Role of the parasympathetic nerves in regulation of periodic secretion of saliva in dogs

1969 ◽  
Vol 67 (3) ◽  
pp. 229-231
Author(s):  
V. D. Sukhodolo
Keyword(s):  
Parasympathetic Nerves ◽  
Periodic Secretion

Origin and modulation of ACh release from rat airway cholinergic nerves

1997 ◽  
Vol 272 (1) ◽  
pp. L8-L14 ◽  
Author(s):  
F. X. Zhu ◽  
X. Y. Zhang ◽  
N. E. Robinson
Keyword(s):  
Synaptic Vesicles ◽  
High Performance ◽  
Electrical Field Stimulation ◽  
Cyclooxygenase Inhibitors ◽  
Ach Release ◽  
Electrical Field ◽  
Parasympathetic Nerves ◽  
Release Of Acetylcholine ◽  
Rat Trachea

The release of acetylcholine (ACh) from airway parasympathetic nerves was studied in rat trachea. We established stimulus parameters, examined the role of extracellular Ca2+, and investigated the origin of the released ACh by use of vesamicol, an inhibitor of ACh uptake in synaptic vesicles. The role of muscarinic autoreceptors and prostanoids on ACh release was also studied. Tracheal rings were incubated in Krebs-Henseleit solution containing neostigmine and guanethidine with or without atropine. ACh release was measured by high-performance liquid chromatography with electrochemical detection. ACh release was dependent on frequency (0.5-16 Hz), voltage (10-25 V), and pulse duration (0.5-4 ms). At 4 Hz, one-fifth of electrical field stimulation-induced ACh release was extracellular Ca2+ independent and vesamicol resistant, indicating its nonvesicular origin. Three-fifths were Ca2+ dependent and vesamicol sensitive, indicating that it was newly synthesized, and one-fifth was Ca2+ dependent but vesamicol resistant, indicating its origin from prestored vesicles. At 16 Hz, two-fifths were nonvesicular and three-fifths were newly synthesized. Blockade of the muscarinic autoreceptor by atropine potentiated the release of ACh four- to fivefold. Neither of the cyclooxygenase inhibitors indomethacin or meclofenamate nor exogenous prostaglandin E2 affected ACh release, indicating that inhibitory prostanoids do not modulate ACh release.

scholarly journals Role of cAMP and neuronal K+channels on α2-AR-induced inhibition of ACh release in equine trachea

1998 ◽  
Vol 274 (5) ◽  
pp. L827-L832
Author(s):  
Xiang-Yang Zhang ◽  
Feng-Xia Zhu ◽  
N. Edward Robinson
Keyword(s):  
Electrical Field Stimulation ◽  
Intracellular Camp ◽  
Field Stimulation ◽  
Ach Release ◽  
Electrical Field ◽  
K Channels ◽  
Parasympathetic Nerves ◽  
Pathway Activation ◽  
Before And After

To investigate the effects of changes in intracellular cAMP on α2-adrenoceptor (AR)-induced inhibition of airway acetylcholine (ACh) release, we examined the effects of the α2-AR agonist clonidine on electrical field stimulation-evoked ACh release from equine tracheal parasympathetic nerves before and after treatment with 8-bromo-cAMP or forskolin. We also tested whether charybdotoxin (ChTX)- or iberiotoxin (IBTX)-sensitive Ca2+-activated K+ channels mediate α2-AR-induced inhibition by examining the effect of clonidine in the absence and presence of ChTX or IBTX on ACh release. The amount of released ACh was measured by HPLC coupled with electrochemical detection. Clonidine (10−7 to 10−5 M) dose dependently inhibited ACh release before and after treatment with 8-bromo-cAMP (10−3 M) or forskolin (3 × 10−5M). ChTX and IBTX, both at the concentration of 5 × 10−7 M, significantly increased ACh release; however, they did not alter the magnitude of clonidine-induced inhibition. These results indicated that in equine tracheal parasympathetic nerves, α2-AR-induced inhibition of ACh release is via an intracellular cAMP-independent pathway. Activation of both ChTX- and IBTX-sensitive Ca2+-activated K+ channels inhibits the electrical field stimulation-evoked ACh release, but these channels are not involved in the α2-AR-induced inhibition of ACh release.

Inhibition of activity-induced parotid growth by submandibular gland ablation or autonomic denervation

1991 ◽  
Vol 261 (5) ◽  
pp. G723-G727 ◽  
Author(s):  
C. A. Schneyer ◽  
M. G. Humphreys-Beher ◽  
H. D. Hall
Keyword(s):  
Parotid Gland ◽  
Submandibular Gland ◽  
Thymidine Incorporation ◽  
Autonomic Nerves ◽  
Autonomic Denervation ◽  
Gland Size ◽  
Parasympathetic Nerves ◽  
Solid Diet ◽  
Rat Parotid

When solid chow was reintroduced for 2 days to rats previously maintained on an all-liquid diet, [3H]thymidine incorporation into rat parotid gland was 2.4-4.4 times that of chow-fed or liquid-fed animals. When the submandibular-sublingual glands were removed before the change in diet from liquid to solid food, values for [3H]thymidine incorporation of parotid gland were not statistically different from those of chow-fed rats: the increase was completely prevented. The increase in gland size that accompanied the change in dietary consistency was not prevented by prior submandibular gland ablation; [3H]uridine incorporation was also not different from that of chow controls. The removal of both the sympathetic and parasympathetic nerves to the parotid gland before the dietary manipulation also suppressed [3H]thymidine incorporation into parotid, and values did not differ from chow controls. Moreover, the return to normal gland size (chow level) also was prevented by autonomic denervation. The data show an important role of the submandibular gland in regulation of the thymidine increase associated with the enhanced parotid activity that accompanies the change from liquid to solid diet. However, the submandibular gland does not have an important role in regulation of the increase in gland size that also accompanies the dietary change, whereas the autonomic nerves have an important role in regulation of hypertrophy and hyperplasia of parotid gland.

The Concept of Cotransmission: Focus on ATP as a Cotransmitter and its Significance in Health and Disease

2014 ◽  
Vol 22 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Geoffrey Burnstock
Keyword(s):  
Sympathetic Nerves ◽  
Purinergic Signalling ◽  
Release Of Noradrenaline ◽  
Spontaneously Hypertensive ◽  
Parasympathetic Nerves ◽  
Sympathetic Pain ◽  
Central Nervous Systems ◽  
Health And Disease ◽  
Nerve Release

The concept of cotransmission, including sympathetic nerve release of noradrenaline and ATP, was formalised in 1976, which challenged the accepted view known as ‘Dale's Principle’ that one nerve released only one transmitter. ATP was also shown to be a cotransmitter with acetylcholine in parasympathetic nerves supplying the urinary bladder and as a cotransmitter with nitric oxide in non-adrenergic, non-cholinergic inhibitory nerves supplying the intestine. It is now recognised that ATP is a cotransmitter in most, if not all, nerves in the peripheral and central nervous systems. The physiological significance of cotransmission will be considered. In pathophysiology, the role of ATP as a cotransmitter appears to increase as shown, for example, in the parasympathetic nerves supplying the diseased human bladder and in sympathetic nerves in spontaneously hypertensive rats. ATP is likely to be involved in sympathetic pain, causalgia and reflex sympathetic dystrophy. Purinergic signalling also appears to be enhanced in inflammatory and stress conditions.

Insulin sensitivity is mediated by the activation of the ACh/NO/cGMP pathway in rat liver

2004 ◽  
Vol 287 (3) ◽  
pp. G527-G532 ◽  
Author(s):  
Maria P. Guarino ◽  
Nina C. Correia ◽  
W. Wayne Lautt ◽  
M. Paula Macedo
Keyword(s):  
Nitric Oxide ◽  
Insulin Sensitivity ◽  
Muscarinic Receptors ◽  
Wistar Rats ◽  
No Donor ◽  
Parasympathetic Nerves ◽  
Cgmp Pathway ◽  
Male Wistar Rats ◽  
Oxide Synthase

The hepatic parasympathetic nerves and hepatic nitric oxide synthase (NOS) are involved in the secretion of a hepatic insulin sensitizing substance (HISS), which mediates peripheral insulin sensitivity. We tested whether binding of ACh to hepatic muscarinic receptors is an upstream event to the synthesis of nitric oxide (NO), which, along with the activation of hepatic guanylate cyclase (GC), permits HISS release. Male Wistar rats (8–9 wk) were anesthetized with pentobarbital sodium (65 mg/kg). Insulin sensitivity was assessed using a euglycemic clamp [the rapid insulin sensitivity test (RIST)]. HISS inhibition was induced by antagonism of muscarinic receptors (atropine, 3 mg/kg iv) or by blockade of NOS [ NG-nitro-l-arginine methyl ester (l-NAME), 1 mg/kg intraportally (ipv)]. After the blockade, HISS action was tentatively restored using a NO donor [3-morpholynosydnonimine (SIN-1), 5–10 mg/kg ipv] or ACh (2.5–5 μg·kg−1·min−1 ipv). SIN-1 (10 mg/kg) reversed the inhibition caused by atropine (RIST postatropine 137.7 ± 8.3 mg glucose/kg; reversed to 288.3 ± 15.5 mg glucose/kg, n = 6) and by l-NAME (RIST post-l-NAME 152.2 ± 21.3 mg glucose/kg; reversed to 321.7 ± 44.7 mg glucose/kg, n = 5). ACh did not reverse HISS inhibition induced by l-NAME. The role of GC in HISS release was assessed using 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 5 nmol/kg ipv), a GC inhibitor that decreased HISS action (control RIST 237.6 ± 18.6 mg glucose/kg; RIST post-ODQ 111.7 ± 6.2 mg glucose/kg, n = 5). We propose that hepatic parasympathetic nerves release ACh, leading to hepatic NO synthesis, which activates GC, triggering HISS action.

Ozone-induced hyperresponsiveness and blockade of M2 muscarinic receptors by eosinophil major basic protein

1999 ◽  
Vol 87 (4) ◽  
pp. 1272-1278 ◽  
Author(s):  
Bethany L. Yost ◽  
Gerald J. Gleich ◽  
Allison D. Fryer
Keyword(s):  
Muscarinic Receptors ◽  
Guinea Pigs ◽  
Basic Protein ◽  
Muscarinic Agonist ◽  
Receptor Function ◽  
Major Basic Protein ◽  
Interleukin 5 ◽  
Parasympathetic Nerves ◽  
Eosinophil Major Basic Protein

Control of airway smooth muscle is provided by parasympathetic nerves that release acetylcholine onto M3 muscarinic receptors. Acetylcholine release is limited by inhibitory M2 muscarinic receptors. In antigen-challenged guinea pigs, hyperresponsiveness is due to blockade of neuronal M2 receptors by eosinophil major basic protein (MBP). Because exposure of guinea pigs to ozone also causes M2dysfunction and airway hyperresponsiveness, the role of eosinophils in ozone-induced hyperresponsiveness was tested. Animals were exposed to filtered air or to 2 parts/million ozone for 4 h. Twenty-four hours later, the muscarinic agonist pilocarpine no longer inhibited vagally induced bronchoconstriction in ozone-exposed animals, indicating M2 dysfunction. M2 receptor function in ozone-exposed animals was protected by depletion of eosinophils with antibody to interleukin-5 and by pretreatment with antibody to guinea pig MBP. M2 function was acutely restored by removal of MBP with heparin. Ozone-induced hyperreactivity was also prevented by antibody to MBP and was reversed by heparin. These data show that loss of neuronal M2 receptor function after ozone is due to release of eosinophil MBP.

Role of macrophages in virus-induced airway hyperresponsiveness and neuronal M2 muscarinic receptor dysfunction

2004 ◽  
Vol 286 (6) ◽  
pp. L1255-L1259 ◽  
Author(s):  
Ann M. Lee ◽  
Allison D. Fryer ◽  
Nico van Rooijen ◽  
David B. Jacoby
Keyword(s):  
Viral Infection ◽  
Airway Hyperresponsiveness ◽  
Viral Infections ◽  
Muscarinic Agonist ◽  
Vagus Nerves ◽  
Ach Release ◽  
Parasympathetic Nerves ◽  
M2 Muscarinic Receptor ◽  
Stimulation Of

Viral infections exacerbate asthma. One of the pathways by which viruses trigger bronchoconstriction and hyperresponsiveness is by causing dysfunction of inhibitory M2 muscarinic receptors on the airway parasympathetic nerves. These receptors normally limit acetylcholine (ACh) release from the parasympathetic nerves. Loss of M2 receptor function increases ACh release, thereby increasing vagally mediated bronchoconstriction. Because viral infection causes an influx of macrophages into the lungs, we tested the role of macrophages in virus-induced airway hyperresponsiveness and M2 receptor dysfunction. Guinea pigs infected with parainfluenza virus were hyperresponsive to electrical stimulation of the vagus nerves but not to intravenous ACh, indicating that hyperresponsiveness was due to increased release of ACh from the nerves. In addition, the muscarinic agonist pilocarpine no longer inhibited vagally induced bronchoconstriction, indicating M2 receptor dysfunction. Treating animals with liposome-encapsulated dichloromethylene-diphosphonate depleted macrophages as assessed histologically. In these animals, viral infection did not cause airway hyperresponsiveness or M2 receptor dysfunction. These data suggest that macrophages mediate virus-induced M2 receptor dysfunction and airway hyperresponsiveness.

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