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Introduction: The factors that control the blood pressure are punctually regulated to keep it in reference values. These are maintained through autoregulatory mechanisms, humoral, nervous and endothelial-related. The humoral mechanisms are complex and modify the long-term blood pressure, in the other hand, the neurogenic mechanisms, are reflexive and can be observed in beat-to-beat changes of blood pressure., Development: The nervous cardiovascular reflexes are mediated by high-pressure and low-pressure baroreceptors, as cardiovagal, cardiosympathetic and vasosympathetic. The arterial baroreceptor are stimulated when the blood volume-ejected by the ventricle distend the arterial walls. The neural discharge travels to the autonomic centers in the brain stem and the result is the modification of the heart rate and the vascular smooth muscle tone. This sudden modification is the responsible of the beat-to-beat (short-term) blood pressure variability., Conclusion: A review was made on the history of the physiology and experiments of the cardiovagal, cardiosympathetic and vasosympathetic baroreflexes and its influence in the short-term blood pressure variability.

INTRODUCTION. The sympathetic skin response (SSR) has been used since its description in 1984 to test the integrity of the sympathetic autonomic nervous system to investigate peripheral and central nervous system diseases. AIM. To present a neurophysiological examination protocol for SSR and the normal parameters for a population of 100 normal subjects. SUBJECTS AND METHODS. To evaluate the characteristics of 200 SSR tests for 100 normal subjects adequately informed: latency, amplitude (peak to peak) and persistence. The subject lays supine and relaxed, with no visual nor auditory stimuli for several minutes. Cutaneous electrodes are used for stimulation and recording, the latter in palm (active) and back (reference) in both hands simultaneously (second interosseous space). The stimulus is applied in the glabela at irregular intervals. RESULTS. We studied 100 normal subjects aged 12 to 89 years (mean: 45.6), 21 men and 79 women. The parameters measured in the 200 SSR are: latency, 1.42 ± 0.03 s; amplitude, 2.44 ± 1.84 mV; persistence, 67.2 ± 19.8%. CONCLUSIONS. SSR is an objective, reproducible, measurable, easy to perform and unpainful for the patient and serves as a basis for further study of other diseases in which there is a dysfunction of the sympathetic autonomic nervous system.

Background: Cardiac sympathovagal balance is altered after resistance exercise. However, the impact of the characteristics of resistance training in this response remains unclear., Objective: Analyze the acute effect of resistance exercise intensity for trunk and upper limbs in cardiac autonomic modulation after exercise., Methods: Fifteen young men performed three experimental sessions in random order: control (C), resistance exercise with 50% of 1-RM (E50%) and resistance exercise with 70% of 1-RM (E70%). The sessions included 05 exercises for the trunk and upper limbs performed in three sets of 12, 9 and 6 repetitions, respectively. Before and at 20 and 50 minutes after the interventions, the heart rate was measured for spectral analysis of variability., Results: In comparison to the values before the intervention, the RR interval and the band of high frequency (HF) increased (major changes: + 112 ± 83 ms; +10 ± 11 un, respectively, p < 0.01), while the low frequency band (LF) and LF/HF ratio decreased (major changes: -10 ± 11 pc; -2 ± 2, respectively, p < 0.01) after the session C. None of these variables changed significantly after the E50% session (p > 0.05). Compared to pre-exercise values, the RR interval and the HF band decreased (major changes: -69 ± 105 ms; -13 ± 14 un, respectively, p <0.01), while the LF band and the LF/HF ratio increased (major changes: -13 ± 14 un, 13 ± 3 14 ± 3 and un, respectively, p <0.01) after E70%., Conclusion: The higher intensity of resistance exercise for trunk and upper limbs promoted, in an acute manner, greater increase in cardiac sympathovagal balance after exercise.

The heart failure (HF) syndrome can be defined as the final pathway of any type of heart disease. The sympatho-inhibitory cardiovascular reflexes, such as the arterial baroreceptor reflex, are significantly decreased in HF. Patients with HF present higher ventilation for a certain workload when compared with normal individuals. This fact generates low ventilatory efficiency and is related to higher ventilation associated with the carbon dioxide production, which is a predictor of bad prognosis, in addition to being a limiting factor for the practice of exercises. There is evidence that the autonomic imbalance contributes to the pathogenesis and the progression of heart failure. The chemoreflexes are the main mechanisms of control and regulation of the ventilatory responses to the changes in concentrations of arterial oxygen and carbon dioxide. The chemoreflex activation causes an increase in the sympathetic activity, heart rate, arterial pressure and minute volume. However, the increase in the minute volume and the arterial pressure, due to negative feedback, cause inhibition of the sympathetic response at the chemoreflex activation. In spite of the functional alterations of the reflexes, their behavior in normal and pathological conditions, especially their contribution to the sympathoexcitatory state observed in HF has not been broadly studied. Therefore, this review aims at integrating the knowledge on central and peripheral chemoreflexes in HF syndrome, as well as clarifying the influence of the heart failure drug therapy on the chemoreflexes.

Serotonin (5-hydroxytryptamine; 5-HT) has been shown to produce vascular sympatho-inhibition in a wide variety of isolated blood vessels by activation of prejunctional 5-HT1 receptors. After considering the mechanisms involved in modulating neuroeffector transmission, the present review analyzes the experimental findings identifying the pharmacological profile of the 5-HT receptors that inhibit the sympathetically-induced vasopressor responses in pithed rats. Thus, 5-HT-induced sympatho-inhibition has been shown to be: (i) unaffected by physiological saline or by the selective antagonists ritanserin (5-HT2), MDL72222 (5-HT3) or tropisetron (5-HT3/4); (ii) blocked by methysergide, a non-selective 5-HT1/2 receptor antagonist; and (iii) potently mimicked by 5-carboxamidotryptamine (5-CT), a non-selective 5-HT1 receptor agonist, as well as by the selective agonists 8-OH-DPAT (5-HT1A), indorenate (5-HT1A), CP93,129 (5-HT1B), and sumatriptan (5-HT1B/1D). These findings show the involvement of prejunctional 5-HT1 receptors. With the use of selective antagonists, it has been shown subsequently that the sympatho-inhibition induced by indorenate, CP93, 129, and sumatriptan was selectively antagonized by WAY100635 (5-HT1A), cyanopindolol (5-HT1A/1B), and GR127935 (5-HT1B/1D), respectively. These results demonstrate that the 5-HT1 receptors mediating sympatho-inhibition on the systemic vasculature of pithed rats resemble the pharmacological profile of the 5-HT1A, 5-HT1B, and 5-HT1D subtypes.

Abstract. The aim of this study was to evaluate the role of AT1 angiotensin II receptor on the sympathetic response to the cold pressor test (CPT) in normotensive healthy volunteers. Eighty-two healthy volunteers were included in this double-blind, placebo-controlled study. Blood pressure and heart rate were determined before and one hundred and seventy five minutes after oral administration of placebo, losartan (50 mg), valsartan (80 mg) or eprosartan (600 mg). Immediately, the subjects underwent CPT and then the same hemodynamic parameters were measured. CPT increased arterial blood pressure (systolic, diastolic and mean) and HR in placebo-treated group. Pretreatment with a single dose of losartan, valsartan or eprosartan blunted CPT-induced pressor response, but not the rise in heart rate. Our results demonstrate that endogenous angiotensin II, through stimulation of AT1 receptor, supports sympathetic mediated stress-response in humans.

Introduction: The autonomic nervous system (ANS) is made up of a complex set of neurons and pathways that control the functioning of the different body systems within the organism. Its overall function is that of maintaining a state of homeostasis in the organism and of performing the adaptation responses when faced with changes in the external and internal environment., Methods: The ANS is composed of visceral afferent pathways, integration centres at the brain stem, hypothalamus and cerebral cortex levels, as well as sympathetic and parasympathetic efferent pathways. The efferent pathways innerve the cardiac muscle, the smooth muscle and the exocrine and endocrine glands, while the afferent pathways are arranged in two patterns: oligosynaptic circuits, which mediate reflex adaptation responses of the visceral systems, and complex circuits, with projections to nuclei in the brain stem and the brain, where the information is collected and responses are produced that affect numerous systems. The afferent signals activate or inhibit the efferent components of the ANS by means of reflex pathways, independently of the will. These reflex circuits are also modulated by means of signals from central structures, and constitute a central autonomic neuronal network that integrates somatic, autonomic and affective responses., Conclusion: Dysfunctions of the ANS are possibly due to increases or decreases in autonomic control activity, which can appear because of lesions to the brain, spinal cord or peripheral nerves.

Introduction: In the diagnosis of autonomic disturbances, the variability of skin blood flow (SBF) and the sympathetic skin response (SSR) in response to several respiratory maneuvers are not routinely studied., Objective: We sought to standardize the method of SBF variability and SSR in healthy subjects during four respiratory maneuvers: 1) spontaneous breathing (SB); 2) rhythmic breathing at a rate of 6 per minute (RB); 3) sudden deep inspiration (SDI); 4) Valsalva maneuver (VM). SUBJECTS, MATERIAL AND METHOD: We studied 30 healthy subjects with a mean age of 32 years, 60% were men and 40% women. We used a photopletysmograph in the finger pad to measure SBF and surface electrodes on the palms of the hand to register the SSR. We also recorded the ECG and the respiratory movements. The variables were: 1) amplitude of SBF; 2) latency and duration of SSR; 3) percentage of decrease of the SBF during the maneuvers compared with the basal flow., Results: During spontaneous breathing there was no respiratory modulation of the SBF and during RB the SBF was modulated with respiration. With SDI there was a 60% decrease of the SBF. VM induced a larger SBF decrease of 72 per cent. A significant statistical difference was revealed when we compared the decrease of SBF basal breathing with SDI and VM (P < 0.001). The difference was also significant between the SDI and VM (P < 0.001). The SBF decrease recovered more slowly after the SDI (beat 7) than after the VM (veat 6). The SBF decrease was more pronounced in magnitude during the VM. The latency of the SSR appears spontaneously and at random in 57% of subjects during normal breathing but it appeared consistently during RB, SDI, and VM. The latency of SSR was longer during SB (1.7 +/- 0.7 s), RB (1.6 +/- 0.7 s) than SDI (0.7 +/- 0.5 s) and VM (0.8 +/- 0.9 s) (P > 0.050). Duration of the SSR was significantly longer in the SDI (around 7.8 +/- 2.4 s) and during the VM (8 +/- 2.5 s) as compared to normal breathing (6.3 +/- 1.0 s) and RB (6.4 +/- 1.5 s) (P < 0.009)., Conclusions: SB and RB induce periodic modulation of sympathetic activity to skin blood vessels and sweat glands. SDI and VM produced a much greater activation of sympathetic skin activity than SB and RB. The increased SSR duration and the profound SBF decrease with SDI and VM as compared to SB or RB are consistent with this hypothesis. The latency of the SSR is much shorter with SDI and VM than with SB or RB. The most likely explanation is that the SSR, under these circumstances, results from a central command. The recovery to normal SBF is faster after the VM as compared to SDI. This suggests that the withdrawal of sympathetic responses is faster after the VM. The explanation for this is unknown but suggests that it might be baroreceptor mediated.

Introduction: From certain experimental data obtained by experimental myocardial perfusion and clinical and animal studies, it would seem that this corroborates the finding that puncture of the acupuncture point (Neiguan, 6PC) has an effect on organic vegetative tone., Objective: We aimed to establish, by means of a simple, conclusive, objective measuring system such as sympathetic electrical response, whether this point had this action and whether its effect was nonspecific or due to activation of a nervous tract subjacent to this point., Patients and Methods: We assessed the sympathetic electrical response in 29 healthy volunteers in whom basal values were recorded and again after orthodox acupuncture stimulus in 6PC, and compared with data obtained of the effects caused by stimulus of an extra-acupunctural point, of a different acupunctural point of the same channel, of bipolar stimulation of the median nerve at the level of 6PC and with the modifications generated in the response by rest lying down during the period of the experiment., Results: A significant increase was observed in the P1 latency of the sympathetic electrical response and significant reduction in its total amplitude, when 6PC was stimulated, an effect not observed in any of the other conditions of the experiment., Conclusion: We conclude that puncture stimulation of 6PC causes significant changes in sympathetic tone, which are not due to nonspecific effects of skin puncture, nor activation of the subjacent median nerve alone.

Background: Therapeutical response to antihypertensive treatment is poorly predicted by individual clinical or biochemical characteristics. Some preliminary data indicate that therapeutical response to atenolol might depend on physical and/or sympathetic activity. The aim of the present study was to evaluate the blood pressure response to atenolol depending on physical and sympathetic activity., Patients and Methods: One thousand one hundred forty hypertensive patients were treated with the beta adrenorecepetor blocker atenolol in an open fashion during 3 months. Before the beginning of the treatment, we evaluated current weekly physical activity (direct interview), as well as sympathetic activity (direct interview and baseline heart rate)., Results: Age or physical activity did not correlate with blood pressure response to atenolol. Conversely, hypertensive patients with symptoms suggesting sympathetic overactivity (three or more of the following symptoms: palpitations, anxiety, diaphoresis, headache, tremor or weakness; n = 456), showed a more pronounced decrease in systolic (27.7 [13.4] vs 25.8 [14.3] mmHg; p = 0.0226) and diastolic (17.6 [8.3] vs 15.5 [8.6] mmHg; p = 0.0001) blood pressures (SBP and DBP), with respect to the remaining hypertensive patients (n = 719). Moreover, we found a statistically significant correlation between blood pressure fall with atenolol and baseline heart rate (r = 0.107, P < 0.001 for SBP, and r = 0.142, p < 0.001 for DBP)., Conclusion: Baseline tachycardia or symptoms suggesting anxiety, emotional tension or sympathetic overactivity are associated with a more pronounced blood pressure fall to antihypertensive treatment with atenolol. These circumstances may play a role when choosing a new antihypertensive therapy.

Introduction: The progress made by contemporary neurobiology opens new horizons both for study and for treatment of disorders of the nervous system. At the present time we are in the age of growth factors. These are molecules which affect survival, development and the normal functioning of cell populations., Development: One of the most widely studied growth factors is nervous growth factor (NGF) which is necessary for normal life of various types of neurones, including sensory nerves and nerves derived from the neural crests. Diabetic neuropathy, worldwide a major neurological disorder, is primarily characterized by involvement of the fine fibres for temperature and pain perception and also by a variety of autonomic disorders. The great dependence of sensory and sympathetic nerves on NGF, the quantity of results which show alterations in the levels of neurotrophic factors in diabetic neuropathy (DN), and the encouraging experimental and clinical results of using NGF as a new alternative to treatment with DN, were the basic reasons which led us to do this study., Conclusions: We started by considering neurotrophic factors, especially NGF and its connection with DN disorders and its clinical applications, we made a summary of the main findings in this field to date.

Introduction and Objectives: Metaiodobenzylguanidine (MIBG) is an analogue of norepinephrine and its cardiac uptake shows sympathetic innervation. During the heart transplantation the allograft becomes completely denervated. The present study was conducted to assess the evolution of sympathetic re-innervation after transplantation, and to related re-innervation with functional status., Patients and Methods: We studied 31 patients from 6 months to 12 years after transplantation by 123I-MIBG studies to evaluate re-innervation and by rest/exercise radionuclide ventriculography to evaluate cardiac function. Myocardial MIBG uptake was quantified by calculating a heart-to-mediastinum ratio (HMR). An HMR > 1.8 was considered normal, moderate between 1.8 and 1.6, mild between 1.6 and 1.3, and absent < 1.3., Results: HMR correlated with time after transplantation (r = 0.607; p < 0.001). HMR of patients studied after 2 years of transplantation was significantly higher (1.62 +/- 0.2 vs 1.34 +/- 0.2; p < 0.05). MIBG uptake was in the anterior region in 3 patients, in the antero-lateral region in 25, and in the antero-lateral and septal regions in 3. From a functional point of view, peak filling rate at exercise was higher in patients studied 2 years after the transplantation (2.7 +/- 0.8 edv/s vs 2.16 +/- 0.5 edv/s; p = 0.02). These patients also showed a higher increase of heart rate with exercise (p < 0.005 vs p < 0.01)., Conclusions: Sympathetic re-innervation increase with time after heart transplantation, and is more frequently seen 2 years after transplantation. Sympathetic re-innervation first appears in the anterior or the antero-lateral regions. A complete re-innervation of the transplanted heart does not occur 12 years after transplantation.

Functional impairment of transplanted kidneys may occur due to circumstances related either directly or indirectly to the donor, the graft or the receptor. In most publications, renal damage is frequently attributed to ischaemia phenomena, mainly host ischaemia, either because of intraoperative interruption of blood flow for an exceedingly long interval, until perfusion and cooling of the removed kidneys, by the duration of cold ischaemia for organ preservation, or during the implant procedure. Also due to the activation of neuroadrenergic reflexes as a consequence of the mechanical stimulation of sympathetic nervous endings during dissection of the vascular pedicle. Earlier studies in animals have demonstrated that direct, low frequency electric stimulation of the splanchnic nerve involves reversible changes in sodium renal excretion, but it does not modify glomerular filtration; when nerve stimulation is done with high frequency there is a decline of renal blood flow and glomerular filtration. The present study tries to associate some of the causes of hot ischaemia during the agony of the corpse donor and to evaluate those that may be caused by sympathetic efference during removal.

The only non-general sensation that can be elicited from the gastrointestinal (GI) tract is that of pain, which can go from slight discomfort to severe pain. However, in certain parts of the intestine, such as the rectum and gastroesophagus, the sensation of pain can be preceded by a non-painful sensation of distension at low levels of stimulation. GI pain is often dull, poorly defined and difficult to pinpoint. In some cases, GI pain is projected to areas of the body distant from the source organ ("referred" pain). These characteristics indicate that the representation of internal organs within the nervous system is very imprecise. Experimental evidence based on behavioral, neurological and clinical testing shows that most GI pain is the result of activity in afferent visceral sensory fibers contained in sympathetic nerves, and that the afferent intestinal innervation by means of parasympathetic nerves is not essentially related to GI pain signalling and transmission. As for the peripheral sensory receptor coding mechanism in the intestine, experimental tests have shown the existence of specific visceral nociceptors in certain places (e.g., the biliary system) and the existence of a king of non-specific "intensity" receptors in others (e.g. the colon). In any case, the number of afferent nociceptive fibers in the intestine is minimal, and this accounts for the fact that large areas of the GI tract appear to be insensitive or to require considerable stimulation before pain can be elicited. The few afferent nociceptive fibers contained in the sympathetic nerves can excite quite a few second order neurons in the medulla spinalis, which in turn generate an extensive divergence within the medulla spinalis and brain stem, including at times long supraspinal branches. This divergent input can activate different motor, autonomous and sensory systems, thus triggering the general reactions which characterize visceral nociception: diffuse pain which is difficult to pinpoint, referred at times to somatic areas, and autonomous and somatic reflexes resulting in prolonged motor activity.

This article discusses the experimental evidence which suggests that the pineal gland and its innervating neurons are useful paradigms for the study of neuroendocrine integrative processes. The obtained results can be summarized as follows: 1) existence of putative receptors for various hormones (estradiol, testosterone, 5 alpha-dihydrotestosterone, progesterone, prolactin) in the mammalian pineal gland; (2) steroid metabolic pattern in the pineal gland resembling other brain areas involved in gonadotrophic regulation; (3) control of pineal estrophilic and androphilic receptors by adrenergic transmitter through beta-adrenergic receptors and at a translational level; (4) denervation supersensitivity of hormone receptors to neurotransmitter; (5) modification of neuronal activity by hormone treatment at ganglionic and preganglionic sites of action; (6) estrophilic binding sites in ganglia; (7) correlation of pineal responsiveness to hormones with activity of sympathetic nerves; (8) modification by hormones of pineal beta-adrenergic mechanisms; (9) dissociation of hormone effects on the pineal gland in those mediated or modulated by changes in afferent neuronal activity and those relatively unaffected by denervation. Collectively these data indicate that neuroendocrine, endocrine-neural and endocrine-endocrine transducing processes occur in the pinealocytes and superior cervical ganglia.

The sympathetic influences on the rabbit unstimulated parotid gland were studied. The experiments were carried out in anaesthetized rabbits with the Stenon aduct cannulated. Direct stimulation of the superior cervical ganglion elicits variable salivary flows. The high amylase content in the saliva points to a sympathetic secretory action upon acinar cells. The administration of alpha-adrenergic blocking agents (dihydroergotamine, phentolamine and phenoxybenzamine) clearly reduces and even abolishes the effect of the sympathetic stimulation upon flow. The administration of a beta-adrenergic blocking agent (propranolol) slightly reduces the sympathetic action. However the amylase activity is greatly reduced. All this suggests that the secretory effects on the fluid fraction should predominantly be alpha-adrenergic while on the secretion of enzymes the beta-receptors should play an important role.

In fifty-five patients who had undergone open-heart surgery, plasma levels of catecholamines and urinary excretion of adrenalin and noradrenalin were studied. We have divided the patients in three groups, according to the analgesic administered during the operation: group A, patients anesthesized with Pentazocina; group B, with Morfine; group C with Fentanest. By determining these catecholamate levels, we have been able to show an increase in sympathetic activity in all three groups. However, during the peroperative period. Fentanest gave the smallest increase and Pentazocina the largest. The more prolonged analgesia of Morfine manifested itself during the post-operative period in a smaller elimination of adrenalin. We then studied the influence of Fentathinil on the sympatho adreno-medullar system. This recently-acquired analgesic, used in extracorporeal perfusion, grave a catecholamine elimination inferior to that found with Fentanest.

Superior cervical ganglion stimulation significantly increases both, flow and amylase activity of saliva. Stimulation provokes two markedly different periods of flow: during the first half, flow is very high and differs significantly from the flow of the second half which closely resembles the one previous to stimulation. Alpha-adrenergic blocking agents, when administered intravenously, abolish the hypersecretion induced by sympathetic stimulation; beta-adrenergic blocking agents do not. These facts strengthen the hypothesis that alpha-adrenoceptors are most important in fluid secretion. The infusion of epinephrine acts similarly on cervical ganglion stimulation, but it differs because of its more diffuse effects and deeper cardiovascular alterations. Isoproterenol, after a long latency period, slightly increases salivary flow, which seemingly indicates that beta-adrenoceptors are involved in the fluid secretory processes although in a lesser degree than alpha-adrenoceptors.