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PubMed1981

[Distribution of horseradish peroxidase-labeled neurons, sources of descending fiber systems, in subcortical brain structures and the hypothalamus of cats].

Location of neurons which initiate different descending fibre systems from amygdaloid nuclei, basal ganglia and hypothalamus to brain stem was studied using the method of horse-radish peroxidase retrograde axonal transport. It was shown that neurons from magnocellular part of the basal amygdaloid nucleus and medial part of central amygdaloid nucleus send their axons to the dorsal hypothalamus, substantia nigra, lateral area of the mesencephalic central grey and midbrain reticular formation at the level of inferior olives. The central amygdaloid nucleus is the main source of projections to the hypothalamus and brain stem structures. It also sends projections to the nucleus of solitary tract and to the dorsal motor nucleus of the vagus. Uncrossed descending fibre systems from the basal ganglia terminate at the pons level, while the uncrossed and crossed fibre systems from dorsolateral and ventromedial areas of hypothalamus descend into the spinal cord. A possible role of the amygdaloid nuclei, basal ganglia, hypothalamus and their different pathways in regulation of somatic and autonomic functions and complex behavioural and emotional responses is discussed.

Amygdala↗
PubMed2004

Dopamine-induced synaptic depression in the parabrachial nucleus is independent of CTX- and PTX-sensitive G-proteins, PKA and PLC signalling pathways.

We have previously reported that dopamine (DA) depresses non-NMDA receptor-mediated glutamatergic transmission in the rat parabrachial nucleus (PBN), an interface between brainstem and forebrain that is implicated in autonomic regulation. This work examined cellular signalling pathways that might underlie this DA-induced synaptic depression. Direct activation of adenylyl cyclase with 10 microM forskolin increased the evoked EPSC but did not occlude DA-induced EPSC depression. Similarly, a preferential protein kinase A inhibitor, H-7 (10 microM), did not block DA's synaptic effects. Incubation of slices with cholera toxin (CTX; 1 microgram/ml) or pertussis toxin (PTX; 0.5 microgram/ml) for 20 h, procedures used to irreversibly activate or disable the G(s) and G(i) proteins, respectively, did not change DA's effects. The putative phospholipase C inhibitor, U-73122 (10 microM) and its inactive analogue U-73343 (10 microM) did not alter DA-induced reduction in the EPSCs. Alterations in signalling molecules downstream of phospholipase C including depleting internal calcium stores by thapsigargin and cyclopiazonic acid and blocking protein kinase C with chelerythrine, had no effect on DA-induced synaptic depression. Furthermore, DA's depression of the non-NMDA response was not blocked by APV, an NMDA receptor antagonist. Finally, DA depressed evoked, pharmacologically isolated NMDA receptor-mediated synaptic responses while increasing NMDA-induced inward currents in the PBN. These results indicate that DA-induced synaptic effects in the PBN are not through the activation of cholera or pertussis toxin sensitive G proteins. Furthermore, it does not employ the adenylyl cyclase-cAMP-PKA cascade, the phospholipase C signalling pathway and NMDA receptor-coupled mechanisms to depress excitatory synaptic transmission in the PBN.

Adjuvants, Immunologic↗
PubMed1993

Central actions of corticotropin-releasing factor on autonomic nervous activity and cardiovascular functioning.

The physiological role of corticotropin-releasing factor (CRF) in mediating stress-induced activation of the pituitary-adrenal axis, together with the neuroanatomical distribution of immunoreactive CRF and CRF receptors, provides a compelling rationale for investigating actions of CRF within the central nervous system (CNS) on autonomic nervous outflow and cardiovascular function. Evidence is reviewed showing that CRF acts within the CNS to elicit stress-like patterns of autonomic nervous outflow and cardiovascular changes in conscious animals. In addition, blockade of CRF-mediated neurotransmission is demonstrated to alter the expression of stress-induced autonomic nervous and cardiovascular responses. Together, the anatomical, pharmacological and physiological data support the hypothesis that the autonomic nervous and cardiovascular responses to selected stressful stimuli may be mediated in part by CRF-containing neuronal pathways.

Animals↗
PubMed1985

Primary afferent projections of the major splanchnic nerve to the spinal cord and gracile nucleus of the cat.

Splanchnic afferent projections to the spinal cord and gracile nucleus were labeled following the application of HRP to the central cut end of the major splanchnic nerve. Labeled afferent fibers were detected in the ipsilateral dorsal column, in Lissauer's tract (LT), in laminae 1, 5, 7, and 10, and in the dorsal gray commissure at T1-T13 levels of the spinal cord. Afferent projections were not identified in laminae 2-4. Collaterals from LT projected ventrally along the lateral and medial margins of the dorsal horn (called lateral and medial pathways, respectively). Afferents in the lateral pathway formed small bundles, spaced rostrocaudally at intervals of 300-1,000 microns, which passed medially at the base of the dorsal horn into laminae 5, 7, and 10 and to the contralateral spinal cord. Some afferents in the lateral pathway projected to the intermediolateral nucleus where labeled sympathetic preganglionic neurons were located. Afferents in the medial pathway entered the lateral aspect of the dorsal column and projected as a group near the midline rostrally to the medulla. The dorsal column pathway terminated in the ventral gracile nucleus in four or five clusters, each occupying a region ranging in size from 0.01-0.1 mm3 and separated in the rostrocaudal axis by distances of 400-800 microns. These clusters were concentrated in the middle and caudal portions of the nucleus below the obex. A comparison of the present results with those from earlier experiments on the central projections of afferent fibers from the heart, kidney, and pelvic organs demonstrates a consistent pattern of visceral afferent termination in the thoracolumbar and sacral segments of the spinal cord. This is not unexpected, since visceral afferent pathways to different organs perform similar functions, such as the transmission of nociceptive information and the initiation of autonomic reflexes.

Afferent Pathways↗
PubMed1995

New model for the regulation of energy balance and adiposity by the central nervous system.

We describe a new model for adiposity regulation in which two distinct classes of peripheral afferent signals modulate neuronal pathways in the brain that control meal initiation, meal termination, and the autonomic outflow influencing the fate of ingested energy. These brain pathways, termed central-effector pathways for the control of energy balance, respond to 1) short-term, situational-, and meal-related signals that are crucial to the size and timing of individual meals, but that are not components of the system serving to regulate adipose stores, and 2) long-term, adiposity-related signals that participate in the negative feedback control of fat stores. Long-term signals, such as the pancreatic hormone insulin, are secreted into the circulation in proportion to energy balance and adipose mass. These signals enter the brain where they influence central-effector pathways, in part by changing the sensitivity of these pathways to short-term signals. Through this mechanism, the central nervous system response to short-term signals is adjusted in proportion to changes in body adiposity, resulting in compensatory changes in food intake and energy expenditure that collectively favor the long-term stability of fat stores. This model provides a comprehensive framework for experimental design and data interpretation in the study of body adiposity regulation.

Adipose Tissue↗
PubMed1986

Physiology and morphology of the lamina I spinomesencephalic projection.

We have examined the physiological and morphological characteristics of spinal dorsal horn lamina I neurons with projections to the midbrain in the cat by combining physiological recording of neurons with the intracellular injection of HRP. Lamina I spinomesencephalic neurons were antidromically activated from the region that included the cuneiform nucleus and lateral periaqueductal gray at the intercollicular level. The majority of mesencephalic projection neurons (50 of 55) responded exclusively to noxious stimulation (nociceptive-specific) of their peripheral receptive fields. Lamina I spinomesencephalic neurons were activated from both the ipsilateral and contralateral midbrain and had slow antidromic conduction velocities (1 to 18 m/second). We identified eight cells with projections to both the midbrain and the thalamus and eight cells that were antidromically activated only from the thalamus. Intracellular injection of HRP revealed that lamina I spinomesencephalic neurons were of diverse morphological types, but generally had extensive, rostrocaudally oriented, dendritic arbors confined to lamina I and the overlying white matter. Axons were observed on nine of the HRP-filled spinomesencephalic neurons; five of the axons issued collateral branches. The morphological characteristics of these neurons did not appear to correlate with functional categories (i.e., wide-dynamic-range- or nociceptive-specific-type neurons). The large number of nociceptive-specific neurons with projections to the midbrain and the interconnections of these midbrain sites with hypothalamic and limbic structures suggest that the lamina I spinomesencephalic pathway plays an important role in the autonomic and affective responses to pain.

Afferent Pathways↗
PubMed2005

Comparison of effects of methylprednisolone and anti-CD11d antibody treatments on autonomic dysreflexia after spinal cord injury.

Autonomic dysreflexia is a condition of episodic hypertension that develops after spinal cord injury (SCI). We previously showed that a two-day anti-inflammatory treatment with an anti-CD11d integrin monoclonal antibody (mAb), soon after SCI in rats, reduced the magnitude of dysreflexia for at least 6 weeks. Effects of methylprednisolone (MP), a commonly used neuroprotective treatment for SCI, on dysreflexia have never been examined. We compared the effects of a 2-day MP treatment and/or the anti-CD11d mAb on autonomic dysreflexia, elicited by colon distension, after clip-compression SCI at the 4th thoracic segment (T4) in rats. We assessed the effects of each treatment on the size of the calcitonin gene-related peptide (CGRP)-immunoreactive afferent arbour in the dorsal horn, as changes in this arbour can correlate with the development of dysreflexia. MP reduced autonomic dysreflexia by approximately 50% at 2 weeks after SCI, but this effect was lost by 6 weeks. At 2 weeks, the combined effects of MP and the mAb were not additive, reducing dysreflexia by approximately 50%. Neither MP nor the mAb treatment altered the area of CGRP-immunoreactive fibres in the lumbar cord, the crucial input region for dysreflexia initiated by colon distension. However, both treatments led to increased fibre areas in the T9 segment, correlated with greater tissue integrity and smaller lesions, delineated by inflammatory cells. In summary, MP only temporarily decreases autonomic dysreflexia after SCI. The early beneficial effects of both treatments on dysreflexia do not relate to changes in the CGRP-immunoreactive afferent arbour but may correlate with decreased lesion progression.

Afferent Pathways↗
PubMed1991

Effect of dialysis and renal transplantation on autonomic dysfunction in chronic renal failure.

Autonomic functions were evaluated in 25 nondialyzed patients with chronic renal failure and eight controls. Eight patients were reassessed after 6.6 +/- 1.0 weeks of hemodialysis and 12 patients were restudied 24 +/- 4.0 weeks after renal transplantation. In addition, six patients who had been on maintenance hemodialysis for a duration of 21.5 +/- 3.0 weeks were also studied. Autonomic function tests, including blood pressure and heart rate response to sudden loud noise, mental arithmetic, hand immersion in cold water, Valsalva maneuver, change in posture and respiration, were performed using brachial artery cannulation and continuous monitoring by electrocardiogram. Baroreceptor sensitivity slope was determined using bolus injections of phenylephrine. Supine and standing plasma norepinephrine levels were measured. The cold pressor test, response to sudden loud noise and mental arithmetic were normal in nondialyzed patients with chronic renal failure, suggesting an intact efferent sympathetic pathway. The plasma norepinephrine concentration varied widely but the mean value was similar to the control group (P greater than 0.05). Expiration/inspiration ratio, lying/standing ratio, Valsalva ratio and the baroreceptor sensitivity slope were significantly abnormal (P less than 0.001) in nondialyzed patients. This indicates a defective efferent parasympathetic pathway and depressed baroreceptor sensitivity. The blood pressure response to phenylephrine was lower in the uremics, suggesting a reduced end-organ responsiveness to alpha agonists. The presence of hypertension did not affect autonomic function. The heart rate response to standing and the baroreceptor sensitivity were significantly lower (P less than 0.05) in patients who developed hypotension during hemodialysis. Lower baroreflex sensitivity could contribute to hypotension during dialysis. Autonomic functions remained unaltered after short- and long-term dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Divergent effects on LH and FSH synthesis and release from intact female rat pituitary glands in vitro by methylxanthines, cyclic AMP derivatives and sodium fluoride.

FSH release from the female rat pituitary gland consists of an LH-like, LRH-dependent component and an autonomous, inhibin-sensitive component. It was investigated whether cyclic AMP mediated FSH release. BrcAMP, theophylline, MIX or NaF stimulated LH release but inhibited FSH release and synthesis. Although dbcAMP had no inhibitory effect on FSH release, it partly reversed the inhibitory action of theophylline. In view of previous and the present results it is concluded that cyclic AMP may mediate the LRH-dependent LH and FSH release and, through a separate pathway, may mediate the inhibition of autonomous FSH release by the ovarian protein inhibin.

1-Methyl-3-isobutylxanthine↗
PubMed1999

Correlation of acetylator phenotype with peripheral, autonomic and central neuropathy in Northern Indian non-insulin-dependent diabetes mellitus patients.

OBJECTIVES: Genetic susceptibility to diabetic neuropathy has been suspected and tentatively explored; however, diabetic autonomic and central neuropathies are poorly investigated areas. Previous trials correlating types of diabetes and diabetic neuropathy with acetylator dimorphisms have not been conclusive. The present study was designed to test peripheral neuropathy, autonomic neuropathy and integrity of central conduction pathways in patients of non-insulin-dependent diabetes mellitus (NIDDM), and to correlate the findings with the acetylator phenotype. METHODS: Twenty-six patients of NIDDM with stable glycaemic control and 11 age- and sex-matched control subjects were recruited, clinically examined and investigated with glycaemic and lipid profile, renal function tests, nerve conduction studies (sensory and motor), auditory brain stem evoked responses (ABERs) and somatosensory evoked potentials (SEPs). Acetylator status of the subjects was determined by sulphadimidine test. RESULTS: Out of 26 NIDDM patients, eight (30.7%; group 1A) were slow acetylators and 18 (69.3%; group 1B) were fast acetylators. The distribution of slow and rapid acetylators in both the groups was similar. Glycaemic and lipid profiles and 24-h urinary albumin excretion in groups 1A and 1B were also similar. Motor nerve conduction velocity, latency of F wave, sensory nerve conduction and amplitudes of sensory nerve action potentials were not different between fast and slow acetylator NIDDM patients. On testing for ABERs, there were no statistically significant differences in peak latencies of waves I, III and V; interpeak latencies (IPLs) I-III, III-V and I-V; amplitude of waves I, III and V on both sides between NIDDM patients and controls. However, peak latencies of wave III (P < 0.01), wave V (P < 0.005), IPLs I-III and I-V (P < 0.005), IPLs III-V (P < 0.05), and amplitudes of wave I (P < 0.05) and wave V (P < 0.05) on the left side were significantly different in slow acetylator NIDDM patients. Increase on the right side for the same group was statistically significant for IPLs I-III and I-V (P < 0.05). SEPs showed no statistically significant difference between NIDDM patients and controls, and slow and fast acetylator NIDDM patients. CONCLUSIONS: No significant association of acetylator status with peripheral neuropathy in NIDDM subjects was observed in the present study. However, central neural conduction, primarily tested by ABERs, was significantly delayed in slow acetylators compared with fast acetylator NIDDM patients. Hence, there may be a predisposition to neuropathy in this group of patients, and such a predisposition may be better detected by studying central rather than peripheral nervous conduction pathways in NIDDM patients.

Adult↗
PubMed2005

Essential role of non-canonical Wnt signalling in neural crest migration.

Migration of neural crest cells is an elaborate process that requires the delamination of cells from an epithelium and cell movement into an extracellular matrix. In this work, it is shown for the first time that the non-canonical Wnt signalling [planar cell polarity (PCP) or Wnt-Ca2+] pathway controls migration of neural crest cells. By using specific Dsh mutants, we show that the canonical Wnt signalling pathway is needed for neural crest induction, while the non-canonical Wnt pathway is required for neural crest migration. Grafts of neural crest tissue expressing non-canonical Dsh mutants, as well as neural crest cultured in vitro, indicate that the PCP pathway works in a cell-autonomous manner to control neural crest migration. Expression analysis of non-canonical Wnt ligands and their putative receptors show that Wnt11 is expressed in tissue adjacent to neural crest cells expressing the Wnt receptor Frizzled7 (Fz7). Furthermore, loss- and gain-of-function experiments reveal that Wnt11 plays an essential role in neural crest migration. Inhibition of neural crest migration by blocking Wnt11 activity can be rescued by intracellular activation of the non-canonical Wnt pathway. When Wnt11 is expressed opposite its normal site of expression, neural crest migration is blocked. Finally, time-lapse analysis of cell movement and cell protrusion in neural crest cultured in vitro shows that the PCP or Wnt-Ca2+ pathway directs the formation of lamellipodia and filopodia in the neural crest cells that are required for their delamination and/or migration.

Adaptor Proteins, Signal Transducing↗
PubMed1993

Physiological assessment of aspects of autonomic function in patients with secondary progressive multiple sclerosis.

A detailed non-invasive study of systemic and regional haemodynamic responses to a range of autonomic tests which assess sympathetic and parasympathetic pathways (mental arithmetic, cutaneous cold, isometric exercise, deep breathing, Valsalva manoeuvre and head-up tilt) were performed in ten patients with secondary progressive multiple sclerosis and ten age- and sex-matched healthy normal subjects (controls). Blood pressure rose in controls during the pressor tests and was maintained during tilt. In six out of ten patients with multiple sclerosis blood pressure was unchanged during one or more of the three pressor tests, but was maintained in all during tilt. In the controls, superior mesenteric artery blood flow fell during pressor tests and head-up tilt. In multiple sclerosis patients, superior mesenteric artery blood flow did not change during pressor tests but fell during tilt. Cardiac index rose during isometric exercise and fell during head-up tilt in controls. Forearm blood flow rose during mental arithmetic in the controls only, but fell during tilt in both groups. Individual analysis indicated that of the ten multiple sclerosis patients, four had responses during the pressor tests similar to controls. Responses to deep breathing and to the Valsalva manoeuvre in controls and multiple sclerosis patients were similar. We conclude that some patients with an aggressive and disabling form of multiple sclerosis have selective autonomic dysfunction, in particular involving pressor responses, despite the lack of postural hypotension. The autonomic abnormality is likely to involve central autonomic interconnections rather than afferent or sympathetic efferent pathways. Further clarification of the nature, site and progression of these lesions is needed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Brain corticotropin-releasing factor acts as inhibitor of stress-induced gastric erosion in rats.

Gastric lesions are known to be caused by stress. Corticotropin-releasing factor (CRF) is a key peptide initiating various stress response. This study was designed to investigate how brain CRF is involved in the occurrence of stress-induced gastric erosion in rats. Intracerebroventricular (icv) administration of CRF suppressed the occurrence of gastric erosion induced by water-immersion restraint stress, and its suppressive effect was blocked by coadministration of a CRF receptor antagonist in rats. The peripheral administration of CRF had no influence on the occurrence of erosion. The icv administration of a CRF receptor antagonist or anti-rat CRF gamma-globulin increased gastric erosion induced by the stress. Ganglionic blockade with chlorisondamine, muscarinic blockade with atropine, or bilateral adrenalectomy by itself significantly inhibited the occurrence of stress-induced gastric erosion, and no additional effect of CRF on these treatments-induced inhibition of erosion was found. These results, therefore, suggest that the occurrence of stress-induced gastric erosion is mediated by the autonomic nervous system- and adrenal-dependent pathway, and that brain CRF reduces the occurrence of stress-induced gastric lesions by acting on its specific receptor within the central nervous system, probably through the autonomic nervous system- and adrenal-dependent mechanism.

Animals↗
PubMed2005

Peroxisomes: another branch of the secretory pathway?

The question of whether new peroxisomes form autonomously has been a subject of debate for more than 30 years. In this issue of Cell, Hoepfner at al. (2005) present the most compelling evidence to date in support of a role for the endoplasmic reticulum in the creation of peroxisomes.

Endoplasmic Reticulum↗
PubMed2006

Segmental organization of spinal reflexes mediating autonomic dysreflexia after spinal cord injury.

Spinal cord injuries above mid-thoracic levels can lead to a potentially life-threatening hypertensive condition termed autonomic dysreflexia that is often triggered by distension of pelvic viscera (bladder or bowel). This syndrome is characterized by episodic hypertension due to sudden, massive discharge of sympathetic preganglionic neurons in the thoracolumbar spinal cord. This hypertension is usually accompanied by bradycardia, particularly if the injury is caudal to the 2nd to 4th thoracic spinal segments. The development of autonomic dysreflexia is correlated with aberrant sprouting of peptidergic afferent fibers into the spinal cord below the injury. In particular, sprouting of nerve growth factor-responsive afferent fibers has been shown to have a major influence on dysreflexia, perhaps by amplifying the activation of disinhibited sympathetic neurons. Using a model of noxious bowel distension after complete thoracic spinal transection at the 4th thoracic segment in rats, we selectively altered C-fiber sprouting, at specified spinal levels caudal to the injury, with microinjections of adenovirus encoding the growth-promoting nerve growth factor or the growth-inhibitory semaphorin 3A. This was followed by assessment of physiological responses to colorectal distension and subsequent histology. Additionally, anterograde tract tracers were injected into the lumbosacral region to compare the extent of labeled propriospinal rostral projections in uninjured cords to those in cords after complete 4th thoracic transection. In summary, overexpression of chemorepulsive semaphorin 3A impeded C-fiber sprouting in lumbosacral segments and mitigated hypertensive autonomic dysreflexia, whereas the opposite results were obtained with nerve growth factor overexpression. Furthermore, compared to naïve rats, there were significantly more labeled lumbosacral propriospinal projections rostrally after thoracic injury. Collectively, our findings suggest that distension of pelvic viscera increases the excitation of expanded afferent terminals in the disinhibited lumbosacral spinal cord. This, in turn, triggers excitation and sprouting of local propriospinal neurons to relay visceral sensory stimuli and amplify the activation of sympathetic preganglionic neurons in the thoracolumbar cord, to enhance transmission in the spinal viscero-sympathetic reflex pathway. These responses are manifested as autonomic dysreflexia.

Adrenergic Fibers↗
PubMed1998

Autonomic dysfunction in chronic intestinal pseudo-obstruction.

Fifteen tests were used to assess adrenergic, non-vagal cholinergic, and cardiovagal functions in 11 patients with chronic intestinal pseudo-obstruction (CIP). The three aims of this study were: 1) to ascertain the presence of and spectrum of autonomic involvement; 2) to assess the level of autonomic dysfunction; and 3) to compare the results of autonomic function tests with gastrointestinal motility patterns. Gastrointestinal motility displayed a neuropathic pattern in 10 patients. Adrenergic functions were abnormal in nine patients and non-vagal cholinergic functions in 10 patients. Cardiovagal functions were abnormal in only seven patients. The autonomic dysfunction was localized mostly to the postganglionic pathways. One patient, who had a myopathic pattern and muscle degeneration on small bowel biopsy, demonstrated normal responses to autonomic function tests. The patients with neuropathic CIP demonstrated widespread, mostly postganglionic autonomic dysfunction. Neuropathic CIP can occur with or without cardiovagal involvement.

Acetylcholine↗
PubMed2005

Anti-CD11d integrin antibody treatment restores normal serotonergic projections to the dorsal, intermediate, and ventral horns of the injured spinal cord.

Spinal serotonergic pathways provide inhibitory and excitatory modulation of sensory, autonomic, and motor processing. After spinal cord injury (SCI), the acute inflammatory response is one process that damages descending pathways. Increases in serotonergic fiber density in spinal segments rostral and decreases caudal to the lesion have been observed previously and may contribute to neuropathic pain and motor dysfunction associated with SCI. We investigated the effect of an acute anti-inflammatory treatment on the density of serotonergic fibers rostral and caudal to a thoracic SCI lesion. This treatment, a monoclonal antibody to the CD11d subunit of the leukocyte CD11d/CD18 integrin, limits the trafficking of neutrophils and macrophages into the SCI site. In the dorsal horn, after treatment, the typically increased serotonin immunoreactivity rostral to injury was reduced, whereas that caudal to the lesion increased toward normal. Coincidently, mechanical allodynia in the dorsal trunk and hindpaws was significantly reduced. Increased serotonergic fiber density below the lesion also occurred in the intermediolateral cell column and ventral horn of treated rats, relative to controls. Improved locomotor recovery paralleled this increased serotonin. The treatment increased compact myelin in and near the lesion epicenter and increased serotonergic fiber bundles coursing around part of the lesion but had no consistent effect on the number of raphe-spinal neurons retrogradely labeled by tracer injection below the injury. In conclusion, this anti-CD11d integrin antibody treatment is neuroprotective after SCI, corresponding with improved patterns of intraspinal serotonergic innervation. The improvement in serotonergic fiber projections paralleled reduced mechanical allodynia and enhanced locomotor recovery.

Animals↗
PubMed1991

Cardiovascular autonomic dysfunction: diagnosis and prognosis.

The symptoms of cardiovascular autonomic dysfunction may be subtle and occur late in the course of diabetes. They include abnormal exercise-induced cardiovascular performance, postural hypotension, and cardiac denervation syndrome. Autonomic nervous system testing involves an evaluation of the responses of complex reflex pathways. Some of the most commonly used and validated cardiovascular autonomic tests are RR-variation, the Valsalva manoeuvre, and postural testing. Sinus arrhythmia during breathing is termed RR-variation. In diabetic patients with autonomic neuropathy the magnitude of the RR-variation is decreased. Abnormal exercise-induced cardiovascular performance has been observed in diabetic subjects with abnormal RR-variation due to autonomic neuropathy. The Valsalva manoeuvre consists of forced expiration against a standardized resistance for a specified period of time. The reflex bradycardia that follows the Valsalva period in normal subjects is lacking in diabetic patients with clinical evidence of autonomic neuropathy. Postural hypotension in diabetics may be due to neuropathy or to a variety of secondary causes. An algorithm is presented to facilitate assessment of diabetic patients with postural symptoms. Treatment of postural hypotension should be directed primarily to the correction of secondary causes, in the absence of which the symptoms can be controlled by mechanical measures, plasma volume expansion, and vasoconstriction. Cardiac denervation syndrome may result in denervation supersensitivity and afferent (pain) nerve dysfunction. The RR-variation is a sensitive indicator of impairment of cardiac autonomic innervation and is a simple method for identifying asymptomatic patients at risk for painless ischaemia. Formal cardiovascular stress testing may be prudent before initiating an exercise programme in such individuals.

Autonomic Nervous System↗