Efecto del manejo farmacológico del sistema nervioso autónomo en la pancreatitis aguda inducida por el veneno de escorpión Tityus zulianus en un modelo ex vivo / Effect of the pharmacological management of the autonomic nervous system in the acute pancreatitis induced by the venom of Tityus zulianus scorpion in an ex vivo model

La pancreatitis es una de las consecuencias principales del envenenamiento escorpiónico producido por el género Tityus. El manejo farmacológico mediante el uso de agonistas y antagonistas α adrenérgicos en modelos experimentales in vivo e in vitro, permiten establecer una aproximación del papel del Sistema Nervioso Simpático (SNS) en el desarrollo de la pancreatitis. Objetivo: determinar el papel del SNS en el desarrollo de la pancreatitis aguda inducida por el veneno de escorpión Tityus zulianus (TzV), por medio del uso de simpaticolíticos como la clonidina y el prazosin. Métodos: La Extravasación de Proteínas Plasmáticas (EPP) en el páncreas se evaluó mediante el método de Azul de Evans (AE), modificado de Saria y Lundberg (1983) a 620 nm; n=3 ratones NIH en cada grupo experimental. Las comparaciones se hicieron por ANOVA de una vía y las pruebas post HOC por Tukey-Kramer. Resultados: Ambos fármacos (1mg/Kg), disminuyeron significativamente p< 0,01 (**) la EPP en el páncreas inducida por el TzV, en comparación con los animales inoculados solo con TzV. No hubo diferencias significativas entre los animales del grupo control y los grupos tratados con los fármacos más el TzV. Conclusiones: El efecto pancreatotóxico del TzV en ratones podría tener un componente autonómico dado que drogas simpaticolíticas al disminuir la actividad noradrenérgica reducen la magnitud del edema. Esto sugiere que ambos fármacos pueden usarse como estrategia terapéutica en estos casos(AU)

Pancreatitis is one of the main consequences of scorpionic poisoning produced by the genus Tityus. The pharmacological management through the use of agonists and α adrenergic antagonists in experimental models in vivo and in vitro, allow us to establish an approximation of the role of the Sympathetic Nervous System (SNS) in the development of pancreatitis. Objective: to determine the role of SNS in the development of acute pancreatitis induced by the scorpion venom Tityus zulianus (TzV), through the use of sympatholytics such as clonidine and prazosin. Methods: Plasma Protein Extravasation (PPE) in the pancreas was evaluated by the method of Evans Blue (EA), modified by Saria and Lundberg (1983) at 620 nm; n = 3 NIH mice in each experimental group. Comparisons were made by one-way ANOVA and post-HOC tests by Tukey-Kramer. Results: Both drugs (1mg / Kg) significantly decreased p <0.01 (**) the EPP in the pancreas induced by TzV, compared to animals inoculated only with TzV. There were no significant differences between the animals in the control group and the groups treated with drugs plus TzV. Conclusions: The pancreatotoxic effect of TzV in mice could have an autonomic component since sympatholytic drugs by decreasing noradrenergic activity reduce the magnitude of edema. This suggests that both drugs can be used as a therapeutic strategy in these cases(AU)

Effect of selective beta-adrenoceptor blockade and surgical resection of the celiac-superior mesenteric ganglion complex on delayed liquid gastric emptying induced by dipyrone, 4-aminoantipyrine, and antipyrine in rats

There is evidence for participation of peripheral β-adrenoceptors in delayed liquid gastric emptying (GE) induced in rats by dipyrone (Dp), 4-aminoantipyrine (AA), and antipyrine (At). The present study aimed to determine whether β-adrenoceptors are involved in delayed GE induced by phenylpyrazole derivatives and the role of the prevertebral sympathetic nervous system in this condition. Male Wistar rats weighing 220-280 g were used in the study. In the first experiment rats were intravenously pretreated with vehicle (V), atenolol 30 mg/kg (ATE, β1-adrenergic antagonist), or butoxamine 25 mg/kg (BUT, β2-adrenergic antagonist). In the second experiment, rats were pretreated with V or SR59230A 2 mg/kg (SRA, β3-adrenergic antagonist). In the third experiment, rats were subjected to surgical resection of the celiac-superior mesenteric ganglion complex or to sham surgery. The groups were intravenously treated with saline (S), 240 µmol/kg Dp, AA, or At, 15 min after pretreatment with the antagonists or V and nine days after surgery. GE was determined 10 min later by measuring the percentage of gastric retention (%GR) of saline labeled with phenol red 10 min after gavage. The %GR (means±SE, n=6) values indicated that BUT abolished the effect of Dp (BUT+Dp vs V+Dp: 35.0%±5.1% vs 56.4%±2.7%) and At (BUT+At vs V+At: 33.5%±4.7% vs 52.9%±2.6%) on GE, and significantly reduced (P<0.05) the effect of AA (BUT+AA vs V+AA: 48.0%±5.0% vs 65.2%±3.8%). ATE, SRA, and sympathectomy did not modify the effects of treatments. These results suggest that β2-adrenoceptor activation occurred in delayed liquid gastric emptying induced by the phenylpyrazole derivatives dipyrone, 4-aminoantipyrine, and antipyrine. Additionally, the released neurotransmitter did not originate in the celiac-superior mesenteric ganglion complex.

Cardiac Sympathetic Hyperactivity after Chemotherapy: Early Sign of Cardiotoxicity? / Hiperatividade Simpática Cardíaca Após Quimioterapia: Sinal Precoce de Cardiotoxicidade?

Background:Chemotherapy with anthracyclines and trastuzumab can cause cardiotoxicity. Alteration of cardiac adrenergic function assessed by metaiodobenzylguanidine labeled with iodine-123 (123I-mIBG) seems to precede the drop in left ventricular ejection fraction.Objective:To evaluate and to compare the presence of cardiovascular abnormalities among patients with breast cancer undergoing chemotherapy with anthracyclines and trastuzumab, and only with anthracycline.Methods:Patients with breast cancer were analyzed clinical, laboratory, electrocardiographic and echocardiographic and cardiac sympathetic activity. In scintigraphic images, the ratio of 123I-mIBG uptake between the heart and mediastinum, and the washout rate were calculated. The variables were compared between patients who received anthracyclines and trastuzumab (Group 1) and only anthracyclines (Group 2).Results:Twenty patients, with mean age 57 ± 14 years, were studied. The mean left ventricular ejection fraction by echocardiography was 67.8 ± 4.0%. Mean washout rate was 28.39 ± 9.23% and the ratio of 123I-mIBG uptake between the heart and mediastinum was 2.07 ± 0.28. Of the patients, 82% showed an increased in washout rate, and the ratio of 123I-mIBG uptake between the heart and mediastinum decreased in 25%. Concerning the groups, the mean washout rate of Group 1 was 32.68 ± 9.30% and of Group 2 was 24.56 ± 7.72% (p = 0,06). The ratio of 123I-mIBG uptake between the heart and mediastinum was normal in all patients in Group 2, however, the Group 1, showed 50% the ratio of 123I-mIBG uptake between the heart and mediastinum ≤ 1.8 (p = 0.02).Conclusion:In women with breast cancer undergoing chemotherapy, assessment of cardiac sympathetic activity with 123I-mIBG appears to be an early marker of cardiotoxicity. The combination of chemotherapy showed higher risk of cardiac adrenergic hyperactivity.

Fundamento:A quimioterapia com antracíclicos e trastuzumabe pode causar cardiotoxicidade. A alteração da função adrenérgica cardíaca, avaliada pela metaiodobenzilguanidina marcada com iodo-123 (123I-mIBG), parece preceder a queda da fração de ejeção do ventrículo esquerdo.Objetivo:Avaliar e comparar a presença de alterações cardiovasculares entre pacientes com câncer de mama submetidas à quimioterapia com antracíclicos e trastuzumabe e apenas a antracíclico.Métodos:Foram analisadas variáveis clínicas, laboratoriais, eletro e ecocardiográficas, além de atividade simpática cardíaca. Nas imagens cintilográficas, foram calculadas a relação da captação do 123I-mIBG entre o coração e o mediastino, e a taxa de clareamento. As variáveis foram comparadas entre os pacientes que receberam antracíclicos e trastuzumabe (Grupo 1) e apenas antracíclicos (Grupo 2).Resultados:Vinte pacientes, com idade média 57 ± 14 anos, participaram deste estudo. A fração de ejeção do ventrículo esquerdo média pelo ecocardiograma foi 67,8 ± 4,0%. A taxa de clareamento média foi 28,39 ± 9,23%, e a relação da captação do 123I-mIBG entre o coração e o mediastino foi de 2,07 ± 0,28. Dentre as pacientes, 82% mostraram taxa de clareamento aumentada e 25%, uma relação da captação do 123I-mIBG entre o coração e o mediastino diminuída. Em relação aos grupos, a média da taxa de clareamento no Grupo 1 foi de 32,68 ± 9,30% e, no Grupo 2, de 24,56 ± 7,72% (p = 0,06). A relação da captação do 123I-mIBG entre o coração e o mediastino foi normal em todas as pacientes do Grupo 2, entretanto, no Grupo 1, 50% mostraram relação da captação do 123I-mIBG entre o coração e o mediastino ≤ 1,8 (p = 0,02).Conclusão:Em mulheres com câncer de mama submetidas à quimioterapia, a avaliação da atividade simpática cardíaca com 123I-mIBG pode ser um marcador precoce de cardiotoxicidade. A associação de quimioterápicos proporcionou maior risco de hiperatividade adrenérgica cardíaca.

Neuropeptides in the posterodorsal medial amygdala modulate central cardiovascular reflex responses in awake male rats

The rat posterodorsal medial amygdala (MePD) links emotionally charged sensory stimuli to social behavior, and is part of the supramedullary control of the cardiovascular system. We studied the effects of microinjections of neuroactive peptides markedly found in the MePD, namely oxytocin (OT, 10 ng and 25 pg; n=6/group), somatostatin (SST, 1 and 0.05 μM; n=8 and 5, respectively), and angiotensin II (Ang II, 50 pmol and 50 fmol; n=7/group), on basal cardiovascular activity and on baroreflex- and chemoreflex-mediated responses in awake adult male rats. Power spectral and symbolic analyses were applied to pulse interval and systolic arterial pressure series to identify centrally mediated sympathetic/parasympathetic components in the heart rate variability (HRV) and arterial pressure variability (APV). No microinjected substance affected basal parameters. On the other hand, compared with the control data (saline, 0.3 µL; n=7), OT (10 ng) decreased mean AP (MAP50) after baroreflex stimulation and increased both the mean AP response after chemoreflex activation and the high-frequency component of the HRV. OT (25 pg) increased overall HRV but did not affect any parameter of the symbolic analysis. SST (1 μM) decreased MAP50, and SST (0.05 μM) enhanced the sympathovagal cardiac index. Both doses of SST increased HRV and its low-frequency component. Ang II (50 pmol) increased HRV and reduced the two unlike variations pattern of the symbolic analysis (P<0.05 in all cases). These results demonstrate neuropeptidergic actions in the MePD for both the increase in the range of the cardiovascular reflex responses and the involvement of the central sympathetic and parasympathetic systems on HRV and APV.

Effects of acute administration of selective serotonin reuptake inhibitors on sympathetic nerve activity

Serotonergic mechanisms have an important function in the central control of circulation. Here, the acute effects of three selective serotonin (5-HT) reuptake inhibitors (SSRIs) on autonomic and cardiorespiratory variables were measured in rats. Although SSRIs require 2-3 weeks to achieve their full antidepressant effects, it has been shown that they cause an immediate inhibition of 5-HT reuptake. Seventy male Wistar rats were anesthetized with urethane and instrumented to record blood pressure, heart rate, renal sympathetic nerve activity (RSNA), and respiratory frequency. At lower doses, the acute cardiovascular effects of fluoxetine, paroxetine and sertraline administered intravenously were insignificant and variable. At middle and higher doses, a general pattern was observed, with significant reductions in sympathetic nerve activity. At 10 min, fluoxetine (3 and 10 mg/kg) reduced RSNA by -33±4.7 and -31±5.4%, respectively, without changes in blood pressure; 3 and 10 mg/kg paroxetine reduced RSNA by -35±5.4 and -31±5.5%, respectively, with an increase in blood pressure +26.3±2.5; 3 mg/kg sertraline reduced RSNA by -59.4±8.6%, without changes in blood pressure. Sympathoinhibition began 5 min after injection and lasted approximately 30 min. For fluoxetine and sertraline, but not paroxetine, there was a reduction in heart rate that was nearly parallel to the sympathoinhibition. The effect of these drugs on the other variables was insignificant. In conclusion, acute peripheral administration of SSRIs caused early autonomic cardiovascular effects, particularly sympathoinhibition, as measured by RSNA. Although a peripheral action cannot be ruled out, such effects are presumably mostly central.

Dexmedetomidine and the perioperative care in Riley-Day syndrome: a case report and literature review

Familial dysautonomia [FD], also known as Riley-Day syndrome, is a disorder of the autonomic nervous system that results in loss of demyelinated nerve fibers of sensory, sympathetic and parasympathetic neurons. Individuals with FD have variable clinical symptoms that may include insensitivity to pain, inability to produce tears, poor oral intake during infancy, repeated vomiting, failure to thrive, wide fluctuations in body temperature, and episodic hypertension and hypotension. These paroxysmal crises are due to dysfunction of the autonomic system with an elevation of both norepinephrine and dopamine levels. Clonidine, an alpha 2-adrenergic agonist, has been previously demonstrated to be an effective pharmacological agent in the treatment of dysautonomic crises related to FD. Dexmedetomidine is an alpha 2-adrenergic agonist with an alpha 2:alpha 1 specificity that is almost 8 times that of clonidine. The authors present the perioperative use of dexmedetomidine in a patient with FD. Previous reports of the use of dexmedetomidine in patients with FD are reviewed and the beneficial physiologic effects discussed

Comportamento dos quimiorreflexos central e periférico na insuficiência cardíaca / Behavior of central and peripheral chemoreflexes in heart failure / Comportamiento de los quimiorreflejos central y periférico en la insuficiencia cardíaca

A síndrome da insuficiência cardíaca (IC) pode ser definida como via final de qualquer forma de doença cardíaca. Os reflexos cardiovasculares simpatoinibitórios como o reflexo arterial barorreceptor estão significativamente suprimidos na IC. Pacientes com IC apresentam maior ventilação para determinada carga de trabalho quando comparados a indivíduos normais. Esse fato gera baixa eficiência ventilatória e relaciona-se com maior ventilação relativa à produção de gás carbônico, que é um preditor de mau prognóstico, além de ser um fator limitante ao exercício. Há evidências de que o desequilíbrio autonômico contribua para a patogênese e a progressão da insuficiência cardíaca. Os quimiorreflexos são os principais mecanismos de controle e regulação das respostas ventilatórias às mudanças de concentração do oxigênio e gás carbônico arterial. A ativação do quimiorreflexo causa aumento da atividade simpática, frequência cardíaca, pressão arterial e volume minuto. No entanto, o aumento do volume minuto e da pressão arterial, pelo feedback negativo provocam inibição da resposta simpática à ativação do quimiorreflexo. Apesar das alterações funcionais dos reflexos, seu comportamento em condições normais e patológicas, especialmente sua contribuição para o estado simpatoexcitatório encontrado na IC, não tem sido amplamente estudado. Dessa forma, esta revisão tem por objetivo integrar os conhecimentos a respeito dos quimiorreflexos central e periférico na síndrome da insuficiência cardíaca, bem como esclarecer a influência da terapêutica medicamentosa da insuficiência cardíaca nos quimiorreflexos.

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.

El síndrome de insuficiencia cardíaca (IC) puede ser definido como vía final de cualquier forma de enfermedad cardíaca. Los reflejos cardiovasculares simpáticoinhibitorios como el reflejo arterial barorreceptor están significativamente suprimidos en la IC. Pacientes con IC presentan mayor ventilación para determinada carga de trabajo cuando son comparados a individuos normales. Ese hecho genera baja eficiencia ventilatoria y se relaciona con mayor ventilación relativa a la producción de gas carbónico, que es un predictor de mal pronóstico, además de ser un factor limitante del ejercicio. Hay evidencias de que el desequilibrio autonómico contribuya a la patogénesis y la progresión de la insuficiencia cardíaca. Los quimiorreflejos son los principales mecanismos de control y regulación de las respuestas ventilatorias a los cambios de concentración del oxígeno y gas carbónico arterial. La activación del quimiorreflejo causa aumento de la actividad simpática, frecuencia cardíaca, presión arterial y volumen minuto. Mientras tanto, el aumento del volumen minuto y de la presión arterial, por el feedback negativo provocan inhibición de la respuesta simpática a la activación del quimiorreflejo. A pesar de las alteraciones funcionales de los reflejos, su comportamiento en condiciones normales y patológicas, especialmente su contribución al estado simpáticoexcitatorio encontrado en la IC, no ha sido ampliamente estudiado. De esa forma, esta revisión tiene por objetivo integrar los conocimientos respecto a los quimiorreflejos central y periférico en el síndrome de insuficiencia cardíaca, así como aclarar la influencia de la terapéutica medicamentosa de la insuficiencia cardíaca en los quimiorreflejos.

Ovariectomy does not affect the cardiac sympathovagal balance of female SHR but estradiol does

The low incidence of cardiovascular diseases, including hypertension, in premenopausal women has led to the conclusion that ovarian hormones may have a protective effect on the cardiovascular system. We evaluated the effects of ovariectomy and/or estradiol on sympathovagal balance and heart rate variability (HRV) in female spontaneously hypertensive rats (SHR) with tachycardia and compared them to Wistar rats (12 weeks old; N = 8-12). Ovariectomy (OVX) and/or estradiol (10 µg/kg) did not affect basal arterial pressure in either rat strain, but estradiol increased basal heart rate (HR) in OVX SHR (454 ± 18 vs 377 ± 9 bpm). HR changes elicited by methylatropine and propranolol were used to evaluate the sympathovagal balance. Ovariectomy did not affect the cardiac sympathovagal balance of any group, while estradiol increased sympathetic tone in OVX SHR (120 ± 8 vs 56 ± 10 bpm) and sham-operated Wistar rats (57 ± 7 vs 28 ± 4 bpm), and decreased the parasympathetic tone only in OVX SHR (26 ± 7 vs 37 ± 5 bpm). HRV was studied in the frequency domain (Fast Fourier Transformation). Spectra of HR series were examined at low frequency (LF: 0.2-0.75 Hz) and high frequency (HF: 0.75-3 Hz) bands. The power of LF, as well as the LF/HF ratio, was not affected by ovariectomy, but estradiol increased both LF (29 ± 4 vs 18 ± 3 nu in Wistar sham-operated, 26 ± 5 vs 15 ± 3 nu in Wistar OVX, 50 ± 3 vs 38 ± 4 nu in SHR sham-operated, and 51 ± 3 vs 42 ± 3 nu in SHR OVX) and LF/HF (0.48 ± 0.08 vs 0.23 ± 0.03 nu in Wistar sham-operated, 0.41 ± 0.14 vs 0.19 ± 0.05 nu in Wistar OVX, 0.98 ± 0.11 vs 0.63 ± 0.11 nu in SHR sham-operated, and 1.10 ± 0.11 vs 0.78 ± 0.1 nu in SHR OVX). Thus, we suggest that ovariectomy did not affect the cardiac sympathovagal balance of SHR or Wistar rats, while estradiol increased the sympathetic modulation of HR.

Short-term red wine consumption promotes differential effects on plasma levels of high-density lipoprotein cholesterol, sympathetic activity, and endothelial function in hypercholesterolemic, hypertensive, and healthy subjects

OBJECTIVES: To compare the metabolic, hemodynamic, autonomic, and endothelial responses to short-term red wine consumption in subjects with hypercholesterolemia or arterial hypertension, and healthy controls. METHODS: Subjects with hypercholesterolemia (n=10) or arterial hypertension (n=9), or healthy controls (n=7) were given red wine (250 mL/night) for 15 days. Analyses were performed before and after red wine intake. RESULTS: Red wine significantly increased the plasma levels of HDL-cholesterol in the controls, but not in the other groups. The effects on hemodynamic measurements were mild, non-significantly more prominent in healthy subjects, and exhibited high interindividual variability. Across all participants, mean blood pressure decreased 7 mmHg (p <0.01) and systemic vascular resistance decreased 7 percent (p = 0.05). Heart rate and cardiac output did not significantly change in any group. Red wine enhanced muscle sympathetic fibular nerve activity in hypercholesterolemic and hypertensive patients, but not in controls. At baseline, brachial artery flow-mediated dilation was impaired in patients with hypercholesterolemia and arterial hypertension; red wine restored the dilation in the hypercholesterolemic group but not in the hypertensive group. CONCLUSIONS: Red wine elicits different metabolic, autonomic, and endothelial responses among individuals with hypercholesterolemia or arterial hypertension and healthy controls. Our findings highlight the need to consider patient characteristics when evaluating the response to red wine.

Oral contraceptive-induced high blood pressure is prevented by renin-angiotensin suppression in female rats but not by sympathetic nervous system blockade.

The use of oral contraceptive (OC) steroids is associated with high blood pressure, although mechanisms responsible are still unclear. This study sought to investigate the possible roles that renin-angiotensin system (RAS) and sympathetic nervous system (SNS) may play in the development of OC-induced hypertension. Administration of OC led to significant increases in blood pressure, heart weight and significant decrease in urinary output in OC-treated and OC+clonidine-treated groups but not in OC+captopril-treated group. The pressor response to angiostensin II was significantly greater in the OC-treated rats than in the control rats. However, the pressor responses induced by norepinephrine were not significantly affected by OC administration. The results of the present study demonstrate that OC-induced high blood pressure is associated with cardiac hypertrophy, enhanced pressor response to angiotensin II and preserved pressor response to sympathetic activation. The study also suggests that the development of the OC-induced hypertension and cardiac hypertrophy is mediated by RAS, but not by SNS.

Defecto en la homeostasis del óxido nítrico: Mecanismo común subyacente de la insulino-resistencia, la hiperactividad simpática y la morbi-mortalidad cardiovascular / Defective nitric oxide homeostasis: Common underlying mechanism between insulin resistance, sympathetic overactivity and cardiovascular morbidity and mortality

La incidencia de la obesidad y de la resistencia a la insulina con sus complicaciones asociadas, como la hipertensión arterial y el aumento de la morbi-mortalidad cardiovascular, alcanzan hoy en día proporciones epidémicas y representan un problema mayor de salud pública. En los últimos años se ha demostrado que la administración de insulina, además de sus efectos metabólicos, posee efectos cardiovasculares importantes. El sistema nervioso simpático y el sistema L-arginina - óxido nítrico son los mediadores centrales de estas acciones cardiovasculares de la insulina. Mostramos, gracias a estudios realizados en animales y en humanos, que no sólo un déficit de la síntesis del óxido nítrico (NO), sino también un aumento exagerado en su producción representan un defecto subyacente central de las anomalías metabólicas, cardiovasculares y del sistema nervioso simpático que caracterizan a la insulino resistencia. Mostramos cómo estos resultados establecen el fundamento científico para la utilización de sustancias farmacológicas capaces de liberar de manera prolongada cantidades fisiológicas de NO o de inhibidores de su sobreproducción como futuros tratamientos para la resistencia a la insulina y sus complicaciones asociadas.

Obesity, insulin resistance and associated cardiovascular complications are reaching epidemic proportions worldwide and represent a major public health problem. Over the past decade, evidence has accumulated indicating that insulin administration, in addition to its metabolic effects, also has important cardiovascular actions. The sympathetic nervous system and the L-arginine-nitric oxide pathway are the central players in the mediation of insulin's cardiovascular actions. Based on recent animal and human research, we demonstrate that both defective and augmented NO synthesis represent a central defect triggering many of the metabolic, vascular and sympathetic abnormalities characteristic of insulin-resistant states. These observations provide the rationale for the use of pharmaceutical drugs releasing small and physiological amounts of NO and/or inhibitors of NO overproduction as a future treatment for insulin resistance and associated comorbidities.

Modifications of the sympathetic skin response in workers chronically exposed to lead

The long-term effects of low-level lead intoxication are not known. The sympathetic skin response (SSR) was evaluated in a group of 60 former workers of a primary lead smelter, located in Santo Amaro, BA, Brazil. The individuals participating in the study were submitted to a clinical-epidemiological evaluation including questions related to potential risk factors for intoxication, complaints related to peripheral nervous system (PNS) involvement, neurological clinical examination, and also to electromyography and nerve conduction studies and SSR evaluation. The sample consisted of 57 men and 3 women aged 34 to 69 years (mean ± SD: 46.8 ± 6.9). The neurophysiologic evaluation showed the presence of lumbosacral radiculopathy in one of the individuals (1.7 percent), axonal sensorimotor polyneuropathy in 2 (3.3 percent), and carpal tunnel syndrome in 6 (10 percent). SSR was abnormal or absent in 12 cases, representing 20 percent of the sample. More than half of the subjects (53.3 percent) reported a history of acute abdominal pain requiring hospitalization during the period of work at the plant. A history of acute palsy of radial and peroneal nerves was reported by about 16.7 and 8.3 percent of the individuals, respectively. Mean SSR amplitude did not differ significantly between patients presenting or not the various characteristics in the current neurological situation, except for diaphoresis. The results suggest that chronic lead intoxication induces PNS damage, particularly affecting unmyelinated small fibers. Further systematic study is needed to more precisely define the role of lead in inducing PNS injury.

Role of renal sympathetic nerves in nitric oxide-induced changes in renal function

Nitric oxide [NO] has been shown to alter kidney function by exerting diuretic and natriuretic effects. No has also been shown to modulate central and peripheral sympathetic activity. Therefore, in order to investigate the possible role of renal sympathetic nerves in the renal effects of NO, the effects of the NO donor sodium nitroprusside [SNP] or the nitric oxide synthase [NOS] inhibitor N-nitro-L-arginine methyl ester [L-NAME] on urine flow and urinary sodium excretion were studied in sham kidney-denewated and bilaterally kidney-denervated water-loaded ethanol-anaesthetized rats. In sham kidney-denervated rats, SNP produced diuretic and natriretic effects, whereas L-NAME caused antidiuresis and antinatriuresis. In kidney-denervated rats, SNP and L-NAME did not cause any significant change in either urine flow or urinary sodium excretion. These results indicate that the renal effects of NO are mediated through inhibition of renal sympathetic nerves activity and therefore has important role in regulating the neural component of renal function

Mechanisms of depressor effect of norepinephrine injected into subnucleus commissuriu of nucleus solitarius tractus in rabbits / 华中科技大学学报（医学）（英德文版）

This experiment aimed to investigate the effect of adrenergic system in the subnucleus commissuriu of nucleus solitrius tractus (CNTS) on renal nerve discharges. Norepinephrine (NE) was microinjected into the CNTS of rabbits and mean arterial blood pressure (MAP) and renal nerve discharges (FRND) were synchronously recorded. The results indicated that (1) microinjection of norepinephine into the CNTS of rabbit could significantly attenuate the frequency of renal nerve discharge, and at the same time decrease markedly the mean arterial pressure. (2) Microinjection of 0.3 nmol yohimbin into CNTS had no significant influence on FRND and MAP, but could attenuate and even reverse the effects of NE on FRND and MAP. These results suggest that microinjection of NE into CNTS may activate the alpha-adrenorecptor located in CNTS and secondarily produce a depressor effect by attenuating the activity of periphenal sympathetic nervous system.

Baroreflex control of sympathetic activity in experimental hypertension

The arterial baroreceptor reflex system is one of the most powerful and rapidly acting mechanisms for controlling arterial pressure. The purpose of the present review is to discuss data relating sympathetic activity to the baroreflex control of arterial pressure in two different experimental models: neurogenic hypertension by sinoaortic denervation (SAD) and high-renin hypertension by total aortic ligation between the renal arteries in the rat. SAD depresses baroreflex regulation of renal sympathetic activity in both the acute and chronic phases. However, increased sympathetic activity (100 percent) was found only in the acute phase of sinoaortic denervation. In the chronic phase of SAD average discharge normalized but the pattern of discharges was different from that found in controls. High-renin hypertensive rats showed overactivity of the renin angiotensin system and a great depression of the baroreflexes, comparable to the depression observed in chronic sinoaortic denervated rats. However, there were no differences in the average tonic sympathetic activity or changes in the pattern of discharges in high-renin rats. We suggest that the difference in the pattern of discharges may contribute to the increase in arterial pressure lability observed in chronic sinoaortic denervated rats.

Insulina, reatividad valcular me hipertension arterial / Insulin, vascular reactiviry and hypertension

Varios estudios epidemiológicos indican que hay una relación entre hiper-insulinemia, resistencia insulínica e hipertensión arterial. La insulina estimula el sistema nervioso simpático, produce retención renal de Na+ y modifica en forma directa mecanismos vasculares (contrayentes y relajantes); estos efectos pueden justificar que la insulina aumente o disminuya la presión arterial. la ausencia de los efectos vasodilatadores debido a resistencia insulínica y/o la mayor manifestación de los efectos hipertensores en caso de hiperinsulinemia podrían ser el nexo entre la insulina y la hipertensión arterial.

Vagal and sympathetic control of heart rate during exercise by sedentary and exercise-trained rats

1. The present investigation was undertaken to study the vagal and sympathetic effects of an acute bout of exercise on ten sedentary (S) and nine trained (T) rats. The exercise training was performed 5 times a week for 13 weeks on a motor treadmill, at 1.0 mph, 15% grade for 60 min. 2. Heart rate (HR) was recorded at rest and during exercise, 15% grade at 0.5, 0.8 and 1.0 mph, for 3 min per stage. Vagal and sympathetic effects were studied after the administration of methylatropine (3 mg/kg) and propranolol (4 mg/kg). 3. Exercise training significantly attenuated cardiac acceleration at 0.8 (441 +/- 8 vs 486 +/- 9 bpm in S, P < 0.05) and 1.0 mph (466 +/- 12 vs 508 +/- 6 bpm in S, P < 0.05). The vagal effect was significantly increased in the T group at 0.8 (72 +/- 5 vs 32 +/- 10 bpm in S, P < 0.05) and 1.0 mph (46 +/- 8 vs 15 +/- 7 bpm in S, P < 0.05). The sympathetic effect was significantly decreased in the T group at 0.8 (73 +/- 9 vs 112 +/- 9 bpm in S, P < 0.05) and 1.0 mph (96 +/- 11 vs 125 +/- 7 bpm in S, P < 0.05). The intrinsic HR behavior was not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The sympathetic neuro-melanophore transmission in a fresh-water Indian major carp, Labeo rohita (Ham.).

Adrenaline was effective in aggregating the melanosomes both in innervated as well as denervated melanophores. Isotonic KCl could induce pigment aggregation only in innervated melanophores. Adrenaline- and K+-induced pigment aggregation response in these melanophores was blocked by phentolamine: propranolol failed to do so. It is suggested that the chromatic nerves in the fish, Labeo rohita are adrenergic and via post-synaptic alpha-adrenoceptors, control the melanosome aggregation.