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PubMed2003

A thermodynamic model of the sympathetic and parasympathetic nervous systems.

In light of the nonequilibrium thermodynamics by I. Prigogine, the autonomic nervous system as a whole may be viewed as a dissipative structure progressively assembled in the course of evolution, plastically and rhythmically interfaced between forebrain, internal and external environments, to regulate energy, matter and information exchanges. In the present paper, this hypothesis is further pursued to verify whether the two main divisions of the autonomic nervous system, the sympathetic and parasympathetic systems, may support different types of exchange with the external environment. Previous data from hypothalamic stimulation experiments, studies of locus coeruleus function and available data on behavioral functional organization indicate that (1) tight engagement with the external environment, (2) high level of energy mobilization and utilization and (3) information mainly related to exteroceptive sensory stimulation characterize a behavioral prevalence of sympathoadrenal activation. On the other hand, (1) disengagement from the external environment, (2) low levels of internal energy and (3) dominance of proprioceptive information characterize a behavioral prevalence of vagal tone. Behavioral matter exchanges such as feeding, drinking, micturition and defecation are equally absent at the extreme of sympathoadrenal and vagally driven behaviors. The autonomic nervous system as a whole is genetically determined, but the sympathoadrenal system has been mainly designed to organize the visceral apparatus for an action to be performed by the biological system in the external environment and to deal with the novelty of task and of the environment, while the functional role of the parasympathetic is to prepare the visceral apparatus for an action to be performed by the biological system on itself, for recovery and self-protection (homeostasis), and is reinforced by repetition of phylo- and ontogenetically determined patterns. The available clinical data further support this interpretation indicating that an increased sympathetic and a decreased vagal tone may represent a consistent risk factor for cardiovascular diseases.

Animals↗
PubMed2005

Socioeconomic status and health: is parasympathetic nervous system activity an intervening mechanism?

BACKGROUND: The link between socioeconomic status (SES) and health is widely recognized but the pathophysiologic mechanisms are not well understood. We tested the hypothesis that parasympathetic nervous system (PNS) regulation is one such mechanism. METHODS: In a cross-sectional study, electrocardiogram-derived RR interval variability (RRV), a non-invasive index of cardiac PNS regulation, and SES, measured as educational attainment and income, were collected in 756 subjects in the CARDIA study of heart disease in young adults. RESULTS: Relative to those with less than a high school education, those with high school to college and post-college education had 26% (beta = 0.233) and 43% (beta = 0.355) greater low frequency (LF) RRV, respectively, adjusted for age, sex, and race. For high frequency (HF) RRV, race interacted with income: relative to low income whites, intermediate and high income whites had 133 and 191% greater HF power, respectively, while intermediate and high income blacks had 32 and 44% greater HF RRV, respectively, relative to low income blacks. CONCLUSIONS: Numerous studies demonstrate that psychosocial stressors reduce cardiac parasympathetic regulation and that SES disparities are associated with increasing social stress proportional to the degree of disparity. Data from the current study suggest that PNS regulation may be a mechanism linking the stressful effects of low SES to increased morbidity and mortality.

Adult↗
PubMed1987

Role of the parasympathetic nervous system in airway hyperresponsiveness after ozone inhalation.

Airway hyperresponsiveness develops in dogs after ozone inhalation. This study examined the role of the parasympathetic nervous system in ozone-induced airway hyperresponsiveness in dogs. Dose-response curves to acetylcholine (n = 8) and histamine (n = 4) were measured before and after exposure to ozone (3 ppm for 30 min). The provocative concentration of each agonist was measured on two randomly assigned days separated by at least 1 wk. On one day a control experiment was performed, and on the other day the dogs were pretreated with the ganglionic blocker hexamethonium bromide in doses that block ganglionic transmission. The acetylcholine provocative concentration decreased on the control day from 5.5 mg/ml (%SE 1.8) before ozone to 0.5 mg/ml (%SE 2.0) after ozone (P less than 0.0001). After pretreatment with hexamethonium the acetylcholine provocative concentration decreased from 9.0 mg/ml (%SE 1.8) before ozone to 1.0 mg/ml (%SE 2.0) after ozone (P = 0.002). The results were similar when histamine was used as the agonist. Therefore, ganglionic blockade does not prevent airway hyperresponsiveness after ozone inhalation, and a parasympathetic reflex mechanism is not responsible for airway hyperresponsiveness after ozone inhalation in dogs.

Acetylcholine↗
PubMed2001

Activation of the parasympathetic nervous system is necessary for normal meal-induced insulin secretion in rhesus macaques.

Meal-induced insulin secretion is thought to be regulated primarily by absorbed nutrients and incretin hormones released from the gastrointestinal tract. In addition, the parasympathetic nervous system (PNS) is known to mediate preabsorptive, or cephalic phase, insulin secretion. Despite evidence that the PNS remains activated during the absorptive phase of the meal, its role in mediating postprandial insulin secretion has not been established. To study the role of the PNS in absorptive phase insulin release, we measured plasma concentrations of glucose as well as islet hormones and incretins in six healthy rhesus monkeys before and for 60 min after meals while they were infused with saline (control), atropine (muscarinic blockade), or trimethaphan (nicotinic blockade). During the infusion of saline, plasma levels of glucose, pancreatic polypeptide (PP), insulin, glucose-dependent insulinotropic polypeptide, and glucagon-like peptide-1 increased promptly after meal ingestion and remained elevated throughout the 60 min of the study. The PP response was nearly abolished in animals treated with trimethaphan, indicating functional blockade of PNS input to the islet, and in contrast to the control study, there were minimal changes in plasma concentrations of glucose, incretin hormones, and insulin. Because trimethaphan inhibited glycemic and incretin stimuli in addition to blocking PNS input to the islet, it was not possible to discern the relative roles of these factors in the stimulation of insulin secretion. Atropine also significantly decreased PNS transmission to the islet, as reflected by PP levels similar to those observed with trimethaphan. Unlike the trimethaphan study, plasma glucose levels rose normally during atropine treatment and were similar to those in the control study over the course of the experiments (114 +/- 22 and 132 +/- 23 mmol/L.60 min, respectively). In addition, the rise in plasma glucagon-like peptide-1 following the meal was not suppressed by atropine, and the glucose-dependent insulinotropic polypeptide responses were only modestly decreased. Despite the significant increases in circulating glucose and incretins, plasma insulin levels were greatly attenuated by atropine, so that the 60 min responses were more comparable to those during trimethaphan treatment than to those in the control study (atropine, 3,576 +/- 1,284; trimethaphan, 4,128 +/- 2,616; control, 15,834 +/- 5,586 pmol/L.60 min; P: < 0.05). Thus, muscarinic blockade markedly suppressed the meal-induced insulin response despite normal postprandial glycemia and significant elevations of incretins. These results indicate that activation of the PNS during the absorptive phase of meals contributes significantly to the postprandial insulin secretory response.

Animals↗
PubMed2003

The parasympathetic nervous system and its influence on heart rate in torpid western pygmy possums, Cercatetus concinnus (Marsupialia: Burramyidae).

We investigated the effect of parasympathetic antagonism on the patterns of heart rate during torpor in the western pygmy possum Cercatetus concinnus (Marsupialia: Burramyidae). This is the first study to examine the influence of the autonomic nervous system on cardiac function in a metatherian hibernator. During torpor, antagonism of the parasympathetic nervous system eliminated the ventilatory tachycardia, variability in instantaneous heart rate, and increased the overall heart rate. These findings are consistent with previous studies on other mammalian heterotherms, which have shown that the parasympathetic nervous system is responsible for these patterns in heart rate. During extended bouts of torpor (2 to 3 days) the ventilatory tachycardia persisted throughout each bout, which indicates that the parasympathetic nervous system remained functional during that time. It has been suggested that the progressive removal of autonomic tone is characteristic of deep steady-state hibernation. There is no evidence to suggest that such a state was going to be reached in the possums in this study. To date there is little evidence that clearly demonstrates a physiological basis for the distinction between shallow, daily torpor and deep hibernation.

Journal Article↗
PubMed1987

Thermic effect of food: possible implication of parasympathetic nervous system.

To investigate the effect of the autonomic nervous system on the thermic response to food ingestion, respiratory exchange measurements were performed on seven healthy young men for 1 h and 45 min before and 6 h after ingestion of a mixed meal, approximately 560 kcal, 53% carbohydrate, 30% fat, and 17% protein (control) and under the same conditions during infusion of either propranolol (80 micrograms/kg bolus and 1 microgram.kg-1.min-1), atropine (10 micrograms/kg and 10 micrograms.kg-1.min-1), or atropine plus propranolol. The postabsorptive resting metabolic rates were the same on each occasion and were slightly altered by drug treatment. The thermic responses to the meal were the same with the control and propranolol tests (9.3 +/- 0.9 and 9.2 +/- 0.5%, respectively) and were greater (P less than 0.001) than with atropine 3.6 +/- 0.6% and atropine plus propranolol 3.3 +/- 0.8%. Blockade of the sympathetic nervous system does not decrease the thermic response to food taken orally, whereas muscarinic receptor blockade does. Although some confounding effects of atropine might explain some of this decrease, our results suggest that the parasympathetic nervous system is involved in the thermic effect of food.

Adult↗
PubMed1984

Role of parasympathetic nervous system in glucagon response to insulin-induced hypoglycemia in normal and diabetic rats.

Effects of cholinergic mechanisms on glucagon and epinephrine responses to insulin-induced hypoglycemia were examined in diabetic and age-matched control male rats. Atropine did not affect plasma glucose levels or plasma glucagon concentrations, in the basal state, in normal or short-term diabetic rats (10 to 15 days following streptozotocin injection). However, atropine blocked the glucagon response to insulin hypoglycemia in both normal and short-term diabetic rats. Subcutaneous injection of carbachol also failed to alter basal plasma glucose, glucagon, or epinephrine values in both normal and diabetic rats. The lack of glucagon and epinephrine responses to insulin hypoglycemia in long-term diabetic rats (80 to 100 days after streptozotocin injection) was reversed with a single dose of carbachol. Carbachol exaggerated the glucagon response to insulin hypoglycemia in normal and short-term diabetic rats. These results demonstrate that the parasympathetic nervus system plays an important role in the glucagon release in response to insulin hypoglycemia in rats. The lack of glucagon response to insulin hypoglycemia observed in long-term diabetic rats could be due to deteriorated parasympathetic nervous system and also could be corrected with carbachol.

Animals↗
PubMed1991

Participation of the parasympathetic nervous system in the development of activity-stress ulcers.

The present study investigates the effects of truncal vagotomy and drug treatment, comprising atropine methylbromide and chlorisondamine, on the development of activity-stress ulcers in rats. To induce gastric lesions, female rats were housed individually in activity-wheel cages and subjected to a food-restricted schedule of only 1 hr food availability per day. Bilateral truncal vagotomy significantly prevented gastric ulceration, while those rats with vagotomy showed more running activity than sham-operated rats. Daily treatment with either methylatropine (3 and 6 mg/kg, s.c.) or chlorisondamine (2 and 4 mg/kg, i.p.) also significantly decreased the severity of lesions without a significant reduction in running activity. This evidence suggests that the development of activity-stress ulcers is mainly due to the hyperactivity of the peripheral parasympathetic nervous system.

Animals↗
PubMed1989

Effect of D-Ala-2-Me-Phe-4-Gly-ol-5 enkephalin on epinephrine-induced arrhythmias in the rat and the interrelationship to the parasympathetic nervous system.

The purpose of this study was to evaluate the effects of the millimicrons opioid agonist D-Ala-2-Me-Phe-4-Gly-ol enkephalin (DAGO) on catecholamine-induced arrhythmias. Arrhythmias were produced, in the rat, by continuous infusion of epinephrine until the development of fatal arrhythmias that were usually ventricular fibrillation. Intracerebroventricular (ICV) administration of DAGO, 3 nmol, significantly (p less than 0.05) shifted to the right the relationship between epinephrine and both the onset of ventricular arrhythmias and the development of fatal arrhythmias. Naloxone, 1 mg/kg i.v., prevented these effects of DAGO. Atropine, 1 mg/kg i.v. or 20 micrograms/kg ICV, prevented the shift in these dose response relationships. Antagonism of DAGO's effects on arrhythmias could not be explained by an alteration of the blood pressure response to epinephrine. However, DAGO significantly increased blood pressure and decreased heart rate in separate experiments in animals that did not receive epinephrine and atropine prevent the heart rate and blood pressure effects of DAGO. These data show that 1) the millimicrons opioid receptor agonist DAGO suppresses epinephrine-induced arrhythmias, 2) the site of action can be within the CNS, 3) there is a role for the central parasympathetic nervous system to mediate the effect of DAGO and 4) endogenous opioids could modulate catecholamine-induced cardiac arrhythmias.

Animals↗