scholarly journals Effects of a novel muscarinic receptor agonist, AF102B, on sympatho- $$$adrenomedullary function in rats

1992 ◽  
Vol 58 ◽  
pp. 170
Author(s):  
Hiroko Togashi ◽  
Yasuko Saito ◽  
Mitsuhiro Yoshioka ◽  
Machiko Matsumoto ◽  
Hideya Saito
Keyword(s):  
Muscarinic Receptor ◽  
Receptor Agonist

Differences between rat dorsal and ventral hippocampus in muscarinic receptor agonist binding and interaction with phospholipase C

1993 ◽  
Vol 244 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Antonio J. Garcia Ruiz ◽  
Matilde Zambelli ◽  
Caterina La Porta ◽  
Herbert Ladinsky ◽  
Silvana Consolo
Keyword(s):  
Phospholipase C ◽  
Muscarinic Receptor ◽  
Receptor Agonist ◽  
Ventral Hippocampus ◽  
Agonist Binding

Effects of MeCh, thapsigargin, and La3+ on plasmalemmal and intracellular Ca2+ transport in lacrimal acinar cells

1990 ◽  
Vol 258 (6) ◽  
pp. C1006-C1015 ◽  
Author(s):  
C. Y. Kwan ◽  
H. Takemura ◽  
J. F. Obie ◽  
O. Thastrup ◽  
J. W. Putney
Keyword(s):  
Plasma Membrane ◽  
Muscarinic Receptor ◽  
Extracellular Space ◽  
Receptor Agonist ◽  
Inositol Phosphates ◽  
Acinar Cells ◽  
Direct Channel ◽  
Physiological Conditions ◽  
Parotid Cells ◽  
Lacrimal Acinar Cells

The Ca2(+)-mobilizing actions of the muscarinic receptor agonist, methacholine (MeCh), and the microsomal Ca2+ pump inhibitor, thapsigargin, were investigated in lacrimal acinar cells. As previously shown for parotid cells (J. Biol. Chem. 264: 12266-12271, 1989), thapsigargin activates both internal Ca2+ release and Ca2+ entry from the extracellular space without increasing cellular inositol phosphates. The inorganic Ca2+ antagonist La3+ inhibited MeCh- or thapsigargin-activated Ca2+ entry. However, when added before MeCh or thapsigargin, La3+ inhibited the extrusion of Ca2+ at the plasma membrane. This phenomenon was exploited in protocols designed to investigate the pathways for filling agonist-sensitive Ca2+ stores in lacrimal cells. The results show that, in contrast to previous suggestions that external Ca2+ is required to replenish agonist-regulated Ca2+ stores, the inhibition of Ca2+ extrusion permits recycling of Ca2+ released by MeCh back into an MeCh- and thapsigargin-sensitive pool. Thus, although extracellular Ca2+ is the major source for refilling the intracellular Ca2+ stores under physiological conditions, the pathway by which this Ca2+ enters the pool need not be a direct one. These results are consistent with the recently revised capacitative model for the refilling of intracellular Ca2+ stores through Ca2+ influx subsequent to Ca2+ depletion, according to which refilling of intracellular Ca2+ stores occurs via a cytoplasmic route rather than a direct channel between intracellular Ca2+ stores and the extracellular space.

Pharmacological Characterization of PD151832, an M1 Muscarinic Receptor Agonist

1997 ◽  
pp. 311-315
Author(s):  
Roy D. Schwarz ◽  
Michael J. Callahan ◽  
Robert E. Davis ◽  
Mark R. Emmerling ◽  
Juan C. Jaen ◽  
...  
Keyword(s):  
Muscarinic Receptor ◽  
Receptor Agonist ◽  
Pharmacological Characterization ◽  
M1 Muscarinic

The contribution of muscarinic-receptor-mediated responses to epineurial vascular diameter at the sciatic nerve

2018 ◽  
Vol 96 (8) ◽  
pp. 855-858
Author(s):  
Chelsa Killey ◽  
Shane Cleary ◽  
Julie Orr ◽  
Jefferson C. Frisbee ◽  
Dwayne Jackson ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Muscarinic Receptor ◽  
Topical Application ◽  
Rat Model ◽  
Receptor Agonist ◽  
Vessel Diameter ◽  
Anaesthetized Rat ◽  
Baseline Diameter

This study used an anaesthetized rat model to directly observe changes in diameter of the vessels supplying the sciatic nerve in response to acetylcholine (10−4 M), a muscarinic receptor agonist, and atropine (10−5 M), a muscarinic receptor antagonist. Topical application of acetylcholine resulted in increases in vessel diameter (baseline: 22.0 ± 2.5 μm, acetylcholine: 28.8 ± 3.3 μm), while topical application of atropine resulted in a decrease in diameter (baseline: 26.6 ± 3.2 μm, atropine: 15.5 ± 3.6 μm) of the epineurial vessels. Mean arterial pressure was not affected by either acetylcholine (baseline: 103.8 ± 1.8 mm Hg, acetylcholine: 102.8 ± 3.2 mm Hg) or atropine (baseline: 104.0 ± 1.9 mm Hg, atropine: 105.2 ± 2.2 mm Hg). These data suggest that muscarinic-receptor-mediated responses can affect the diameter of the epineurial vessels at the sciatic nerve. In addition, muscarinic-receptor-mediated responses appear to contribute to baseline diameter of epineurial vessels at the sciatic nerve.

Pharmacokinetics and Metabolism of Radiolabelled SNI-2011, a Novel Muscarinic Receptor Agonist, in Healthy Volunteers

2011 ◽  
Vol 53 (02) ◽  
pp. 80-86
Author(s):  
Takuo Washio ◽  
Kazuhiro Kohsaka ◽  
Hirohiko Arisawa ◽  
Hiroaki Masunaga ◽  
Shin-ichiro Nagatsuka ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Muscarinic Receptor ◽  
Receptor Agonist

Neurochemical evaluation of the selective m1 muscarinic receptor agonist CDD-0097-A

Life Sciences ◽  
1995 ◽  
Vol 56 (11-12) ◽  
pp. 1005
Author(s):  
W.S Messer ◽  
Y.F Abuh ◽  
A.A El-Assadi ◽  
Y Liu ◽  
B Ojo ◽  
...  
Keyword(s):  
Muscarinic Receptor ◽  
Receptor Agonist ◽  
M1 Muscarinic

scholarly journals Protein kinase C is involved in desensitization of muscarinic receptors induced by phorbol esters but not by receptor agonists

1990 ◽  
Vol 267 (1) ◽  
pp. 23-29 ◽  
Author(s):  
W S Lai ◽  
T B Rogers ◽  
E E el-Fakahany
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Surface ◽  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Receptor Agonist ◽  
Phorbol Esters ◽  
Down Regulation ◽  
Receptor Agonists ◽  
Kinase C

Preincubation with receptor agonists or phorbol esters desensitized muscarinic-receptor-mediated [3H]cyclic GMP responses in mouse neuroblastoma N1E-115 cells. However, desensitization mediated by phorbol esters was heterologous, whereas that effected by receptor agonist was specific towards the muscarinic receptors. In addition, there was no loss of cell surface muscarinic receptors, as measured by the binding of the hydrophilic ligand [3H]N-methylscopolamine, when cells were treated with phorbol esters, but receptor-agonist-induced desensitization was accompanied by a decrease in cell surface receptor density. We examined the role of protein kinase C (PKC) in the desensitization of muscarinic receptors by employing a kinase inhibitor and by down-regulation of PKC by long-term incubation of cells with phorbol esters. Whereas these manoeuvres had marked effects on phorbol-ester-induced desensitization of muscarinic responses, they did not block agonist-induced down-regulation and desensitization of muscarinic receptors. In addition, when phosphoinositide hydrolysis was suppressed, the muscarinic agonist was still capable of mediating receptor sequestration and desensitization. These results suggest that the mechanisms for regulating muscarinic receptor sensitivity could be both PKC-dependent and PKC-independent, being mediated by phorbol esters and receptor agonists respectively.

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