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PubMed2000

Central neural regulation of penile erection.

Penile erection is caused by a change of the activity of efferent autonomic pathways to the erectile tissues and of somatic pathways to the perineal striated muscles. The spinal cord contains the cell bodies of autonomic and somatic motoneurons that innervate the peripheral targets. The sympathetic outflow is mainly antierectile, the sacral parasympathetic outflow is proerectile, and the pudendal outflow, through contraction of the perineal striated muscles, enhances an erection already present. The shift from flaccidity to erection suggests relations among these neuronal populations in response to a variety of informations. Spinal neurons controlling erection are activated by information from peripheral and supraspinal origin. Both peripheral and supraspinal information is capable of eliciting erection, or modulating or inhibiting an erection already present. One can hypothesize a spinal network consisting of primary afferents from the genitals, spinal interneurons and sympathetic, parasympathetic and somatic nuclei. This system is capable of integrating information from the periphery and eliciting reflexive erections. The same spinal network, eventually including different populations of spinal interneurons, would be the recipient of supraspinal information. Premotor neurons that project directly onto spinal sympathetic, parasympathetic or somatic motoneurons, are present in the medulla, pons and diencephalon. Several of these premotor neurons may in turn be activated by sensory information from the genitals. Aminergic and peptidergic descending pathways in the vicinity of spinal neurons, exert complex effects on the spinal network that control penile erection. This is caused by the potential interaction of a great variety of receptors and receptor subtypes present in the spinal cord. Brainstem and hypothalamic nuclei (among the latter, the paraventricular nucleus and the medial preoptic area) may not necessarily reach spinal neurons directly. However they are prone to regulate penile erection in more integrated and coordinated responses of the body, such as those occurring during sexual behavior. Finally, the central and spinal role of regulatory peptides (oxytocin, melanocortins, endorphins) has only recently been elucidated.

Animals↗
PubMed1994

Alterations in neural pathways to the urinary bladder of the rat in response to streptozotocin-induced diabetes.

Voiding dysfunction in diabetics has been attributed to a variety of causes including an axonopathy in autonomic pathways to the urinary bladder. The present study was undertaken to determine whether changes occurred in afferent and efferent neurons supplying bladders of streptozotocin (STZ)-induced diabetic rats. Nine weeks after STZ treatment, the mean cross-sectional area for retrogradely labeled (Fluoro-Gold) bladder neurons in the major pelvic ganglion (MPG) was greater in diabetics (364 microns 2) than controls (300 microns 2). The number of labeled neurons was similar in these groups. In contrast, mean cross-sectional areas of bladder afferent neurons labeled with WGA-HRP in the L6 and S1 dorsal root ganglia (DRG) were smaller (393 microns 2) in diabetics than in normal rats (528 microns 2). In addition, very few DRG neurons were labeled in STZ-treated rats and transganglionic labeling of bladder afferent projections in the L6 and S1 spinal cord with WGA-HRP was sparse. Radioimmunoassay studies revealed that substance P was reduced by 70% in the MPG and by 40% in L6 DRG, yet this peptide was unchanged in the bladders of diabetic rats. The amounts of VIP in the MPG and DRG of diabetics and controls were similar, while VIP in the bladder was increased in diabetics. These observations indicate that both afferent and efferent neurons innervating the urinary bladder are altered in the STZ-induced diabetic rat. In addition, axonal transport in visceral afferent pathways may be disrupted.

Afferent Pathways↗
PubMed1993

The circulation in diabetes, from HL523 to the NO era.

In 1955, F R Barany, a Swedish research physician interested in diabetes, summarised his dissertation (Acta Med Scand 1955; suppl 1304: 127) with the words "The ultimate cause of the various abnormal vascular reactions in diabetes might be assumed to be the cause of diabetic neuropathy in which autonomic pathways are the first to be destroyed...". That diabetes might involve a microcirculatory disease affecting the autonomic nervous system may be more relevant to the following reminiscence about the agent HL523 than I realised.

Diabetes Mellitus↗
PubMed1992

Neural regulation of the vas deferens in the rat: an electrophysiological analysis.

Electrophysiological analysis of the neural control of the vas deferens was performed in urethan-anesthetized rats. Intraluminal distension (0.2 ml/min) or electrical stimulation of hypogastric (threshold 1-5 V, 20 Hz) and pelvic nerves (2-5 V, 20 Hz) produced contractions of the vas deferens. Distension-evoked contractile activity was not abolished by nicotinic ganglionic blockade or ipsilateral hypogastric and pelvic nerve transection. Contractions following hypogastric nerve stimulation were abolished by prazosin, while pelvic nerve-evoked responses were partially blocked by atropine. Hypogastric nerve, pelvic nerve, and sympathetic chain stimulation evoked volleys with latencies of 10-30 ms in vasal nerves. Crude estimates for conduction velocities for these responses (less than 0.5 m/s) corresponded to activation of unmyelinated C-fibers. Stimulation of the dorsal nerve of the penis (DNP) (10-16 V, 10-40 Hz) or administration of 5-methoxy-N,N-dimethyltryptamine, both of which produce seminal emission, elicited reflex discharges in nerves to the vas deferens. Hypogastric nerve but not pelvic nerve transection abolished both spontaneous and evoked (105- to 380-ms latency) reflex activity. These experiments provide insight into the organization of afferents in the DNP and efferents conveyed by autonomic pathways that regulate male reproduction.

Animals↗
PubMed1986

Autonomic dysreflexia in a paraplegic man with catecholamine-secreting neuroblastoma.

Autonomic dysreflexia and catecholamine secreting tumor, each of which causes paroxysmal hypertension, coexisted in a young man. Two years after neuroblastoma was diagnosed, he developed T4 incomplete paraplegia due to metastases to the spine at T5 and L3 levels. Shortly after the onset of paraplegia, paroxysmal hypertension developed. The hypertension was controlled adequately by good bowel and bladder management and oral clonidine. The paroxysmal hypertension is believed to have resulted from the synergistic effect of the high levels of circulating catecholamines from the tumor and the disruption of autonomic pathways.

Adult↗
PubMed1988

Marked depletion of dorsal spinal cord substance P and calcitonin gene-related peptide with intact skin flare responses in multiple system atrophy.

In view of the presence of neuropeptides in spinal cord autonomic pathways, their regional concentration was studied in post mortem thoracic cord from four cases of multiple system atrophy with progressive autonomic failure (MSA). A marked depletion was observed of substance P, its related peptide substance K, and of calcitonin gene-related peptide (CGRP), particularly in dorsal regions where peptide-containing sensory fibres terminate. As substance P and CGRP in primary sensory fibres are considered mediators of skin flares in Lewis' triple response, histamine-induced skin flares were measured in 12 MSA patients and were found to be preserved. These results provide a new key to the classification and aetiology of autonomic and multiple system degenerations, as well as a model to study the role of sensory neuropeptides in man.

Aged↗
PubMed1986

Alpha-adrenoreceptors in hypertension.

The most important central autonomic pathways in the control of arterial blood pressure are the baroreceptor reflex pathway and descending pathways from the hypothalamus. Central neurotransmitters in these pathways are L-glutamate, substance P, norepinephrine (NE), gamma-aminobutyric acid, epinephrine, neuropeptide Y, and acetylcholine. At peripheral autonomic neurovascular junctions, there are prejunctional alpha 2- and dopamine-2 receptors, which inhibit NE release, and beta- and serotonin receptors, which stimulate NE release. Postjunctional alpha 1-receptors open sodium channels, open calcium channels via phosphoinositol release, and release intracytoplasmic calcium. Postjunctional alpha 2-receptors, which are extrasynaptic, inhibit adenylate cyclase and also open calcium channels. In animal models of hypertension, changes in alpha-receptor density have been reported. In spontaneously hypertensive rats, increased renal beta- and alpha 2-receptors, respectively, may enhance renin release and cause sodium and water retention. In experimental (renovascular) hypertension, vascular postsynaptic (vasoconstrictor) alpha 1- and alpha 2-receptors are increased. In both models of hypertension, beta-receptors are down-regulated. Selective alpha 1-antagonists, such as indoramin and prazosin, decrease arterial blood pressure by postsynaptic alpha 1-blockade; alpha 2-receptor inhibition of NE release is unaffected so that there is no beta-receptor-mediated tachycardia.

Adrenergic alpha-Agonists↗
PubMed1998

Angiotensin receptors in the nervous system.

In addition to its traditional role as a circulating hormone, angiotensin is also involved in local functions through the activity of tissue renin-angiotensin systems that occur in many organs, including the brain. In the brain, both systemic and presumptive neurally derived angiotensin and angiotensin metabolites act through specific receptors to modulate many functions. This review examines the distribution of these specific angiotensin receptors and discusses evidence regarding the function of angiotensin peptides in various brain regions. Angiotensin AT1 and AT2 receptors occur in characteristic distributions that are highly correlated with the distribution of angiotensin-like immunoreactivity in nerve terminals. Acting through the AT1 receptor in the brain, angiotensin has effects on fluid and electrolyte homeostasis, neuroendocrine systems, autonomic pathways regulating cardiovascular function and behavior. Angiotensin AT1 receptors are also found in many afferent and efferent components of the peripheral autonomic nervous system. The role of the AT2 receptor in the brain is less well understood, although recent knockout studies point to an involvement with behavioral and cardiovascular functions. In addition to the AT1 and AT2 receptors, receptors for other fragments of angiotensin have been proposed. The AT4 binding site, which binds angiotensin, has a widespread distribution in the brain quite distinct from that of the AT1 and AT2 receptors. It is associated with many cholinergic neuronal groups and also several sensory nuclei, but its function remains to be determined. Our discovery that another brain-derived peptide binds to the AT4 binding site in the brain and may represent the native ligand is discussed. Overall, the distribution of angiotensin receptors in the brain indicate that they play diverse and important physiological roles in the nervous system.

Animals↗
PubMed1985

Autonomic nervous system and epilepsy.

Seizures frequently manifest autonomic dysfunction clinically, and seizure discharges commonly spread into and involve autonomic pathways. These associations are direct and simple in some instances, and the result of multiple indirect and complex relationships in others. Effects of epileptic discharge on the autonomic nervous system are mediated through the cortical, limbic, and hypothalamic systems. Some significant consequences of altered autonomic function include convulsive apnea, abnormal sexual function, and potentially fatal effects on the cardiovascular system.

Adult↗
PubMed1982

Effects of kainic acid applied to the ventral surface of the medulla oblongata on vasomotor tone, the baroreceptor reflex and hypothalamic autonomic responses.

Application of an excitotoxic amino acid, kainic acid, to the ventral medullary surface just caudal to the trapezoid bodies (at Feldberg and Guertzenstein's glycine-sensitive area) led to the following observations. (1) Blood pressure began to rise within 25 s and by 10 min rose to high levels (200-240 mm Hg). Blood pressure subsequently fell to levels at or approaching those of a spinal animal. (2) Sympathetic vasomotor activity became insensitive to baroreceptor inhibition shortly after the peak in blood pressure, and the cardioinhibitory action of the reflex was enhanced during this time. (3) The autonomic effects of hypothalamic stimulation were differentially affected--pupillary dilatation and retraction of the nictitating membranes were unaffected, while the increases in blood pressure and renal nerve activity were blocked. (4) Recovery from these effects was observed on two occasions, when the animals were infused with a pressor agent and allowed to survive beyond 6 h after the kainic acid application. These results support the view that vasomotor tone is dependent upon the activity of relatively superficial cells in the ventral medulla. We further suggest that baroreceptor inhibition of sympathetic vasomotor activity acts via these cells and that descending hypothalamic autonomic pathways are organized at this level in terms of separate end organs.

Animals↗
PubMed1979

Anaesthetic considerations in idiopathic orthostatic hypotension and the Shy-Drager syndrome.

Orthostatic hypotension due to autonomic failure may occur secondary to systemic disease states (notably diabetes) or as a disease entity in its own right with a variable degree of neurological involvement that has resulted in a confused classification. The diagnosis, classification and treatment of these latter forms of orthostatic hypotension is reviewed. The pathology is in the central and efferent autonomic pathway, resulting in a disordered baro-receptor reflex, postural hypotension, abnormal responses to tilting and the Valsalva manoeuvre, an inappropriately fixed heart rate and other autonomic features. Anaesthesia may be associated with profound hypotension and some of the signs of anaesthesia may be absent. The response to cardiac depressant drugs and reduction of circulating blood volume may be exaggerated due to absence of compensatory mechanisms. The response to vasoactive agents is unpredictable. The importance of preoperative evaluation, monitoring during operation and the careful selection of anaesthetic agents and techniques is discussed.

Adult↗
PubMed1988

Localization of corticotropin-releasing factor, somatostatin, and vasoactive intestinal polypeptide in the parabrachial nuclei of the human brain.

The immunocytochemical localizations of corticotropin-releasing factor (CRF), somatostatin (SRIF), and vasoactive intestinal polypeptide (VIP) were studied in the human parabrachial nuclei (PBN) using the avidin-biotin complex (ABC) technique. The brains were obtained from seven adult male human subjects of 38-74 years. In three cases, the brains were fixed within 2 hr, in four cases within 5 hr, postmortem. All of these peptides were detected in fibers through the orocaudal extent of the lateral PBN, whereas the medial nucleus contained only CRF immunoreactive fibers. Immunoreactive fibers were distributed unevenly within the lateral nucleus with the highest density in the dorsal and much fewer in the ventral part of the lateral subdivision. The highest to lowest density of immunostained processes were detected using CRF, SRIF, and VIP antisera, respectively. Since NPB is known as an important relay nucleus for the central autonomic pathway, the presence of the above noted neuropeptides in nerve fibers in this area may suggest a neurotransmitter or neuromodulatory role of CRF, somatostatin, and VIP in certain autonomic nervous mechanism of the human brain.

Adult↗
PubMed1980

The neuroanatomical basis of central cardiovascular control.

A brief review is given of some of the recent neuroanatomical studies of the central autonomic pathways. Two major points are discussed. 1) There are several descending inputs to the intermediolateral cell column that have recently been demonstrated; these include the A5 catecholamine cell group, certain of the raphe nuclei, the nucleus of the solitary tract, the Kölliker Fuse nucleus, and the paraventricular nucleus of the hypothalamus. 2) Certain nuclei of the brain that function as autonomic centers are extensively interconnected: the nucleus of the solitary tract, the parabrachial nucleus, the paraventricular nucleus of the hypothalamus, the central nucleus of the amygdala, and the bed nucleus of the stria terminalis. This network may play an important role in cardiovascular regulation and related neuroendocrine functions.

Amygdala↗
PubMed1993

Do nonimmunologically mediated pathways play a role in the pathogenesis of rheumatoid arthritis?

The association between elevated serum rheumatoid factor and rheumatoid arthritis (RA) has been confirmed repeatedly and interpreted as strong evidence for an immunologic basis for the disease. In recent years, considerable additional evidence supporting this view has been obtained, strongly suggesting a role for CD4+ T cells in the pathogenesis of RA. An alternative view has also gained support, however. Based on studies of animal models and of RA itself, several lines of evidence have emerged that indicate that nonimmunologic pathways are operative in established RA. These observations have fostered the hypothesis that the evolution of RA may be associated with the emergence of non-T-cell-dependent autonomous pathways that dominate the latter stages of the disease.

Antibody Formation↗
PubMed1991

Surgical interruption of postganglionic innervation of the sinoatrial nodal region.

Recent experiments have revealed synapses that selectively mediate right and left vagal regulation of sinoatrial function in the fat pad overlying and surrounding the right pulmonary vein complex. However, precise vagal postganglionic pathways to the sinoatrial region have remained obscure. Such pathways, including critically important neural inputs to sinoatrial and atrioventricular nodal regions, may be vulnerable to surgical approaches to atrial or intracardiac repair. The present experiments seek to delineate specific autonomic pathways to the sinoatrial region of the canine heart. The distal ends of the cut right and left cervical vagi and the right and left ansae subclaviae were electrically stimulated (10 to 20 Hz, 1 msec, 2 to 3 V) before and after surgical incisions were placed. Cut No. 1 was made longitudinally along the ventral caval surface from the pericardial reflection caudally to the pulmonary vein fat pad, cut No. 2 was made from the caudal end of cut No. 1 transversely across the sulcus terminalis to a point midway across the anterior (ventral) surface of the right atrium. Each incision was closed with 4-0 silk, with care being taken to avoid injury to either the sinoatrial nodal or the pulmonary fat pad regions. In four of seven animals, these two incisions totally interrupted vagal input to the sinoatrial node, whereas in the remaining three dogs a residual inhibitory influence remained. These residual fibers were surgically ablated by excision of globular fat pads situated on the rostrodorsal surfaces of the right superior pulmonary vein, suggesting a dorsorostral route into the interatrial septum and thence to the sinoatrial node. There was little or no interruption of either right or left vagal input to the atrioventricular nodal region; sympathetic supplies to both sinoatrial nodal and atrioventricular nodal regions remained essentially intact after the two incisions. Thus the major parasympathetic postganglionic projections to the sinoatrial node in the dog heart are by way of the free wall of the right atrium and are vulnerable to surgical interventions in this portion of the heart.

Animals↗
PubMedDate not supplied

Vestibular influences on autonomic cardiovascular control in humans.

There is substantial evidence that anatomical connections exist between vestibular and autonomic nuclei. Animal studies have shown functional interactions between the vestibular and autonomic systems. The nature of these interactions, however, is complex and has not been fully defined. Vestibular stimulation has been consistently found to reduce blood pressure in animals. Given the potential interaction between vestibular and autonomic pathways this finding could be explained by a reduction in sympathetic activity. However, rather than sympathetic inhibition, vestibular stimulation has consistently been shown to increase sympathetic outflow in cardiac and splanchnic vascular beds in most experimental models. Several clinical observations suggest that a link between vestibular and autonomic systems may also exist in humans. However, direct evidence for vestibular/autonomic interactions in humans is sparse. Motion sickness has been found to induce forearm vasodilation and reduce baroreflex gain, and head down neck flexion induces transient forearm and calf vasoconstriction. On the other hand, studies using optokinetic stimulation have found either very small, variable, or inconsistent changes in heart rate and blood pressure, despite substantial symptoms of motion sickness. Furthermore, caloric stimulation severe enough to produce nystagmus, dizziness, and nausea had no effect on sympathetic nerve activity measured directly with microneurography. No effect was observed on heart rate, blood pressure, or plasma norepinephrine. Several factors may explain the apparent discordance of these results, but more research is needed before we can define the potential importance of vestibular input to cardiovascular regulation and orthostatic tolerance in humans.

Animals↗
PubMed1999

Intracavernous pressure during erection in rats: an integrative approach based on telemetric recording.

To better understand the similarities and differences in the neural control of penile erection occurring in different contexts, we recorded intracavernous pressure (ICP) in conscious rats using a miniaturized telemetric device. ICP changes during reflexive, noncontact, and apomorphine-induced erections were characterized by a plateau increase surmounted by peaks. Plateaus were also elicited by cavernous nerve stimulation in anesthetized rats, suggesting that the cavernous nerve represents the final common proerectile autonomic pathway in these contexts and that it responds similarly to information originating in the periphery or in supraspinal nuclei. During reflexive, noncontact, and apomorphine-induced erections, activation of spinal autonomic nuclei, considered the spinal generators of erection, would take place first, representing a prerequisite for the occurrence of peaks. Suprasystolic peaks would result from the addition of pudendal motoneuron activity. In contrast, only peaks were recorded during copulation. In this context, the convergence of peripheral and supraspinal information apparently elicits the best temporal arrangement of autonomic and somatic outflows, reflecting a highly organized and integrated spinal activity.

Animals↗
PubMed1999

Autonomic nervous system disorders in stroke.

Disturbances of the autonomic nervous system are common in patients with various cerebrovascular diseases. They are attributed to damage of the central autonomic network, particularly in the frontoparietal cortical areas and in the brain stem, or to a disruption of the autonomic pathways descending from the hypothalamus via the mesencephalon, pons, and medulla to the spinal cord. The most common clinical problems include abnormalities in heart rate and blood pressure regulation, reflecting cardiovascular autonomic dysfunction, and asymmetric sweating with cold hemiplegic limbs, reflecting changes in the sudomotor and vasomotor regulatory systems. Bladder and bowel dysfunction and impotence are also frequent complaints after stroke, but the present knowledge concerning their prevalence and clinical significance is still limited. Cardiovascular autonomic dysfunction, which is mainly related to increased sympathetic activity, is most evident in the acute phase of stroke, whereas other autonomic disorders, such as abnormal sweating, are long-standing or even irreversible. In addition to the well-established sympathetic hyperfunction, abnormalities of the parasympathetic nervous system may also contribute to the autonomic imbalance after stroke. Reliable recognition of autonomic dysfunction using quantitative analysis methods is important, because these disturbances are not only subjectively disabling and uncomfortable, but they may also be prognostically unfavorable. Moreover, quantitative measurements also form the ground for successive treatment of various stroke-related autonomic disorders.

Autonomic Nervous System Diseases↗