immunohistochemical and neurochemical techniques in intact and brainstem-operated rats. The transection of the neuronal arc resulted in an accumulation of tyrosine hydroxylase immunoreactivity in a small group of cells in the NTS adjacent to the area postrema, ipsilateral to the knife cut. Decreased angiotensinogen mRNA and atrial natriuretic peptide concentrations were measured in the ventrolateral medulla after the cut, and an accumulation of angiotensin II-immunoreactivity was found in neuronal perikarya in the ipsilateral NTS. Intracranial vagotomy caused marked depletions in glutamate levels in the subcommissural portion of the NTS and in the caudal ventrolateral medulla but nowhere else in the brainstem investigated including the rostral ventrolateral medulla.

Role of nitric oxide in regulation of baroreceptor reflex

The possible role of nitric oxide (NO) on modulating sympathetic nerve activity through its action on baroreceptor reflex arc was investigated. l-Arginine, a precursor of NO, and N G - monomethyl- l-arginine ( l-NMMA) , an inhibitor of NO synthase, were separately infused intravenously in increasing doses in 126 pentobarbital-anesthetized rabbits. Mean arterial pressure (MAP), heart rate (HR), aortic nerve activity (ANA), cervical (CSNA) and renal sympathetic nerve activities (RSNA) were recorded. l-Arginine infusion decreased MAP ( P < 0.05), ANA ( P < 0.05), CSNA ( P < 0.05) and RSNA ( P < 0.05) without changes in HR. Infusion of d-arginine, an enantiomer of l-arginine, and simultaneous infusion of l-arginine and l-NMMA, did not elicit such changes. l-NMMA infusion increased MAP ( P < 0.05) and ANA ( P < 0.05) and decreased HR ( P < 0.05), while it tended to increase CSNA and RSNA without significance. Infusion of l-arginine or l-NMMA did not alter the slope of ANA, CSNA, RSNA, or HR in relation to MAP. These results suggest that NO modulates efferent sympathetic nerve activity, not by altering the afferent or efferent limbs of the baroreceptor reflex arc, but by interacting with the sympathetic pathway in the central nervous system.

Acute alcohol administration stimulates baroreceptor discharge in the dog.

It has been shown that alcohol administration causes baroreceptor reflex inhibition. The site of action of alcohol could reside anywhere within the baroreceptor reflex arc. Therefore, the goal of this study was to determine the effects of acute administration of alcohol on carotid sinus baroreceptor discharge characteristics. In pentobarbital-anesthetized dogs, the carotid sinus was isolated and perfused. Single unit baroreceptor discharge was recorded from the carotid sinus nerve along with carotid sinus diameter using sonomicrometry. Carotid sinus pressure-baroreceptor discharge and carotid sinus pressure-diameter curves were constructed. Perfusion of the carotid sinus with alcohol (100 mmol/L) significantly decreased the pressure threshold from 91.1 +/- 2.8 to 86.4 +/- 2.9 mm Hg (p < 0.05) and increased the peak discharge rate from 45.8 +/- 3.4 to 52.8 +/- 3.6 spikes per second (p < 0.01). The same phenomenon was seen during perfusion of the carotid sinus with acetaldehyde (2.5 mmol/L) but was not seen during perfusion with acetate (2.5 mmol/L). During perfusion of the carotid sinus with alcohol, the carotid sinus pressure-carotid sinus diameter relation did not change. The baroreceptor sensitization induced by alcohol is not an endothelium-dependent mechanism, because endothelial denudation did not block this alcohol-induced effect. Measurement of the duration of postexcitatory depression of carotid sinus baroreceptors, which is related to Na+,K(+)-ATPase activity, showed that perfusion of the carotid sinus with alcohol or acetaldehyde significantly reduced the duration of postexcitatory depression, indicating that the alcohol- and acetaldehyde-induced effect on baroreceptor discharge is most likely mediated by an inhibition of Na+,K(+)-ATPase.(ABSTRACT TRUNCATED AT 250 WORDS)

Identification of baroreceptor reflex interneurons in the caudal ventrolateral medulla.

Interrupting neuronal activity in the caudal ventrolateral medulla (CVL) abolishes baroreceptor-mediated sympathoinhibition and vasodepressor responses. In the present study we identified CVL neurons that function as interneurons in the baroreceptor reflex arc. The mean antidromic onset latency of CVL neurons (5 ms) after stimulation in the rostral ventrolateral medulla (RVL) suggests that they transmit information to the RVL via unmyelinated axons. Stimulation of baroreceptor afferents in the aortic depressor nerve (ADN) excited CVL neurons projecting to the RVL with onset latencies between 15 and 45 ms. The short-latency ADN stimulus-evoked excitation of CVL barosensory interneurons preceded the onset of the ADN stimulus-evoked inhibition of RVL-spinal sympathoexcitatory neurons. Longer-latency ADN-evoked CVL neuronal responses may arise from activation of unmyelinated ADN afferents that can prolong the inhibition of RVL sympathoexcitatory neurons. The excitation of CVL barosensory interneurons resulting from the systolic pressure rise was followed by a period of decreased excitability of RVL sympatho-excitatory neurons, which was of comparable duration to the increase in the discharge probability of CVL neurons. Our characterization of baroreceptor reflex interneurons in the CVL suggests that transmission of baroreceptor information involves a complex activation of medullary interneurons responding selectively to different aspects of the arterial pressure stimulus.

9 On the location of the defect in the carotid sinus baroreceptor reflex arc in human essential hypertension

9 On the location of the defect in the carotid sinus baroreceptor reflex arc in human essential hypertension

Modulation of brown adipose tissue-mediated thermogenesis by lesions to the nucleus tractus solitarius in the rat

Given that relatively little is known regarding the central control of brown adipose tissue (BAT)-mediated thermogenesis the present study assessed whether the direct pharmacological stimulation of β- or α-adrenergic receptors located on the brown adipocytes would result in a typical thermogenic response following electrolytic lesions to the nucleus tractus solitarius (NTS). Bilateral electrolytic lesions to the NTS in the rat effectively disrupted the baroreceptor reflex arc. It was observed that the metabolic and temperature responses to either norepinephrine (1, 5, or 25 μg/kg/min) or to the β-agonist isoproterenol (0.5 μg/kg/min) were significantly attenuated in the NTS-lesioned rats relative to the control animals with an intact baroreflex. Conversely, the cardiovascular effects of norepinephrine or of the α-agonist phenylephrine (10 μg/kg/min) were enhanced in the NTS-lesioned animals. The results suggest that the functional capacity of the brown adipocytes was reduced following NTS lesions and points to an alteration in the ability of β-receptors to respond to pharmacological stimulation with a typical thermogenic response.

Clinical features of patients with dysfunction in the afferent limb of the baroreceptor reflex arc

Clinical features of patients with dysfunction in the afferent limb of the baroreceptor reflex arc