Central cholinergic stimulation causes adrenal epinephrine release.

Kennedy, Brian P.; Janowsky, David S.; Risch, S. Craig

doi:10.1172/jci111517

Cited by 36 publications

(13 citation statements)

References 25 publications

(15 reference statements)

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“…Stimulation of the SSN alone resulted in a slight decrease in tarsal muscle tension (-113 + 11 mg, Figure la and Ib), as reported previously (Smith & Beauregard, 1993;Beauregard & Smith, 1994). Administration of physostigmine in the absence of stimulation resulted in a gradual increase in muscle tension that reached its maximum (525 + 33 mg) in approximately 1 min; this is consistent with reports that cholinesterase inhibition can increase sympathetic tone by eliciting spontaneous discharge of ganglionic neurones (Gilman et al, 1990) and by activating central sympathoadrenal pathways (Kennedy et al, 1984). Tension returned to baseline values over a period of 5 to 10 min.…”

Section: Resultssupporting

confidence: 88%

Parasympathetic excitation of sympathetic innervation after cholinesterase inhibition

Beauregard

Smith

1996

British J Pharmacology

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1 Orbital parasympathetic innervation normally provides prejunctional muscarinic inhibition of sympathetic neurotransmission without activation of excitatory muscarinic receptors located on the innervated smooth muscle. The present study examines the role of acetylcholinesterase (AChE) in limiting the effects of parasympathetically released acetycholine to prejunctional receptors. 2 Urethane anaesthetized rats were placed in a stereotaxic frame, and parasympathetic activation was achieved by electrical stimulation (20 Hz, <2.0 V) of the ipsilateral superior salivatory nucleus. Drugs were administered through a femoral venous cannula. Superior tarsal smooth muscle responses were measured by recording eyelid tension. 3 Parasympathetic stimulation alone caused a small decrease in resting tension; previous studies have shown this to be attributable to attenuation of resting sympathetic tone. Parasympathetic activation following physostigmine administration, however, evoked a large contractile response. Contractions were resistant to atropine but were blocked by gallamine, guanethidine, and phentolamine. 4 We conclude that AChE inhibition results in conversion of orbital parasympathetic nerve function from inhibition of sympathetic neurotransmission to smooth muscle excitation. This occurs as a result of cholinergic activation of excitatory nicotinic receptors on sympathetic varicosities, which elicit the release of noradrenaline.

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Section: Resultssupporting

confidence: 88%

Parasympathetic excitation of sympathetic innervation after cholinesterase inhibition

Beauregard

Smith

1996

British J Pharmacology

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“…In turn, this results in enhanced sympathoexcitatory mechanisms through increased neurotransmission of cholinergic neurons in the rostral ventrolateral medulla (5,32). Cholinergic pathways are independently involved in the central control of MABP through SNS activation as well (3,18,34,35). The activation of sympathetic responses plays a central role in orchestrating hemodynamic counterregulation to blood loss, increasing systemic vascular resistance and cardiac output, which ultimately contributes to restoration of MABP (7).…”

Section: Discussionmentioning

confidence: 99%

Central acetylcholinesterase inhibition improves hemodynamic counterregulation to severe blood loss in alcohol-intoxicated rats

Mathis¹,

Molina²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Acute alcohol intoxication results in impaired hemodynamic counterregulation to blood loss and is associated with an attenuated hemorrhage-induced release of catecholamines and AVP. We speculated that restoration of the neuroendocrine response to hemorrhage would improve mean arterial blood pressure (MABP) recovery during acute alcohol intoxication. Previously, we demonstrated that intracerebroventricular (i.c.v.) choline, a precursor of acetylcholine, transiently increases sympathetic nervous system (SNS) outflow but is not capable of improving neuroendocrine and hemodynamic compensation to hemorrhage in alcohol-treated rats. We hypothesized that prolongation of the observed effect via i.c.v. neostigmine, an acetylcholinesterase inhibitor, would enhance SNS outflow, restore the neuroendocrine response, and in turn improve hemodynamic responses to hemorrhage during acute alcohol intoxication. I.c.v. neostigmine (1 microg) increased MABP, catecholamines, and AVP within 5 min and reversed hypotension due to 40% hemorrhage and intragastric alcohol (30% wt/vol, 2.5 g/kg) administration in chronically catheterized male Sprague-Dawley rats (225-250 g body wt). Acute alcohol intoxication before 50% hemorrhage decreased basal MABP, accentuated hypotension midhemorrhage, suppressed the hemorrhage-induced release of norepinephrine and AVP, and prevented restoration of MABP to basal levels after fluid resuscitation with lactated Ringer solution. I.c.v. neostigmine (0.5 microg) produced a sustained increase in MABP beginning at 30 min of hemorrhage that persisted throughout fluid resuscitation in control and alcohol-treated animals. I.c.v. neostigmine enhanced epinephrine responses and restored the hemorrhage-induced release of norepinephrine and AVP in alcohol-treated rats. These results demonstrate that inhibition of acetylcholinesterase in the central nervous system enhances SNS outflow, restores the neuroendocrine response to severe blood loss, and thereby improves hemodynamic counterregulation during acute alcohol intoxication. This study provides evidence for a central (and not peripheral) role of alcohol in impairing hemodynamic stability during hemorrhagic shock.

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“…OPC intoxication leads to changes in blood pressure, which can be dose-depen dent [15,16]. A low dose could result in vasoconstriction of small arteries whereas a high dose leads to vasodilata tion.…”

Section: Discussionmentioning

confidence: 99%

Effect of Organophosphorus Compound Intoxication on Auditory Brainstem Response in Mini Pigs

Bergler¹,

Juncker²,

Petroianu

et al. 1996

ORL

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Organophosphorus compounds (OPC) are widely used as insecticides and cause a high number of acute and chronic intoxications in man. Their toxico logical properties lead among others to disturbances of the central nervous system. Hearing disturbances have been reported after chronic exposure to OPC, and changes in bioelectric brain activity have been observed during the acute state of intoxication. The EEG showed no characteristic alterations. We performed a threshold auditory brainstem response (ABR) in 12 mini pigs before, during and after paraoxon (a typical OPC) intoxication with a high dose of 27 mg/kg BW. During the application of paraoxon we saw a prolongation of the interpeak latencies Jewett I-V of approximately 1 ms. A threshold shift of 10–20 dB was seen in 8 animals. After the application, while the systemic effect of the paraoxon intoxication was still apparent, the threshold shift disappeared except for 2 animals and the prolongation of the interpeak latencies could not be observed any more. No characteristic signs of paraoxon intoxication could be seen in the ABR after the application was completed. Acute intoxication with an OPC only leads to temporary, limited hearing impairment and increased interpeak latency. We could not observe characteristic changes in the ABR corresponding to the state of intoxication.

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Central cholinergic stimulation causes adrenal epinephrine release.

Cited by 36 publications

References 25 publications

Parasympathetic excitation of sympathetic innervation after cholinesterase inhibition

Parasympathetic excitation of sympathetic innervation after cholinesterase inhibition

Central acetylcholinesterase inhibition improves hemodynamic counterregulation to severe blood loss in alcohol-intoxicated rats

Effect of Organophosphorus Compound Intoxication on Auditory Brainstem Response in Mini Pigs

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