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At least 19 recordsLinked to original sources
PubMed1993

[Interaction between the renin system and parasympathetic nervous system in heart failure].

UNLABELLED: The increase of sympathetic activity in heart failure is accompanied by a reduced parasympathetic tone. The renin-angiotensin system has not only multiple interactions with the sympathetic nervous system, but may also influence vagal tone directly by angiotensin II. Animal studies show a reduction of parasympathetic tone by a direct action of angiotensin II in the area postrema where the blood brain barrier is absent. It is possible that, in addition to the sympathetic and renin-angiotensin system, the parasympathetic nervous system may also influence prognosis in heart failure. Therefore, baroreflex sensitivity as (CBS) an index of vagal tone was examined in 35 patients with moderate to severe heart failure (NYHA II-III). Independent of the severity of heart failure BS was the lower the higher plasma-renin-activity was. Fifty-six months after the initial examination a comparison of the surviving patients (Group 1, n = 20) with the patients who died or underwent heart transplantation (Group 2, n = 15) did not reveal significant differences in the initial hemodynamic data. However, group 2 patients showed a tendency to higher initial plasma-renin-activity and significantly lower BS 1.3 +/- 0.2 vs. 2.2 +/- 0.3 ms/mm Hg; p < 0.05). CONCLUSION: In patients with heart failure a relation between the renin-angiotensin system and the parasympathetic nervous system is likely as there is a significant negative relationship between BS and plasma-renin-activity. Among patients with a similar degree of heart failure a low vagal tone identifies patients with a poor prognosis.

Adult↗
PubMed1994

Interactions between the renin-angiotensin system and the parasympathetic nervous system in heart failure.

The increase of sympathetic activity in heart failure is accompanied by reduced parasympathetic tone. The renin-angiotensin system (RAS) is often activated in heart failure. It not only has multiple interactions with the sympathetic nervous system but also may influence vagal tone directly via angiotensin II. Animal studies show a reduction of parasympathetic tone by a direct action of angiotensin II in the area postrema, where the blood-brain barrier is absent. It is possible that in addition to the sympathetic and renin-angiotensin systems the parasympathetic nervous system may also influence prognosis in heart failure. Therefore, baroreflex sensitivity (BS) as an index of vagal tone was examined in 35 patients with moderate-to-severe heart failure (NYHA II-III). Independent of the severity of heart failure, BS was lower the higher the plasma renin activity. At 56 months after initial examination, a comparison of the surviving patients (group 1, n = 20) with the patients who died or underwent heart transplantation (group 2, n = 15) did not reveal significant differences in the initial hemodynamic data. However, group 2 patients showed a tendency to higher initial plasma renin activity and a significantly lower BS (1.3 +/- 0.2 versus 2.2 +/- 0.3 ms/mm Hg; p < 0.05). It is concluded that in patients with heart failure a relation between the RAS and the parasympathetic nervous system is likely, as there is a significant negative relationship between BS and plasma renin activity. Among patients with similar degrees of heart failure, low vagal tone identifies patients with a poor prognosis.

Age Factors↗
PubMed1986

The hemodynamic response of conscious normotensive rats to atriopeptin III: Lack of a role of the parasympathetic nervous system.

The influence of the parasympathetic nervous system on the cardiovascular response to a synthetic atrial peptide (atriopeptin III) was examined in conscious normotensive rats by utilizing radiolabelled microspheres. Atriopeptin III was infused intravenously for 30 min at a rate of 1 microgram/min per rat in animals pretreated with a bolus intravenous injection of atropine, (150 micrograms/rat, n = 8) or of its vehicle (n = 8). Additional animals (n = 9) received the vehicle of both atropine and atriopeptin III. The atrial peptide decreased mean blood pressure to a similar extent in rats pretreated with atropine (from 124 +/- 4.5 to 108 +/- 5.3 mm Hg, mean +/- S.E.M., P less than 0.05) and in the controls (from 123 +/- 3.8 to 105 +/- 3.8 mm Hg, P less than 0.05). Heart rate rose significantly after administration of atropine. After the 30 min infusion, the cardiac index was significantly lower (P less than 0.05) in both groups infused with atriopeptin III (23.7 +/- 2.3 after atropine pretreatment and 25.1 +/- 2.2 ml X min-1 X 100 g-1 without atropine) than in the group of rats given only the vehicle of both atropine and atriopeptin III (32.4 +/- 2.8 ml X min-1 X 100 g-1). Calculated systemic vascular resistance tended to be higher in the former two groups than in the latter. There was no significant difference in regional blood flow distribution within the three groups of rats. These data therefore indicate that in conscious rats atriopeptin III reduces blood pressure and cardiac output without concomitantly diminishing total peripheral vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Role of the parasympathetic nervous system and interaction with the sympathetic nervous system in the early phase of hypertension.

The role of the peripheral parasympathetic nervous system in the development of hypertension was investigated in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Animals were 5-7 weeks old, anesthetized, and in the open-chest condition. The decrement in heart rate evoked by parasympathetic nerve stimulation (62 +/- 8 beats/min) in SHR was greater (p < 0.01) than that in WKY rats (23 +/- 4 beats/min). Furthermore, the decrease in heart rate (73 +/- 9 beats/min) in response to combined stimulation of sympathetic and parasympathetic nerves in SHR was greater (p < 0.05) than that in response to vagal stimulation alone. The extent of the interaction of sympathetic and parasympathetic nerves was calculated as the difference between the decrease in heart rate during combined stimulation and that during vagal nerve stimulation alone. The extent of the interaction in SHR (-11 +/- 5) was not significantly different from that in WKY rats (-8 +/- 3 beats/min). Therefore, the influence of the peripheral parasympathetic nervous system in the early phase of hypertension may be greater than that in the normotensive state. Interaction between the two branches of the autonomic nervous system may occur as accentuated antagonism originating in the early phase of hypertension. The interaction during the early phase of hypertension may not be different in extent from that of the normotensive state.

Animals↗
PubMed1987

Physiology of the parasympathetic nervous system of the lung.

Parasympathetic nerves play an important role in modulating smooth muscle tone and mucus secretion in the airways. This modulation can occur through a variety of afferent inputs, from the central nervous system, at parasympathetic ganglia, and on post-ganglionic efferent fibres themselves. Abnormalities at any of these sites could, and in some patients probably do, contribute to the abnormalities in smooth muscle contraction and mucus secretion that characterize a number of airway diseases, including asthma. Because these pathways play little or no role in the exaggerated bronchoconstrictor responses in many patients, however, an abnormality of the parasympathetic pathway cannot be the sole explanation for abnormal airway hyperresponsiveness.

Bronchi↗
PubMed1994

Parasympathetic nervous system control of heart rate responses to stress in offspring of hypertensives.

The elevated heart rate response to stress in normotensive offspring of hypertensives (PH+) has been suggested to be a function of sympathetic nervous system activity. This study examined whether parasympathetic nervous system activity may also underlie familial differences in the heart rate response. Twenty-four subjects, half of whom were PH+, were exposed to four stressor tasks administered in counterbalanced order. Stressors were chosen based on previous research that suggested vagal contributions to the heart rate response. Stressors were a cold pack to the forehead, isometric hand grip, a noxious film, and a shock-avoidance video game task. Physiological measures included heart rate (HR), respiration rate (RR), and respiratory sinus arrhythmia (RSA). RSA values were corrected for corresponding RR by analysis of covariance. Familial differences in HR were observed in response to the hand grip and video game tasks. However, in both cases analyses suggest that familial differences in reactivity were a function of primarily sympathetic as opposed to parasympathetic influences. Familial differences in RSA were not observed for rest or tasks. This study found no evidence for parasympathetic mediation of familial differences in the heart rate response to the stressors employed.

Adult↗
PubMed1986

Role of the parasympathetic nervous system and of cholinergic mechanisms in bronchial hyperreactivity.

The parasympathetic nervous system of the respiratory tract is involved in the control of airway calibre in three ways: through afferent nerve pathways (pulmonary reflexes); through efferent nerve pathways (reflexes, interaction between efferent vagus and mediators or modulating transmitter substances) and through cholinergic muscarinic receptors and postreceptor mechanisms in the target organ. To what extent do these mechanisms contribute to airway hyperreactivity? Pulmonary reflexes: Reflex bronchoconstriction has been established in divided lung experiments for histamine and in experiments involving an isolated segment of trachea for SO2. A reflex pathway is the most likely explanation for the heightened reactivity induced by aerosols of prostaglandin E2 and by maximal respiratory manoeuvers. Reflex bronchoconstriction is mediated through rapidly adapting ("irritant") receptors and through C-fibre endings. The influence of C-fibre endings is greater than hitherto suspected and many effects ascribed to irritant receptors are probably due to stimulation of C-fibre endings which outnumber myelinated fibres 3-4 to 1. From studies on the control of respiration (which reflect more directly the state of sensory receptors in the airways than studies of airway calibre) it appears that the activity of C-fibre endings increases during ozone-induced hyperreactivity. This could explain the increased bronchial reactivity seen in this condition. Interaction: Aerosols of serotonin cause bronchoconstriction when the vagus nerve is intact but have little effect during vagal block. This is an effect neither on afferent receptors nor on the end organ, but on the efferent nerve pathway. Interaction effects of this type ("cholinergic facilitation") are frequent and may be more important quantitatively than reflex effects. From data on serotonin and by analogy to other systems it appears that preganglionic and ganglionic sites are important points of interaction. Parasympathetic ganglia are located in the airway wall. Several transmitter substances have been identified in airway ganglia and in autonomic nerves, sensory and motor. Thus there seem to be convergent inputs capable of modulating transmission through the ganglia. An altered balance of converging ganglionic inputs may cause hyperreactivity. Receptors in airway smooth muscle may not be a homogeneous population. Muscarinic receptors are being classified into subgroups and the existence of at least 3 subtypes: M-1, M-2 and M-3 has been postulated. Their distribution depends on the tissue studied. They differ in agonist affinity messenger systems.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1979

Evaluation of the control of glucagon secretion by the parasympathetic nervous system in man.

To evaluate the influence of the parasympathetic nervous system on human glucagon secretion, we have measured the plasma immunoreactive glucagon (IRG) levels after the administration of edrophonium, bethanechol chloride, and 2-deoxyglucose, and have compared the IRG responses to hypoglycemia in normal, atropinized, and vagotomized man. Edrophonium administered i.v. and bethanechol chloride administered s.c. did not affect IRG levels. Two-deoxy-glucose resulted in symptomatic neuroglucopenia with resultant vagal discharge, as evidenced by increased gastric acid secretion; but no changes in IRG concentrations were observed. The IRG response to insulin-induced hypoglycemia in normal subjects was not influenced by the administration of atropine. In seven subjects with a truncal vagotomy and no increased gastric acid secretion during insulin-induced hypoglycemia, the IRG increases were indistinguishable from those of control subjects in terms of timing, peak level obtained, or total glucagon response. We conclude that the cholinergic system is unlikely to play an important role in modulating glucagon secretion in man.

Adult↗
PubMed1996

Cardiac parasympathetic nervous system activity does not increase in anticipation of sleep.

Parasympathetic Nervous System (PNS) activity increases while Sympathetic Nervous System (SNS) activity remains relatively stable from wakefulness to NREM sleep. However, it is not clear whether these changes are specifically associated with NREM sleep, or whether they anticipate sleep onset. The latter may occur if ANS activity was influenced by the circadian system. This issue was investigated by conducting spectral analysis of heart beat-to-beat intervals (Periodogram method), collected from 20 healthy male and female subjects at three different times across 24 h; in the morning, just prior to normal sleep onset time, and in slow-wave sleep (SWS). Subjects were supine in all conditions and awake in the first two conditions. The high- and low-frequency peaks, reflecting PNS and SNS activity, respectively, were expressed as proportions of the total power. PNS activity decreased significantly from the morning (0.22) to the presleep period (0.19), before it increased to its maximum during SWS (0.33). In contrast, SNS activity was similar in each of the three conditions (0.07, 0.06, and 0.05 for morning, presleep and SWS, respectively). Thus there do not appear to be changes in PNS activity in anticipation of sleep, as would be predicted on the basis of a circadian influence on the PNS. Instead the increased PNS activity appears to be sleep dependent.

Adolescent↗
PubMed1991

The parasympathetic nervous system takes part in the immuno-neuroendocrine dialogue.

In a series of experiments the communication between the parasympathetic nervous system and the immune system was examined in rats. The data are summarized as follows: (1) In vivo administration of physostigmine increased the number of plaque-forming cells whereas in vitro addition of cholinergic agonists decreased the specific antibody response. (2) Prolonged in vivo treatment with atropine or physostigmine influenced concanavalin A stimulation of lymphocytes of different compartments in different ways. (3) Immunization with sheep red blood cells changed the number and the affinity of muscarinic cholinergic receptors in the hippocampus. (4) Cholinergic stimulation in vivo inhibited the transient increase of plasma corticosterone following immunization. Our results provide evidence that the parasympathetic nervous system is included in the dialogue between the neuro-endocrine and the immune systems.

Animals↗
PubMed1990

Parasympathetic nervous system activity in hypothyroidism determined by R-R interval variations on electrocardiogram.

Little is known about the relationship between hypothyroidism and the parasympathetic nervous system. R-R interval variations revealed by electrocardiogram (ECG) are known to be a useful clinical indicator of abnormalities of parasympathetic nervous system activity. Studies were conducted in hypothyroid patients, and significant reductions in R-R interval variations were observed in patients with primary severe hypothyroidism due to Hashimoto's thyroiditis, and in patients with Graves' disease who became severely hypothyroid during antithyroid drug therapy. R-R interval variations were restored to normal levels in both groups of patients after treatment. The present investigation suggests that in marked hypothyroidism there are hypofunctional abnormalities in the parasympathetic nervous system in association with a reduction in the levels of serum T4 and T3.

Adult↗
PubMed1990

Parasympathetic nervous system in patients with Graves' disease determined by R-R interval variations on electrocardiogram.

Little is known about an interrelationship between thyroid dysfunction and parasympathetic nervous system. R-R interval variations on electrocardiogram (ECG) have been considered to be reliable indicator reflecting abnormalities of parasympathetic nervous system. We have attempted to apply this technique in patients with hyperthyroidism. Studies were conducted in 60 healthy subjects and 57 patients with Graves' disease. R-R interval variations were expressed as coefficient of variation on 100 heart rates at the time of resting (CVq) and deep respiration (CVd). A negative correlation between R-R interval variations (CVq, CVd) and ages was observed in healthy subjects. CVq was significantly lower in untreated Graves' disease than in antithyroid drug-treated Graves' disease and control subjects. A similar result also was obtained in CVd. Decreased CVq in untreated patients with Graves' disease was restored by administration of beta blockades, propranolol and metoprolol, but not by administration of alpha blockade, bunazosine. The present investigation suggests that there are hypofunctions in parasympathetic nervous system associated with beta (especially beta one) effects in patients with hyperthyroidism due to Graves' disease.

Adrenergic alpha-Antagonists↗
PubMed1988

The interrelationship of morphine and the parasympathetic nervous system in digoxin-induced arrhythmias in the guinea-pig.

1. The role of the parasympathetic nervous system and the effect of morphine on cardiac arrhythmias induced by digitalis was assessed in guinea-pigs that had digitalis arrhythmias produced by digoxin 50 micrograms/kg intravenously plus 500 micrograms/kg per h. 2. Morphine produced a dose-dependent rightward shift in the relationship between digoxin dose and arrhythmias. Morphine 5 mg/kg subcutaneously (s.q.) was associated with significantly (P less than 0.05) higher digoxin doses both at the onset of ventricular arrhythmias and at development of fatal arrhythmias compared with the control group that received saline s.q. 3. Vagotomy and atropine prevented the effect of morphine so that the dose-response relationships and the mean digoxin dose at onset of ventricular arrhythmias and the development of fatal arrhythmias were not significantly different from the control group receiving saline. 4. These data indicate that morphine limits the development of digitalis arrhythmias and this effect is, at least in part, mediated through the parasympathetic nervous system.

Animals↗
PubMedDate not supplied

[The role of the parasympathetic nervous system in regulating the kinetics of the regional blood circulation in the digestive system organs].

Cranio-bulbar part of the parasympathetic nervous system proved to be important for regulation of the blood flow distribution between the organs of the gastroduodenal complex (liver, stomach, and small intestine), rate of the local blood flow and its kinetics. Investigation of the blood supply of the above mentioned organs various periods (1-60 days) after bilateral subdiaphragmatic truncal vagotomy has demonstrated the most pronounced transformations in macro- and micro-hemodynamics in the 14-30 days period. Time pattern of these changes has one maximum in liver and stomach (14-30 days) and two maxima (7 and 30 days) in small intestine.

Animals↗
PubMed1986

[Absence of a role for the parasympathetic nervous system in the hemodynamic response to atriopeptin III in the normotensive rat].

The influence of the parasympathetic nervous system on the cardiovascular response to a synthetic atrial peptide (atriopeptin III) was examined in conscious normotensive rats utilizing the technique of radiolabelled microspheres. Atriopeptin III was infused intravenously for 30 min at a rate of 1 microgram/min in rats pretreated with a bolus intravenous injection of atropine, 150 micrograms (n = 8), or of its vehicle (n = 8). Additional animals (n = 9) received the vehicle of both atropine and atriopeptin III. The atrial peptide decreased mean blood pressure to similar extent in rats pretreated with atropine (from 124 +/- 4.5 to 108 +/- 5.3 mmHg, mean +/- SEM, p less than 0.05) and in the controls (from 123 +/- 3.8 to 105 +/- 3.8 mmHg, p less than 0.05). Heart rate rose significantly after administration of atropine. After the 30 minute infusion, cardiac index was significantly lower (p less than 0.05) in both groups infused with atriopeptin III (23.4 +/- 2.3 after atropine pretreatment and 25.1 +/- 2.2 ml/min X 100 g without atropine) than in the group of rats given only the vehicle of both atropine and atriopeptin III (32.4 +/- 2.8 ml/min X 100 g). There was no significant difference in regional blood flow distribution within the three groups of rats. These data therefore indicate that in conscious rats atriopeptin III reduces blood pressure and cardiac output without concomitantly modifying regional blood flow distribution. They also suggest that the parasympathetic nervous system does not contribute to the hemodynamic response to atriopeptin III.

Animals↗
PubMed1986

Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm.

We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 micrograms ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of the 25 of the 27 patients. The injection of 20 to 100 micrograms ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm.

Acetylcholine↗