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1 ignificantly decreased after 0.2% or greater pirenzepine.
2  using the muscarinic cholinergic antagonist pirenzepine.
3 ased 20 to 40 minutes after 0.02% or greater pirenzepine.
4 brium and kinetic pharmacological values for pirenzepine.
5 binding than the prototypical m1 antagonist, pirenzepine.
6 ramine but not by the M1 receptor antagonist pirenzepine.
7 sts methoctramine and tropicamide but not by pirenzepine.
8 mally observed after infusion of atropine or pirenzepine.
9                       Atropine (1 microM) or pirenzepine (0.05-0.1 microM) blocked the CS- or eserine
10  reversed with either atropine (1 microM) or pirenzepine (1 microM).
11                         When challenged with pirenzepine (1 uM), an antagonist selective for M1-type
12 nduced secretion was inhibited 54% +/- 8% by pirenzepine (10(-5) M), 69% +/- 14% by gallamine (10(-5)
13 fted to the right by a factor of about 10 by pirenzepine (100 nM), suggesting a pKB (-log of the appa
14                                              Pirenzepine (3.0 mM), which blocks postsynaptic m1 recep
15 l interaction test, the anxiogenic effect of pirenzepine (30-100 ng) provided evidence for a tonic ch
16 sts with a rank order of potency (atropine > pirenzepine = 4-DAMP >> gallamine) consistent with regul
17            Although sustained treatment with pirenzepine also resulted in marked up-regulation of the
18          Although the M1 receptor antagonist pirenzepine also reversed the inhibition of IPSCs by mus
19 mAChR (M(2)R) antagonist AFDX-116 and not by pirenzepine, an M(1)-mAChR (M(1)R) antagonist.
20 a2+ transients were antagonized by 10 nmol/L pirenzepine, an m1 mAChR-selective antagonist.
21       Hence, we explored the nature of [(3)H]pirenzepine and [(3)H]NMS binding to human cortex and sh
22 nding to human cortex and showed total [(3)H]pirenzepine and [(3)H]NMS binding was reduced by Zn(2+),
23 dition, two muscarinic receptor antagonists (pirenzepine and atropine) are assayed to compare their r
24 terizing the muscarinic receptor antagonists pirenzepine and atropine.
25 e muscarinic M1 and M2 receptor antagonists, pirenzepine and gallamine, and the nicotinic receptor an
26 t analysis using the competitive antagonists pirenzepine and himbacine indicated that the effect of m
27 a previous 5-min experience of the plus-maze pirenzepine and mecamylamine had anxiogenic effects in t
28                     Prior microinjections of pirenzepine and methoctramine (1 mM, each) into the PMN,
29                                        Since pirenzepine and methoctramine microinjections into the P
30                                              Pirenzepine and MT7 also prevented peripheral neuropathy
31 d five antagonists, atropine (nonselective), pirenzepine and telenzepine (M1), gallamine (M2), and 4-
32 ferring muscarinic antagonists, telenzepine, pirenzepine, and trihexyphenidyl, which alleviate dyston
33 c (scopolamine) and specific (methoctramine, pirenzepine) antagonists of muscarinic cholinergic trans
34  a significant increase in the number of [3H]pirenzepine binding sites compared to normotensive WKY i
35 because of a profound loss of cortical [(3)H]pirenzepine binding.
36 eas BQCA effects on [(3)H]NMS, but not [(3)H]pirenzepine, binding was enhanced by Mg(2+) and Zn(2+).
37                                              Pirenzepine blocks the B50-elicited motor program, the p
38 a2+ current by CCh was antagonized by 100 nM pirenzepine but not by 6 nM tripitramine, indicating tha
39            The M1-selective mAChR antagonist pirenzepine completely blocked the carbachol effect at 1
40 nized by 6 nM tripitramine but not by 100 nM pirenzepine, consistent with activation of endogenous M2
41 Pseudo-analogues of the tricyclic antagonist pirenzepine demonstrate that this is an effective strate
42 pport the definition of two groups of Bodipy-pirenzepine derivatives exhibiting distinct allosteric b
43 e the applied chemical modifications to make pirenzepine derivatives sensitive to light stimuli, the
44         We provide evidence that fluorescent pirenzepine derivatives, with the M1 antagonist fused to
45                                 Furthermore, pirenzepine, diphenyl-acetoxy-N-methyl-piperidine and me
46 Subconjunctival injections of 0.002% or less pirenzepine do not decrease EW-stimulated accommodation.
47        The M1 muscarinic receptor antagonist pirenzepine dose dependently inhibited the action of ace
48 from the norepinephrine transporter, and [3H]pirenzepine from muscarinic m1 receptors.
49  potency of carbachol (EC50=10.5 microM) and pirenzepine (IC50=4.2 muM), with the same accuracy as st
50 ubconjunctival injections of 0.0002% to 0.2% pirenzepine in log unit dilutions were tested in three m
51 ed by 100 nM methoctramine but not by 100 nM pirenzepine, indicating that it was mediated by M(2) mus
52                                              Pirenzepine inhibited sulfate incorporation by chondrocy
53                    At 40 to 50 minutes after pirenzepine injection, accommodation was stimulated phar
54                                     After 2% pirenzepine injection, pupil size increased 2.02 +/- 0.4
55                                              Pirenzepine is suggested to be a relatively selective mu
56 rinic receptor-subtype-selective antagonists pirenzepine (M1), gallamine (M2), and 4-4-diphenylacetox
57 phenidol (M3, 8.0) > tropicamide (M4, 6.4) > pirenzepine (M1, 6.1) > methoctramine (M2, 5.9).
58 4-DAMP) was 57-244-fold smaller than that of pirenzepine, methoctramine, and tropicamide to inhibit t
59                         In contrast, neither pirenzepine nor telenzepine altered the quaternary organ
60         In the current study, the effects of pirenzepine on pupil diameter, resting refraction, and a
61                 The effect of the antagonist pirenzepine on the carbachol-induced intracellular calci
62 week-old SHR and WKY were incubated with [3H]pirenzepine or [3H]AFDX 384 to label M1 and M2 receptors
63 not blocked by the M1-selective antagonists, pirenzepine or telenzepine or by the M2/M4-selective ant
64 arinic acetylcholine receptors (mAChRs; with pirenzepine) or disruption of calcium/calmodulin (Ca(2+)
65 se curve to methoctramine but not to 4-DAMP, pirenzepine, or tropicamide.
66 ide), OXO plus the M(1) selective antagonist pirenzepine (PIRENZ; 0.3 nmol/side) or aCSF 15 min befor
67    The muscarinic M(1) preferring antagonist pirenzepine potently blocked pilocarpine-induced increas
68              A mixture of methoctramine plus pirenzepine recapitulated the place-cell effects of scop
69 bconjunctival injections of 0.02% or greater pirenzepine result in a significant decrease in accommod
70 m treatment with the selective M1 antagonist pirenzepine resulted in a large shift in the distributio
71 pproximately 60% reduction of an M1-coupled, pirenzepine-sensitive depolarizing current, which appear
72 of an afterdepolarization, both triggered by pirenzepine-sensitive M1 receptors.
73 cates that PV neurons in rats rarely express pirenzepine-sensitive muscarinic AChRs.
74 ) neurons in macaque V1 express the m1-type (pirenzepine-sensitive, Gq-coupled) muscarinic ACh recept
75            In the present study, atropine or pirenzepine significantly inhibited the ability of eithe
76 ilitation of LTD was blocked by atropine and pirenzepine, suggesting involvement of M1 receptors.
77 icroscopic autoradiography, using 1-2 nM [3H]pirenzepine to assess unoccupied M(1) receptors.
78 M1R using specific or selective antagonists, pirenzepine, VU0255035, or muscarinic toxin 7 (MT7) acti
79  Zn(2+), acetylcholine displacement of [(3)H]pirenzepine was reduced by Mg(2+) and enhanced by Zn(2+)
80 driasis from subconjunctival injection of 2% pirenzepine were determined in five normal rhesus monkey