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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.
11 nduced secretion was inhibited 54% +/- 8% by pirenzepine (10(-5) M), 69% +/- 14% by gallamine (10(-5)
12 fted to the right by a factor of about 10 by pirenzepine (100 nM), suggesting a pKB (-log of the appa
14 l interaction test, the anxiogenic effect of pirenzepine (30-100 ng) provided evidence for a tonic ch
15 sts with a rank order of potency (atropine > pirenzepine = 4-DAMP >> gallamine) consistent with regul
20 nding to human cortex and showed total [(3)H]pirenzepine and [(3)H]NMS binding was reduced by Zn(2+),
21 dition, two muscarinic receptor antagonists (pirenzepine and atropine) are assayed to compare their r
23 e muscarinic M1 and M2 receptor antagonists, pirenzepine and gallamine, and the nicotinic receptor an
24 t analysis using the competitive antagonists pirenzepine and himbacine indicated that the effect of m
25 a previous 5-min experience of the plus-maze pirenzepine and mecamylamine had anxiogenic effects in t
29 d five antagonists, atropine (nonselective), pirenzepine and telenzepine (M1), gallamine (M2), and 4-
30 ferring muscarinic antagonists, telenzepine, pirenzepine, and trihexyphenidyl, which alleviate dyston
31 c (scopolamine) and specific (methoctramine, pirenzepine) antagonists of muscarinic cholinergic trans
32 a significant increase in the number of [3H]pirenzepine binding sites compared to normotensive WKY i
34 eas BQCA effects on [(3)H]NMS, but not [(3)H]pirenzepine, binding was enhanced by Mg(2+) and Zn(2+).
36 a2+ current by CCh was antagonized by 100 nM pirenzepine but not by 6 nM tripitramine, indicating tha
38 nized by 6 nM tripitramine but not by 100 nM pirenzepine, consistent with activation of endogenous M2
39 pport the definition of two groups of Bodipy-pirenzepine derivatives exhibiting distinct allosteric b
42 Subconjunctival injections of 0.002% or less pirenzepine do not decrease EW-stimulated accommodation.
45 potency of carbachol (EC50=10.5 microM) and pirenzepine (IC50=4.2 muM), with the same accuracy as st
46 ubconjunctival injections of 0.0002% to 0.2% pirenzepine in log unit dilutions were tested in three m
47 ed by 100 nM methoctramine but not by 100 nM pirenzepine, indicating that it was mediated by M(2) mus
52 rinic receptor-subtype-selective antagonists pirenzepine (M1), gallamine (M2), and 4-4-diphenylacetox
54 4-DAMP) was 57-244-fold smaller than that of pirenzepine, methoctramine, and tropicamide to inhibit t
58 week-old SHR and WKY were incubated with [3H]pirenzepine or [3H]AFDX 384 to label M1 and M2 receptors
59 not blocked by the M1-selective antagonists, pirenzepine or telenzepine or by the M2/M4-selective ant
61 ide), OXO plus the M(1) selective antagonist pirenzepine (PIRENZ; 0.3 nmol/side) or aCSF 15 min befor
62 The muscarinic M(1) preferring antagonist pirenzepine potently blocked pilocarpine-induced increas
64 bconjunctival injections of 0.02% or greater pirenzepine result in a significant decrease in accommod
65 m treatment with the selective M1 antagonist pirenzepine resulted in a large shift in the distributio
66 pproximately 60% reduction of an M1-coupled, pirenzepine-sensitive depolarizing current, which appear
69 ) neurons in macaque V1 express the m1-type (pirenzepine-sensitive, Gq-coupled) muscarinic ACh recept
71 ilitation of LTD was blocked by atropine and pirenzepine, suggesting involvement of M1 receptors.
73 M1R using specific or selective antagonists, pirenzepine, VU0255035, or muscarinic toxin 7 (MT7) acti
74 Zn(2+), acetylcholine displacement of [(3)H]pirenzepine was reduced by Mg(2+) and enhanced by Zn(2+)
75 driasis from subconjunctival injection of 2% pirenzepine were determined in five normal rhesus monkey
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