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At least 181 records · Page 10Linked to original sources
PubMed1994

Interaction of iodinated quinuclidinyl benzilate enantiomers with M3 muscarinic receptors.

We examined the interaction of 3-quinuclidinyl-4-iodobenzilate enantiomers, (RR)- and (SS)-IQNB, relatively receptor-active and -inactive, respectively, with M3-muscarinic receptors (mAChRs) in rat parotid acinar cells in vitro. This stereospecific antagonist pair has often been used for in vivo studies of mAChRs. There was a 16-fold difference in the ability of (RR)- and (SS)-IQNB to bind in vitro to mAChRs; Ki values estimated by competition with N-methylscopolamine were 5.3 and 84.2 nM, respectively. However, the ability of these antagonists to inhibit carbachol-stimulated inositol trisphosphate formation (Ki values determined by Schild analyses) was more similar, 16.3 and 47.7 nM, respectively for (RR)- and (SS)-IQNB. These data suggest that while it may be useful to employ this antagonist pair to evaluate some mAChR subtypes in vivo, it is difficult to use them in studies of M3-mAChRs.

Animals↗
PubMed1984

The binding of 3H-quinuclidinyl benzilate to cholinergic muscarinic receptors in rat brain region following chronic treatment with morphine and during abstinence.

Chronic morphine treatment (subcutaneous pellet implantation of four morphine pellets) caused significant tolerance to morphine analgesia as observed at zero and 6 hrs. after pellet removal. However, such treatment failed to elicit any changes in striatal muscarinic receptors using (3H)-QNB binding studies. At 24 hours after pellet removal there was significant development of physical dependence but the affinity (Kd) as well as density (Bmax) of striatal muscarinic receptors remained unaffected. Although naloxone caused marked precipitation of abrupt withdrawal in morphine tolerant rats, it also failed to produce any changes in striatal muscarinic receptors. Results indicate that any cholinergic involvement in opiate tolerance and physical dependence does not involve an effect on muscarinic receptors.

Animals↗
PubMed1985

Comparison of the affinity constant of some muscarinic receptor antagonists with their displacement of [3H]quinuclidinyl benzilate binding in atrial and ileal longitudinal muscle of the guinea-pig.

The ability of the muscarinic receptor antagonists fenipramide, 4-diphenylacetoxy-N-methyl piperidine methiodide (4-DAMP) and secoverine to displace [3H]QNB binding was correlated with the inhibition of responses of cholinomimetics at muscarinic receptors in the atria and ileal longitudinal muscle of the guinea-pig. Fenipramide and 4-DAMP exhibited a 2-4 fold higher affinity for muscarinic receptors in ileal longitudinal muscle in both types of experiments. Secoverine exhibited no difference in affinity in the two tissues.

Animals↗
PubMed1998

[Effect of lysophasphatidylcholine on sensitivity of the heart to acetylcholine and binding of quinuclidinyl benzilate to myocardial membranes].

Chemical nature of the blood serum factor exerting cholinolytic effect on the animal heart, was determined. The effect is due to the serum lipid component: lysophosphatidylcholine. The latter in concentration 1-25 microM suppresses the sensitivity of the frog perfused heart ventricle to acetylcholine. Phosphatidylcholine was found to protect the heart from the lysophosphatidylcholine effect. Lysophosphatidylcholine also affected the binding of the acetylcholine high affinity antagonist [3H]-quinuclidinylbenzilate to the rabbit atria cell membranes. The mechanism of this effect is related to an increased ability of muscarinic receptors to form oligomeric complexes in presence of lysophosphatidylcholine, the latter manifesting a positive cooperativity on binding to ligand.

Acetylcholine↗