Differential Regulation of Putative M1/M2 Muscarinic Receptors: Implications for Different Receptor-Effector Coupling Mechanisms

1984 ◽  
pp. 99-114 ◽  
Author(s):  
Thomas W. Vickroy ◽  
Mark Watson ◽  
Henry I. Yamamura ◽  
William R. Roeske
Keyword(s):  
Muscarinic Receptors ◽  
Differential Regulation ◽  
Coupling Mechanisms ◽  
M2 Muscarinic Receptors

Dysfunction of M2-muscarinic receptors in pulmonary parasympathetic nerves after antigen challenge

1991 ◽  
Vol 71 (6) ◽  
pp. 2255-2261 ◽  
Author(s):  
A. D. Fryer ◽  
M. Wills-Karp
Keyword(s):  
Muscarinic Receptors ◽  
Guinea Pigs ◽  
Antigen Challenge ◽  
Saline Control ◽  
Control Group ◽  
Vagus Nerves ◽  
Parasympathetic Nerves ◽  
Volume Blood ◽  
M2 Muscarinic Receptors ◽  
Stimulation Of

The effect of antigen challenge on the function of neuronal M2-muscarinic autoreceptors in the lungs was studied in anesthetized guinea pigs. Guinea pigs were injected intraperitoneally with saline (control group) or ovalbumin (10 mg/kg) on days 1, 3, and 5. One group of sensitized animals was challenged on days 20–25 with aerosolized ovalbumin for 5 min/day (challenged group), while another group of the sensitized animals was not challenged (sensitized group). On day 26 the animals were anesthetized, paralyzed, tracheostomized, and artificially ventilated. Pulmonary inflation pressure (Ppi), tidal volume, blood pressure, and heart rate were recorded. Both vagus nerves were cut, and electrical stimulation of the distal portions caused bronchoconstriction (measured as an increase in Ppi) and bradycardia. In the control group, pilocarpine (1–100 micrograms/kg iv) attenuated vagally induced bronchoconstriction by stimulating inhibitory M2-muscarinic receptors on parasympathetic nerves in the lungs. Conversely, blockade of these receptors with the antagonist gallamine (0.1–10 mg/kg iv) produced a marked potentiation of vagally induced bronchoconstriction. These results confirm previous findings. In the challenged guinea pigs, pilocarpine did not inhibit vagally induced bronchoconstriction. Furthermore, gallamine did not potentiate vagally induced bronchoconstriction to the same degree as in the controls. In the group of animals that was sensitized but not challenged, the potentiation of vagally induced bronchoconstriction by gallamine was identical to the controls. There was no increase in baseline Ppi in the sensitized or challenged animals compared with the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Involvement of M2 muscarinic receptors in relaxant response of circular muscle of mouse gastric antrum.

2006 ◽  
Vol 18 (3) ◽  
pp. 226-233 ◽  
Author(s):  
t. takeuchi ◽  
m. toyoshima ◽  
k. mukai ◽  
k. hagi ◽  
m. matsui ◽  
...  
Keyword(s):  
Muscarinic Receptors ◽  
Circular Muscle ◽  
Gastric Antrum ◽  
Relaxant Response ◽  
M2 Muscarinic Receptors

Multiple Autoantibodies against Cardiovascular Receptors as Biomarkers in Hypertensive Heart Disease

Cardiology ◽  
2019 ◽  
Vol 142 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Xin Wang ◽  
Yuan Zhang ◽  
Juan Zhang ◽  
Yu-Xing Wang ◽  
Xiao-Rong Xu ◽  
...  
Keyword(s):  
Heart Disease ◽  
Angiotensin Ii ◽  
Muscarinic Receptors ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ventricular Ejection Fraction ◽  
M2 Muscarinic Receptors ◽  
Normal Controls

Objectives: The pathogenesis of hypertensive heart disease (HHD) remains unclear, which might include autoimmunity. The aim of the present study was to determine whether a relationship exists between the presence of autoantibodies against β1, β2, α1 adrenoreceptors, M2-muscarinic receptors, angiotensin II type1 receptors and HHD. Methods: In the present study, 44 patients diagnosed with HHD, 36 patients with hypertension, and 40 controls were also enrolled. The measurement of these 5 autoantibodies was performed by enzyme-linked immunosorbent assay. Results: The frequencies of autoantibodies against β1, β2, α1 adrenoreceptors, autoantibodies against M2-muscarinic receptors and autoantibodies against angiotensin II type1 receptors were significantly higher in patients with HHD, when compared to patients with hypertension and normal controls (all p < 0.001). In addition, the titers of these 5 autoantibodies significantly increased in patients with HHD. Patients who were positive for all 5 autoantibodies had larger left ventricular end-diastolic diameter (60.5 ± 4.9 vs. 57.8 ± 5.0 vs. 52.5 ± 5.3 mm) and worse left ventricular ejection fraction (45.0 ± 11.0 vs. 56.6 ± 10.4 vs. 57.8 ± 5.3%), when compared to patients not positive for all the 5 autoantibodies and patients negative for all the 5 autoantibodies (χ2 = 9.524, p = 0.009 and χ2 = 7.689, p = 0.021). Furthermore, a significant positive correlation was observed between each 2 autoantibodies of these 5 autoantibodies (all p < 0.001). Conclusion: Multiple autoantibodies of cardiovascular receptors may be involved in the pathogenesis and may be predictive factors of HHD.

Ozone-induced airway hyperresponsiveness and loss of neuronal M2 muscarinic receptor function

1994 ◽  
Vol 76 (3) ◽  
pp. 1088-1097 ◽  
Author(s):  
A. H. Schultheis ◽  
D. J. Bassett ◽  
A. D. Fryer
Keyword(s):  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Ozone Exposure ◽  
Muscarinic Agonist ◽  
Receptor Function ◽  
Vagus Nerves ◽  
Parasympathetic Nerves ◽  
M2 Muscarinic Receptor ◽  
Release Of Acetylcholine ◽  
M2 Muscarinic Receptors

The effect of acute ozone exposure on the function of efferent parasympathetic nerves, M3 muscarinic receptors on airway smooth muscle, and inhibitory M2 muscarinic receptors on the parasympathetic nerves was studied. Immediately after exposure to 2.0 ppm ozone for 4 h, guinea pigs became hyperresponsive to electrical stimulation of the vagus nerves. The normal airway response to intravenous cholinergic agonists at this time demonstrates normal M3 receptor function. M2 muscarinic receptors on the nerves, which normally inhibit release of acetylcholine, were dysfunctional after ozone exposure, as demonstrated by the failure of the muscarinic agonist pilocarpine to inhibit, and the failure of the M2 antagonist gallamine to potentiate, vagally mediated bronchoconstriction. Thus, loss of inhibitory M2 muscarinic receptor function after ozone exposure potentiates release of acetylcholine from the vagus nerves, increasing vagally mediated bronchoconstriction. By 14 days, postozone responses to vagal nerve stimulation were not different from those of air-exposed animals and the function of the neuronal M2 muscarinic receptor was normal, confirming that ozone-induced hyperresponsiveness is reversible.

scholarly journals Adrenomedullin upregulates M2 -muscarinic receptors in cardiomyocytes from P19 cell line

2003 ◽  
Vol 139 (6) ◽  
pp. 1219-1227 ◽  
Author(s):  
Sophie Buys ◽  
Fatima Smih ◽  
Atul Pathak ◽  
Pierre Philip-Couderc ◽  
Patrick Verwaerde ◽  
...  
Keyword(s):  
Cell Line ◽  
Muscarinic Receptors ◽  
M2 Muscarinic Receptors
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