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PubMed2003

Involvement of cyclic AMP-mediated pathway in neural release of noradrenaline in canine isolated mesenteric artery and vein.

OBJECTIVE: Our major hypothesis is that cyclic adenosine-3',5'-monophosphate (cAMP)-mediated modulation of neurotransmitter release plays different roles at low and high activity of the sympathetic nervous system. We further hypothesize that cAMP-mediated neuromodulation might underlie disparate neurovascular control in mesenteric arteries and veins. METHODS: Electrical field stimulation (EFS)-evoked overflow of noradrenaline (NA) was evaluated in the absence or presence of activators and inhibitors of cAMP-dependent pathway at low (4 Hz) and high (16 Hz) frequencies of stimulation of endothelium-denuded secondary and tertiary branches of the canine isolated inferior mesenteric arteries and veins. The content of NA in samples of the superfusates collected before and during nerve stimulation was assayed by high-performance liquid chromatography (HPLC) technique in conjunction with electrochemical detection. Student's t-test and ANOVA analyses were applied for statistical analysis. RESULTS: Activation of cAMP-dependent pathway with either isoproterenol (ISO, 10 microM), forskolin (1 microM), dibutyryl cAMP (100 microM) or combined site-specific activators of cAMP-dependent protein kinase (PKA) [i.e. N(6)-phenyl-adenosine-3',5'-cyclic monophosphate, 8-(6-aminohexyl) aminoadenosine-3',5'-cyclic monophosphate, and the Sp-isomer of 5,6-dichloro-1-D-ribofuranosylbenzimidazole-3',5'-cyclic monophosphorothioate, each 100 microM] caused an enhancement of the EFS-evoked overflow of endogenous NA at 16 Hz of stimulation but was without an effect at 4 Hz of stimulation both in artery and vein. The EFS (16 Hz)-evoked overflow of NA in vein was also increased in the presence of inhibitors of phosphodiesterase (PDE) III and PDE IV (i.e. milrinone, 0.4 microM, and roilpram, 30 microM), whereas these inhibitors did not affect the overflow of NA in the artery. The facilitating effect of activators of cAMP-dependent pathway on the EFS-evoked release of NA at 16 Hz appears to be more pronounced in the vein than in artery. The increasing effect of ISO (10 microM) was inhibited with either propranolol (1 microM) or the adenylyl cyclase (AC) inhibitor [9-(tetrahydro-2'-furyl)adenine] (SQ 22,536, 100 microM) in both blood vessels. The ISO effect was inhibited by the PKA inhibitor 14-22 amide (PKI(14-22)), 1 microM, in the artery but not in vein. The enhancing effect of FSK was inhibited by pretreatment of the tissue with SQ 22,536, 100 microM, or the PKA inhibitors PKI(14-22), 1 microM, and 4-cyano-3-methylisoquinoline, 50 nM. However, the inhibitors alone did not significantly change the EFS-evoked overflow of NA in both blood vessels. CONCLUSIONS: Activation of AC-cAMP-PKA pathway appears to play a role in modulating NA release at higher stimulation frequencies as might be expected during stress, strenuous exercise, or hemorrhage. The AC-cAMP pathway plays a more pronounced role in the autonomic neural control of mesenteric veins than of the corresponding arteries, whereas the PKA contribution is more distinct in the arteries.

Adenine↗
PubMed2005

[False recognition of faces associated with fronto-temporal dementia with prosopagnosia].

INTRODUCTION: The association of prosopagnosia and false recognition of faces is unusual and contributes to our understanding of the generation of facial familiarity. METHOD: A 67-year-old man with a left prefrontal traumatic lesion, developed a temporal variety of fronto-temporal dementia (semantic dementia) with amyotrophic lateral sclerosis. Cerebral imagery demonstrated a bilateral, temporal anterior atrophy predominating in the right hemisphere. The main cognitive signs consisted in severe difficulties to recognize faces of familiar people (prosopagnosia), associated with systematic false recognition of unfamiliar people. RESULT: Neuropsychological testing indicated that the prosopagnosia probably resulted from the association of an associative/mnemonic mechanism (inability to activate the Face Recognition Units (FRU) from the visual input) and a semantic mechanism (degradation of semantic/biographical information or deconnexion between FRU and this information). At the early stage of the disease, the patient could activate residual semantic information about individuals from their names, but after a 4-year course, he failed to do so. This worsening could be attributed to the extension of the degenerative lesions to the left temporal lobe. Familiar and unfamiliar faces triggered a marked feeling of knowing. False recognition concerned all the unfamiliar faces, and the patient claimed spontaneously that they corresponded to actors, but he could not provide any additional information about their specific identities. The coexistence of prosopagnosia and false recognition suggests the existence of different interconnected systems processing face recognition, one intended to identification of individuals, and the other producing the sense of familiarity. Dysfunctions at different stages of one or the other of these two processes could result in distortions in the feeling of knowing. CONCLUSION: From this case and others reported in literature, we propose to complete the classical model of face processing by adding a pathway linked to limbic system and frontal structures. This later pathway could normally emit signals for familiarity, essentially autonomic, in response to the familiar faces. These signals, primitively unconscious, secondly reach consciousness and are then integrated by a central supervisor system which evaluates and verifies identity-specific biographical information in order to make a decision about the sense of familiarity.

Aged↗
PubMed1987

Cardiovascular abnormalities accompanying acute spinal cord injury in humans: incidence, time course and severity.

The frequency of cardiovascular abnormalities was evaluated in 71 consecutive patients with acute injury to the spinal cord. Persistent bradycardia was universal in all 31 patients with severe cervical cord injury and less common in milder cervical injury (6 of 17) or thoracolumbar injury (3 of 23) (p less than 0.00001). Marked sinus slowing (71 versus 12 versus 4%, respectively, p less than 0.00001), hypotension (68 versus 0 versus 0%, p less than 0.00001), supraventricular arrhythmias (19 versus 6 versus 0%, p = 0.05) and primary cardiac arrest (16 versus 0 versus 0%, p less than 0.05) were significantly more frequent in the severe cervical injury group. The frequency of bradyarrhythmias peaked on day 4 after injury and gradually declined thereafter. All observed abnormalities resolved spontaneously within 2 to 6 weeks. The primary mechanism underlying these observations appears to involve the acute autonomic imbalance created by the disruption of sympathetic pathways located in the cervical cord. Acute severe injury to the cervical spinal cord is regularly accompanied by arrhythmias and hemodynamic abnormalities not found with thoracolumbar cord trauma. These abnormalities are limited to the first 14 days after injury, a period in which life-threatening disturbances must be anticipated.

Adolescent↗
PubMed2000

Functional and chemical anatomy of the afferent vagal system.

The results of neural tracing studies suggest that vagal afferent fibers in cervical and thoracic branches innervate the esophagus, lower airways, heart, aorta, and possibly the thymus, and via abdominal branches the entire gastrointestinal tract, liver, portal vein, billiary system, pancreas, but not the spleen. In addition, vagal afferents innervate numerous thoracic and abdominal paraganglia associated with the vagus nerves. Specific terminal structures such as flower basket terminals, intraganglionic laminar endings and intramuscular arrays have been identified in the various organs and organ compartments, suggesting functional specializations. Electrophysiological recording studies have identified mechano- and chemo-receptors, as well as temperature- and osmo-sensors. In the rat and several other species, mostly polymodal units, while in the cat more specialized units have been reported. Few details of the peripheral transduction cascades and the transmitters for signal propagation in the CNS are known. Glutamate and its various receptors are likely to play an important role at the level of primary afferent signaling to the solitary nucleus. The vagal afferent system is thus in an excellent position to detect immune-related events in the periphery and generate appropriate autonomic, endocrine, and behavioral responses via central reflex pathways. There is also good evidence for a role of vagal afferents in nociception, as manifested by affective-emotional responses such as increased blood pressure and tachycardia, typically associated with the perception of pain, and mediated via central reflex pathways involving the amygdala and other parts of the limbic system. The massive central projections are likely to be responsible for the antiepileptic properties of afferent vagal stimulation in humans. Furthermore, these functions are in line with a general defensive character ascribed to the vagal afferent, paraventricular system in lower vertebrates.

Animals↗
PubMed2004

Vagal afferent is involved in short-pulse gastric electrical stimulation in rats.

This study investigated the effect of gastric electrical stimulation (GES) on vagal activity and its possible vagal afferent-mediated mechanisms. Sixty rats implanted with gastric serosal electrodes were divided into six groups (control, vehicle, local capsaicin, perivagal capsaicin, systemic capsaicin, and vagotomy). GES with six sets of parameters was performed in the control group; and GES with one set of effective parameters was performed in the other five groups. Spectral analysis of heart rate variability was used to assess vagal activity. Regular gastric slow waves were recorded in the control rats with a frequency of 4.8 cycles/min. Vagotomy significantly reduced the frequency of the gastric slow wave but did not induce dysrhythmia. Capsaicin did not alter the gastric slow wave. Short-pulse (300-microsec) GES significantly increased vagal activity at a frequency four times the intrinsic slow-wave frequency. Stimulation at a lower frequency or with a long pulse (300 msec) had no effect on vagal activity. Vagotomy or capsaicin administered perivagally, systemically, or locally abolished the effect of GES on the vagal activity. GES with short but not long pulses is capable of altering vagal activity. This effect is mediated by capsaicin-sensitive vagal afferent fibers.

Afferent Pathways↗
PubMed1999

Sucrose availability on the aerial part of the plant promotes morphogenesis and flowering of Arabidopsis in the dark.

Conditions to promote dark morphogenesis and flower-ing in Arabidopsis have previously been limited to liquid cultures and to a few laboratory ecotypes. We have obtained development and flowering of Arabidopsis plants under complete darkness by growing them on vertical Petri dishes containing solid agar medium with sucrose. Under these conditions, all the ecotypes tested were able to develop, giving rise to etiolated plants that flowered after producing a certain number of leaves. Dark-grown plants showed similarities with phytochrome-deficient mutants and were different from de-etiolated or constitutive photomorphogenesis mutants such as det and cop. Late- and early-flowering ecotypes, showing large differences in flowering time and leaf number under long days, flowered with a similar number of leaves when grown in the dark. Rapid dark flowering of late-flowering ecotypes was not an effect of darkness but the result of the interaction between dark and sucrose availability at the aerial part of the plant, since sucrose also had an effect when plants were grown in the light. Gibberellin-deficient and insensitive mutants were delayed in the initiation of flowers in the dark, indicating a role for these hormones in flowering promotion in the dark. The late-flowering phenotype of mutants at different loci of the autonomous and long-day-dependent flowering induction pathways was rescued in dark growth conditions. However, the late-flowering phenotype of ft and fwa mutants was not rescued by sucrose either in the dark or in the light, suggesting a different role for these genes in flowering induction.

Arabidopsis↗
PubMed1994

Autonomic changes during hypnosis: a heart rate variability power spectrum analysis as a marker of sympatho-vagal balance.

Spectral analysis of beat-to-beat variability in electrocardiography is a simple, noninvasive method to analyze sympatho-vagal interaction. The electrocardiogram is analyzed by means of an automatic, autoregressive modeling algorithm that provides a quantitative estimate of R-R interval variability by the computation of power spectral density. Two major peaks are recognizable in this specter: a low-frequency peak (LF, -0.1 Hz), related to the overall autonomic activity (ortho+parasympathetic) and a high-frequency peak (HF, -0.25 Hz), representative of the vagal activity. The LF/HF ratio is an index of the sympatho-vagal interaction. This technique was applied, using a computer-assisted electrocardiograph, to 10 healthy volunteers (6 high and 4 low hypnotizable subjects as determined by the Stanford Hypnotic Susceptibility Scale, Form C) in randomized awake and neutral hypnosis conditions. Preliminary results indicated that hypnosis affects heart rate variability, shifting the balance of the sympatho-vagal interaction toward an enhanced parasympathetic activity, concomitant with a reduction of the sympathetic tone. A positive correlation between hypnotic susceptibility and autonomic responsiveness during hypnosis was also found, with high hypnotizable subjects showing a trend toward a greater increase of vagal efferent activity than did low hypnotizables.

Adult↗
PubMed1999

Aging alteration of cardiac vagosympathetic balance assessed through the tone-entropy analysis.

BACKGROUND: Age-associated alterations of cardiac autonomic functions have been investigated intensively through heart rate variability analyses. However, changes with age in cardiac vagosympathetic balance remain to be elucidated. METHODS: We studied 142 male subjects (30-69 yr) at a health care center in Kyoto, Japan. Electrocardiographic data were collected from subjects in a recumbent position for 10 min in the morning. Analysis was done by classifying the subjects into four age groups. In a pharmacological experiment carried out in December 1996, tone was verified to reflect the cardiac vagosympathetic balance, and entropy the total autonomic neural efferent activity. We assessed the heart rate variability through the tone-entropy (T-E) analysis that was described previously. In essence, two indexes, tone and entropy, were defined on a distribution of successive variations of heart period. RESULTS: No significant differences were detected in clinical conditions among the four age groups. Tone increased and entropy decreased significantly with age. The aging process was expressed as a curvilinear path in T-E space. Compared to the pharmacological experiment, it was observed that aging degenerated the heart function from an ordinary to a denervated one. The same aging path was superimposed in the opposite direction on the heart recovery path after dynamic exercise in which cardiac vagosympathetic balance tended toward vagus division, corresponding with restoration of total autonomic activity. CONCLUSIONS: An age-related reduction in cardiac autonomic function was consistent with previous reports. The vagosympathetic balance was altered with this reduction: vagal predominance was impaired significantly in proportion to the withdrawal of total cardiac autonomic activity.

Adrenergic beta-Antagonists↗
PubMed1978

Causalgia.

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Adrenergic Fibers↗
PubMed2005

Molecular pathology of aging and its implications for senescent coronary atherosclerosis.

PURPOSE OF REVIEW: This review highlights common mechanisms of organismal aging and inflammatory coronary atherosclerosis. RECENT FINDINGS: A substantial body of evidence now indicates that aging is largely due to molecular damage inflicted by reactive oxygen species, electrophiles, and other reactive endobiotic and xenobiotic metabolites. Our understanding of genetic pathways regulating longevity began 12 years ago with the discovery that a developmental-arrest program in the nematode Caenorhabditis elegans also has marked effects on adult lifespan. This pathway, closely related to the insulin and insulinlike growth factor-signaling pathways of mammals, modulates longevity and stress resistance in several model organisms. Insulin-like signaling also has an impact on redox signaling, antioxidant defenses, and metabolic generation of oxidative stress. Recently, additional signaling pathways--involving Sirtuins, AMP kinase, Jun N-terminal kinase 1, and other master regulatory proteins--have been implicated in longevity and stress-resistance mechanisms. The inflammatory process involves acute production of reactive oxygen species by specialized cells responding to infection, exposure to toxins or allergens, cell damage, hypoxia, ischemia/reperfusion, and other factors, initiating signaling through several of these pathways. Free radical chain reactions arise from lipid oxidation and generate oxidized low-density lipoprotein, a powerful inflammatory signal and potentiator of atherosclerosis. Oxidized low-density lipoprotein accumulates in atherosclerotic arteries, particularly in rupture-prone regions. Inflammation involving oxidative stress, by way of the production of reactive oxygen species, is a hallmark of coronary atherosclerosis. SUMMARY: Common pathways underlie both organismal aging and tissue-autonomous senescent pathologic processes, such as coronary atherosclerosis. The mechanisms discovered in model organisms may lead to pharmacotherapeutic interventions.

Aging↗
PubMed2004

Differential involvement of rat medial prefrontal cortex dopamine receptors in modulation of hypothalamic-pituitary-adrenal axis responses to different stressors.

Recent investigations have implicated the medial prefrontal cortex (mPFC) in modulation of subcortical pathways that contribute to the generation of behavioural, autonomic and endocrine responses to stress. However, little is known of the mechanisms involved. One of the key neurotransmitters involved in mPFC function is dopamine, and we therefore aimed, in this investigation, to examine the role of mPFC dopamine in response to stress in Wistar rats. In this regard, we infused dopamine antagonists SCH23390 or sulpiride into the mPFC via retrodialysis. We then examined changes in numbers of cells expressing the c-fos immediate-early gene protein product, Fos, in subcortical neuronal populations associated with regulation of hypothalamic-pituitary-adrenal (HPA) axis stress responses in response to either of two stressors; systemic injection of interleukin-1 beta, or air puff. The D1 antagonist, SCH23390, and the D2 antagonist, sulpiride, both attenuated expression of Fos in the medial parvocellular hypothalamic paraventricular nucleus (mpPVN) corticotropin-releasing factor cells at the apex of the HPA axis, as well as in most extra-hypothalamic brain regions examined in response to interleukin-1 beta. By contrast, SCH23390 failed to affect Fos expression in response to air puff in any brain region examined, while sulpiride resulted in an attenuation of the air puff-induced response in only the mpPVN and the bed nucleus of the stria terminalis. These results indicate that the mPFC differentially processes the response to different stressors and that the two types of dopamine receptor may have different roles.

Adrenocorticotropic Hormone↗
PubMed2004

Activation of 5-HT1A receptors in raphe pallidus inhibits leptin-evoked increases in brown adipose tissue thermogenesis.

To elucidate the central neural pathways contributing to the thermogenic component of the autonomic response to intravenous administration of leptin, experiments were conducted in urethane-chloralose-anesthetized, ventilated rats to address 1) the role of neurons in the rostral ventromedial medulla, including raphe pallidus (RPa), in the leptin-evoked stimulation of brown adipose tissue (BAT) sympathetic nerve activity (SNA); and 2) the potential thermolytic effect of 5-hydroxytryptamine(1A) (5-HT(1A)) receptors on RPa neurons that influence BAT thermogenesis. Leptin (1 mg/kg) administration increased BAT SNA by 1,219% of control, BAT temperature by 2.8 degrees C, expired CO(2) by 1.8%, heart rate by 90 beats/min, and mean arterial pressure by 12 mmHg. Microinjection of the 5-HT(1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) into RPa resulted in a prompt and sustained reversal of the leptin-evoked stimulation of BAT SNA, BAT thermogenesis, and heart rate, with these variables returning to their pre-leptin control levels. Subsequent microinjection of the selective 5-HT(1A) receptor antagonist WAY-100635 into RPa reversed the BAT thermolytic effects of 8-OH-DPAT, returning BAT SNA and BAT temperature to the elevated levels after leptin. In conclusion, activation of neurons in RPa, possibly BAT sympathetic premotor neurons, is essential for the increases in BAT SNA, BAT thermogenesis, and heart rate stimulated by intravenous administration of leptin. Neurons in RPa express 5-HT(1A) receptors whose activation leads to reversal of the BAT thermogenic and the cardiovascular responses to intravenous leptin, possibly through hyperpolarization of local sympathetic premotor neurons. These results contribute to our understanding of central neural substrates for the augmented energy expenditure stimulated by leptin.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2001

The sleep apnoea/hypopnoea syndrome depresses waking vagal tone independent of sympathetic activation.

The modest daytime hypertension and sympathetic upregulation associated with the sleep apnoea/hypopnoea syndrome (SAHS), does not explain the relatively large increased risk of cardiac morbidity and mortality in the SAHS patients population. Therefore, efferent vagal and sympathetic activity was evaluated during wakefulness in SAHS subjects and matched healthy controls, in order to determine if vagal downregulation may play a role in the aetiology of cardiac disease in the SAHS. The awake autonomic nervous system function of 15 male subjects, with mild-to-moderate SAHS was compared to that of 14 healthy controls matched for age, body mass index, gender and blood pressure. All subjects were free from comorbidity. Vagal activity was estimated from measurements of heart rate variability high frequency power (HF) and sympathetic activity was measured from urine catecholamine excretion. The %HF power was significantly (p < 0.03) reduced in SAHS patients (10+/-1.6 (mean+/-SEM)) as compared to controls (17 +/- 3). In addition, HF power correlated with the apnoea/hypopnoea index in the SAHS subjects (R = -0.592, p = 0.02). There was no statistically significant difference in the daytime excretion of nonadrenaline between control (242 +/- 30 nmol x collection(-1)) and SAHS (316 +/- 46 nmol x collection(-1)) subjects (p = 0.38). In these sleep apnoea/hypopnoea syndrome patients there was limited evidence of increased waking levels of urine catecholamines. The principal component altering waking autonomic nervous system function, in the sleep apnoea/hypopnoea syndrome subjects, was a reduced daytime efferent vagal tone.

Adult↗
PubMed1998

Effects of adrenergic and nitrergic blockade on theophylline-induced increase in peripheral blood flow in rat ear.

A bolus injection of theophylline produced a significant increase in peripheral blood flow in anesthetized rat ear, monitored by laser-Doppler flowmetry, with increases in arterial blood pressure and heart rate. These effects were attenuated by previous treatment with reserpine, but reserpine had no effect on the blood flow increase produced by acetylcholine. A dose of propranolol, which caused attenuation of the theophylline-induced increase in heart rate, did not change the peripheral blood flow. The higher dose of propranolol, which nearly canceled the increases in blood pressure and heart rate, caused attenuation of the blood flow increase but did not cancel it. However, the theophylline-induced flow increase was completely reversed by a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, which alone had no effect, without any change in arterial blood pressure and heart rate. Treatment of the rats with the dose of inhibitor slightly and significantly reduced the response of peripheral blood flow to acetylcholine. The other isomer, NG-nitro-D-arginine methyl ester, and the other inhibitor, NG-monomethyl-L-arginine, did not have such an effect. These results suggest that the flow increase is due to an independent effect on the heart with modification by autonomic reflexes and involves the adrenergic and nitrergic pathways.

Acetylcholine↗
PubMed2003

Analysis of hydrogen peroxide-independent expression of the high-light-inducible ELIP2 gene with the aid of the ELIP2 promoter-luciferase fusions.

Intense and excessive light triggers the evolution of reactive oxygen species in chloroplasts, and these have the potential to cause damage. However, plants are able to respond to light stress and protect the chloroplasts by various means, including transcriptional regulation at the nucleus. Activation of light stress-responsive genes is mediated via hydrogen peroxide-dependent and -independent pathways. In this study, we characterized the Early-Light-Inducible Protein 2 (ELIP2) promoter-luciferase gene fusion (ELIP2::LUC), which responds only to the hydrogen peroxide-independent pathway. Our results show that ELIP2::LUC is expressed under nonstressful conditions in green tissue containing juvenile and developing chloroplasts. Upon light stress, expression was activated in leaves with mature as well as developing chloroplasts. In contrast to another high-light-inducible gene, APX2, which responds to the hydrogen peroxide-dependent pathway, the activation of ELIP2::LUC was cell autonomous. The activation was suppressed by application of 3-(3,4)-dichlorophenyl-1,1-dimethylurea, an inhibitor of the reduction of plastoquinone, whereas 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone, an inhibitor of the oxidation of plastoquinone, gave the contrasting effect, which may suggest that the redox state of the plastoquinone plays an important role in triggering the hydrogen peroxide-independent light stress signaling.

Arabidopsis↗
PubMed1997

Neural reflex regulation of arterial pressure in pathophysiological conditions: interplay among the baroreflex, the cardiopulmonary reflexes and the chemoreflex.

The maintenance of arterial pressure at levels adequate to perfuse the tissues is a basic requirement for the constancy of the internal environment and survival. The objective of the present review was to provide information about the basic reflex mechanisms that are responsible for the moment-to-moment regulation of the cardiovascular system. We demonstrate that this control is largely provided by the action of arterial and non-arterial reflexes that detect and correct changes in arterial pressure (baroreflex), blood volume or chemical composition (mechano- and chemosensitive cardiopulmonary reflexes), and changes in blood-gas composition (chemoreceptor reflex). The importance of the integration of these cardiovascular reflexes is well understood and it is clear that processing mainly occurs in the nucleus tractus solitarii, although the mechanism is poorly understood. There are several indications that the interactions of baroreflex, chemoreflex and Bezold-Jarisch reflex inputs, and the central nervous system control the activity of autonomic preganglionic neurons through parallel afferent and efferent pathways to achieve cardiovascular homeostasis. It is surprising that so little appears in the literature about the integration of these neural reflexes in cardiovascular function. Thus, our purpose was to review the interplay between peripheral neural reflex mechanisms of arterial blood pressure and blood volume regulation in physiological and pathophysiological states. Special emphasis is placed on the experimental model of arterial hypertension induced by N-nitro-L-arginine methyl ester (L-NAME) in which the interplay of these three reflexes is demonstrable.

Animals↗