Atropine methyl nitrate increases myenteric but not dorsal vagal complex Fos-like immunoreactivity in the rat

2006 ◽  
Vol 88 (4-5) ◽  
pp. 448-452 ◽  
Author(s):  
S RABOIN ◽  
S GULLEY ◽  
S HENLEY ◽  
W CHAN ◽  
A ESDAILE ◽  
...  
Keyword(s):  
Dorsal Vagal Complex ◽  
Methyl Nitrate ◽  
Atropine Methyl Nitrate

Central neuropeptide Y induces proximal stomach relaxation via Y1 receptors in the dorsal vagal complex of the rat

2006 ◽  
Vol 290 (2) ◽  
pp. R290-R297 ◽  
Author(s):  
Motoi Kobashi ◽  
Yuichi Shimatani ◽  
Keisuke Shirota ◽  
Song-Yu Xuan ◽  
Yoshihiro Mitoh ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Fourth Ventricle ◽  
Cholinergic Neurons ◽  
Proximal Part ◽  
Dependent Manner ◽  
Dorsal Vagal Complex ◽  
Proximal Stomach ◽  
Y1 Receptors ◽  
Atropine Methyl Nitrate ◽  
Intermediate Part

Effects of neuropeptide Y (NPY) on motility of the proximal stomach was examined in anesthetized rats. Intragastric pressure was measured using a balloon situated in the proximal part of the stomach. Administration of NPY into the fourth ventricle induced relaxation of the proximal stomach in a dose-dependent manner. Administration of an Y1 receptor (Y1R) agonist [Leu31, Pro34]NPY induced a larger relaxation than NPY. The administration of an Y2 receptor agonist (NPY 13-36) did not induce significant changes in motility. Microinjections of [Leu31, Pro34]NPY into the caudal part of the dorsal vagal complex (DVC) induced relaxation of the proximal stomach. In contrast, similar injections into the intermediate part of the DVC increased IGP of the proximal stomach. Administration of NPY into the fourth ventricle did not induce relaxation after bilateral injections of the Y1R antagonist (1229U91) into the caudal DVC. These results indicate that NPY induces relaxation in the proximal stomach via Y1Rs situated in the DVC. Because bilateral vagotomy below the diaphragm abolished the relaxation induced by the administration of NPY into the fourth ventricle, relaxation induced by NPY is probably mediated by vagal preganglionic neurons. Intravenous injection of atropine methyl nitrate reduced relaxation induced by administration of NPY. Therefore, relaxation induced by NPY is likely mediated by peripheral cholinergic neurons.

Atropine methyl nitrate inhibits sham feeding in the rat

1978 ◽  
Vol 8 (4) ◽  
pp. 405-407 ◽  
Author(s):  
D. Lorenz ◽  
P. Nardi ◽  
G.P. Smith
Keyword(s):  
Sham Feeding ◽  
Methyl Nitrate ◽  
Atropine Methyl Nitrate

scholarly journals Heterogeneity of muscarinic receptor-mediated Ca2+ responses in cultured urothelial cells from rat

2008 ◽  
Vol 294 (4) ◽  
pp. F971-F981 ◽  
Author(s):  
F. Aura Kullmann ◽  
D. Artim ◽  
J. Beckel ◽  
S. Barrick ◽  
W. C. de Groat ◽  
...  
Keyword(s):  
Muscarinic Receptors ◽  
Calcium Concentration ◽  
Atp Release ◽  
Urothelial Cells ◽  
Muscarinic Agonists ◽  
Rt Pcr ◽  
Methyl Nitrate ◽  
Atropine Methyl Nitrate ◽  
And Function ◽  
Sensory Mechanisms

Muscarinic receptors (mAChRs) have been identified in the urothelium, a tissue that may be involved in bladder sensory mechanisms. This study investigates the expression and function of mAChRs using cultured urothelial cells from the rat. RT-PCR established the expression of all five mAChR subtypes. Muscarinic agonists acetylcholine (ACh; 10 μM), muscarine (Musc; 20 μM), and oxotremorine methiodide (OxoM; 0.001–20 μM) elicited transient repeatable increases in the intracellular calcium concentration ([Ca2+]i) in ∼50% of cells. These effects were blocked by the mAChR antagonist atropine methyl nitrate (10 μM). The sources of [Ca2+]i changes included influx from external milieu in 63% of cells and influx from external milieu plus release from internal stores in 27% of cells. The use of specific agonists and antagonists (10 μM M1 agonist McN-A-343; 10 μM M2, M3 antagonists AF-DX 116, 4-DAMP) revealed that M1, M2, M3 subtypes were involved in [Ca2+]i changes. The PLC inhibitor U-73122 (10 μM) abolished OxoM-elicited Ca2+ responses in the presence of the M2 antagonist AF-DX 116, suggesting that M1, M3, or M5 mediates [Ca2+]i increases via PLC pathway. ACh (0.1 μM), Musc (10 μM), oxotremorine sesquifumarate (20 μM), and McN-A-343 (1 μM) acting on M1, M2, and M3 mAChR subtypes stimulated ATP release from cultured urothelial cells. In summary, cultured urothelial cells express functional M1, M2, and M3 mAChR subtypes whose activation results in ATP release, possibly through mechanisms involving [Ca2+]i changes.

Effects of atropine methyl nitrate on sham feeding in the rat

1982 ◽  
Vol 17 (4) ◽  
pp. 863-867 ◽  
Author(s):  
Harvey P. Weingarten ◽  
Susan D. Watson
Keyword(s):  
Sham Feeding ◽  
Methyl Nitrate ◽  
Atropine Methyl Nitrate

CRF in the paraventricular nucleus mediates gastric and colonic motor response to restraint stress

1992 ◽  
Vol 262 (1) ◽  
pp. G137-G143 ◽  
Author(s):  
H. Monnikes ◽  
B. G. Schmidt ◽  
H. E. Raybould ◽  
Y. Tache
Keyword(s):  
Gastric Emptying ◽  
Paraventricular Nucleus ◽  
Restraint Stress ◽  
Gastrointestinal Transit ◽  
Proximal Colon ◽  
Colonic Transit ◽  
Dependent Inhibition ◽  
Methyl Nitrate ◽  
Atropine Methyl Nitrate ◽  
Stimulation Of

The role of corticotropin-releasing factor (CRF) in the paraventricular nucleus of the hypothalamus (PVN) in the control of gastric emptying of a nonnutrient meal and colonic transit was investigated in conscious fasted rats chronically implanted with hypothalamic cannulas and catheters in both the stomach and proximal colon. CRF (0.06-0.6 nmol) microinfused unilaterally into the PVN resulted in a dose-dependent inhibition of gastric emptying (0-51%) and stimulation of colonic transit (0-93%). CRF (0.6 nmol)-induced delay in gastric emptying was inhibited by 50% by subdiaphragmatic vagotomy or atropine methyl nitrate (1 mg/kg ip), whereas the stimulation of colonic transit was completely abolished by atropine methyl nitrate and reduced by 19% by vagotomy. Microinfusion of CRF (0.6 nmol) into the lateral hypothalamus or central amygdala had no effect. Restraint exposure for 1 h delayed gastric emptying and stimulated colonic transit by 28 and 78%, respectively. Bilateral microinfusion of the CRF antagonist alpha-helical CRF-(9-41) (13 nmol) into the PVN before restraint abolished stress-induced alterations of gastric and colonic transit. The CRF antagonist did not alter basal gastric and colonic transit under basal conditions. These data indicate that the PVN is a specific responsive site for central CRF-induced alterations of gastric and colonic transit and suggest that endogenous CRF in the PVN plays a role in mediating restraint stress-related alterations of gastrointestinal transit.

Effect of N-methyl-D-aspartate applied to the ventral surface of the medulla on the trachea

1987 ◽  
Vol 63 (3) ◽  
pp. 1268-1274 ◽  
Author(s):  
M. A. Haxhiu ◽  
E. C. Deal ◽  
M. P. Norcia ◽  
E. van Lunteren ◽  
N. S. Cherniack
Keyword(s):  
Respiratory Activity ◽  
Excitatory Amino Acid ◽  
Ventral Surface ◽  
Intermediate Area ◽  
Cholinergic Antagonist ◽  
Tracheal Pressure ◽  
Area Increase ◽  
Specific Antagonist ◽  
Methyl Nitrate ◽  
Atropine Methyl Nitrate

Structures located near the ventral surface of the medulla (VMS) affect both cardiovascular tone and respiratory activity. In addition cooling the intermediate area of the VMS blocks the increases in parasympathetic activity and tracheal tone resulting from ventilation with hypercapnic or hypoxic gas mixtures, or due to stimulation of mechanoreceptors within the lung. Since cooling the surface of the VMS may affect fibers of passage as well as cell bodies, we performed studies in which pledgets containing N-methyl-D-aspartic acid (NMDA), a synthetic excitatory amino acid, were applied to intermediate area of the VMS. The studies were performed in chloralose-anesthetized, artificially ventilated cats. Application of pledgets containing NMDA (10(-7) mol at 10(-3) M) caused increases in tracheal pressure and the onset of phasic phrenic activity, but application of 10(-8) mol at 10(-4) M of NMDA could produce tracheal constriction without the appearance of phasic phrenic activity. Applying to the entire VMS either 2-amino-5-phosphonovalerate (2-APV, 10(-6) M), a specific antagonist to NMDA, or lidocaine (2%), a local anesthetic, 60 s before the application of pledgets containing NMDA, prevented the increase in tracheal tone and phasic phrenic activity. Intravenous administration of atropine methyl nitrate 0.5 mg/kg, a cholinergic antagonist, blocked tracheal responses to local application of pledgets containing NMDA but did not affect the increase in phasic phrenic nerve activity. These findings suggest that when stimulated, neurons near the surface of the VMS in the vicinity of the intermediate area increase the activity of parasympathetic fibers to the airway.

Central autonomic modulation of cardiac baroreflex by corticotropin-releasing factor

1989 ◽  
Vol 256 (4) ◽  
pp. H949-H955 ◽  
Author(s):  
L. A. Fisher
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Arterial Pressure ◽  
Corticotropin Releasing Factor ◽  
Pulse Interval ◽  
Response Range ◽  
Reflex Gain ◽  
Methyl Nitrate ◽  
Atropine Methyl Nitrate ◽  
Interval Response

The effects of intracerebroventricular administration of corticotropin-releasing factor (CRF) on baroreflex control of heart rate were studied in conscious, unrestrained rats. Stimulus-response curves relating mean arterial pressure (MAP) to pulse interval were constructed for assessment of baroreflex function. CRF, intracerebroventricularly injected, elicited dose-related reductions of resting pulse interval, response range, and reflex gain and elevations of resting arterial pressure and MAP50 (arterial pressure at midrange). Earlier peripheral blockade of cardiac vagal influences with atropine methyl nitrate greatly attenuated the effects of CRF on resting pulse interval, response range, and reflex gain. In contrast, earlier blockade of cardiac sympathetic influences with intravenous propranolol treatment did not alter the ability of CRF to reduce resting pulse interval, response range, and reflex gain. The central nervous system effects of CRF on cardiac baroreflex function were qualitatively similar to the actions of atropine methyl nitrate. It is concluded that CRF alters transmission in central nervous system pathways mediating baroreceptor-induced activation of cardiac vagal motor neurons.

Nodulus-uvula depressor response: central GABA-mediated inhibition of alpha-adrenergic outflow

1989 ◽  
Vol 256 (6) ◽  
pp. H1601-H1608 ◽  
Author(s):  
R. T. Henry ◽  
J. D. Connor ◽  
C. D. Balaban
Keyword(s):  
Vestibular Nucleus ◽  
Abrupt Onset ◽  
Neural Pathways ◽  
Superior Cerebellar Peduncle ◽  
Depressor Response ◽  
Arterial Blood ◽  
Methyl Nitrate ◽  
Cerebellar Peduncle ◽  
Atropine Methyl Nitrate ◽  
Hypotensive Response

Electrical stimulation of a lateral region of the cerebellar nodulus-uvula transition zone in anesthetized albino rabbits decreases mean arterial blood pressure in direct proportion to stimulus intensity. The hypotension has an abrupt onset and is phasic; heart rate is unaffected. Neural pathways that might mediate the depressor response were studied using autonomic-blocking agents. Pretreatment with 2 mg/kg iv of either propranolol HCl or atropine methyl nitrate did not alter the onset or duration of the hypotensive response. However, pretreatment with 2 mg/kg iv phentolamine HCl abolished the depressor response, and 7 mg.kg-1.min-1 iv tetraethylammonium infusion decreased the response by more than 50%. Ipsilateral injections of 200 ng bicuculline methiodide into an area immediately dorsal to the superior cerebellar peduncle or the dorsal aspect of the superior vestibular nucleus reversibly attenuated the nodulus-uvula evoked depression. Anterograde horseradish peroxidase-wheat germ agglutinin (HRP-WGA) transport experiments revealed that both these regions receive direct inputs from the nodulus-uvula. These data suggest that hypotensive events elicited by lateral nodulus-uvula stimuli represent a central, alpha-aminobutyric acid-mediated, phasic inhibition of vasomotor drive mediated through autonomic ganglia to alpha-adrenoreceptors in the vasculature.

scholarly journals Esophageal-gastric relaxation reflex in rat: dual control of peripheral nitrergic and cholinergic transmission

2006 ◽  
Vol 290 (6) ◽  
pp. R1570-R1576 ◽  
Author(s):  
Gerlinda E. Hermann ◽  
R. Alberto Travagli ◽  
Richard C. Rogers
Keyword(s):  
Nucleus Tractus Solitarius ◽  
Concomitant Administration ◽  
Inhibitory Response ◽  
Motor Nucleus ◽  
Neural Pathways ◽  
Cholinergic Transmission ◽  
Dorsal Motor Nucleus ◽  
Balloon Distension ◽  
Methyl Nitrate ◽  
Atropine Methyl Nitrate

It has long been known that the esophageal distension produced by swallowing elicits a powerful proximal gastric relaxation. Gastroinhibitory control by the esophagus involves neural pathways from esophageal distension-sensitive neurons in the nucleus tractus solitarius centralis (cNTS) with connections to virtually all levels of the dorsal motor nucleus of the vagus (DMV). We have shown recently that cNTS responses are excitatory and primarily involve tyrosine hydroxylase-immunoreactive cells, whereas the DMV response involves both an α1 excitatory and an α2 inhibitory response. In the present study, using an esophageal balloon distension to evoke gastric relaxation (esophageal-gastric reflex, EGR), we investigated the peripheral pharmacological basis responsible for this reflex. Systemic administration of atropine methyl nitrate reduced the amplitude of the gastric relaxation to 52.0 ± 4.4% of the original EGR, whereas NG-nitro-l-arginine methyl ester (l-NAME) reduced it to 26.3 ± 7.2% of the original EGR. Concomitant administration of atropine methyl nitrate and l-NAME reduced the amplitude of the gastric relaxation to 4.0 ± 2.5% of control. This reduction in the amplitude of induced EGR is quite comparable (4.3 ± 2.6%) to that seen when the animal was pretreated with the nicotinic ganglionic blocker hexamethonium. In the presence of bethanechol, the amplitude of the esophageal distension-induced gastric relaxation was increased to 177.0 ± 10.0% of control; administration of l-NAME reduced this amplitude to 19.9 ± 9.5%. Our data provide a clear demonstration that the gastroinhibitory control by the esophagus is mediated via a dual vagal innervation consisting of inhibitory nitrergic and excitatory cholinergic transmission.

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