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1 ) directly indicate the SR Ca2+ leak (before tetracaine).
2 revented by the ryanodine receptor inhibitor tetracaine.
3 versed by traditional RyR inhibitors such as tetracaine.
4 s were sensitive to block by both Mg(2+) and tetracaine.
5 aradoxically did not modify these actions of tetracaine.
6  an increase of cell Ca2+ during exposure to tetracaine.
7 eviously abolished by the addition of 2.0 mM tetracaine.
8 d relatively high, 1-2 mM, concentrations of tetracaine.
9 a2+ efflux) was increased in the presence of tetracaine.
10 lcium efflux per unit time was unaffected by tetracaine.
11 r the quiescent period following addition of tetracaine.
12 s were dose dependent, from 25 to 200 microM tetracaine.
13 in the presence of various concentrations of tetracaine.
14  waves that were insensitive to ryanodine or tetracaine.
15 odology was developed and demonstrated using tetracaine.
16 several orders of magnitude more potent than tetracaine.
17 ose observed during perfusion with 50 microM tetracaine.
18                                In all cases, tetracaine (0.2 mM) abolished Ca(2+) spark activity, whe
19                                              Tetracaine (0.75 mM) caused transient complete inhibitio
20 y decreasing ryanodine receptor opening with tetracaine (1 mm).
21    In some experiments, the local anesthetic tetracaine (10 microg) was then microinjected near the A
22 h field-stimulated and voltage-clamped cells tetracaine (100-200 microM) produced an initial decrease
23 iperidine ([(3)H]TCP), [(3)H]ethidium, [(3)H]tetracaine, [(14)C]amobarbital, and 3-(trifluoromethyl)-
24 perchlorate (8.0 mM) or caffeine (0.2 mM) to tetracaine (2.0 mM)-treated fibres, also known to restor
25                                              Tetracaine (200 microM) reversibly abolished sparks and
26 4-AP and Ba(2+)) but completely inhibited by tetracaine (200 microM), an inhibitor of TREK channels.
27     Here we have synthesized a derivative of tetracaine, 3-[(aminopropyl)amino]-N,N-dimethyl-N-(2-[[4
28        Reduction of RyR2 Ca2+ sensitivity by tetracaine (50 microM) reduced the spontaneous Ca2+ rele
29 , neither steroid inhibited binding of [(3)H]tetracaine, a closed-state selective channel blocker, or
30 ii) blocking Ca(2+) release from the SR with tetracaine, a membrane-permeant, reversible ryanodine-se
31 odulation to detect the interactions between tetracaine, a positively charged small molecule used as
32          At high concentrations (> 1.25 mM), tetracaine abolished all forms of spontaneous release.
33           Resting [Ca2+]i declined 25% after tetracaine addition (126+/-6 versus 94+/-6 nmol/L; P<0.0
34 opical administration of anesthetics such as tetracaine, adrenaline, and cocaine and lidocaine, epine
35                   In contrast, inhalation of tetracaine aerosol (mass median aerodynamic diameter of
36                    We examined the effect of tetracaine aerosol inhalation, a local anesthetic, on lu
37                                Inhalation of tetracaine aerosol resulted in marked reductions in ozon
38 iodophenyl)diazirine ([(125)I]TID) and [(3)H]tetracaine, an aromatic amine, are noncompetitive antago
39 ated channels relative to a multiply charged tetracaine analogue described previously.
40                                          The tetracaine analogues described here have apparent affini
41                                     Five new tetracaine analogues were synthesized and evaluated for
42 ding of the noncompetitive antagonists [(3)H]tetracaine and [(3)H]phencyclidine to Torpedo nAChR-rich
43  by acute block of the ryanodine receptor by tetracaine and assessment of the consequent shift of Ca
44 ted, e.g. at a membrane potential of -70 mV) tetracaine and dantrolene each blocked IP3-evoked Ca2+ i
45 the use of blocking drugs such as ryanodine, tetracaine and dantrolene, reportedly specific inhibitor
46 taF/Fo, and FWHM were gradually decreased by tetracaine and increased by caffeine.
47 ermal thresholds to a different extent, with tetracaine and lidocaine being most efficient.
48 , hydrophobic and ionic interactions between tetracaine and lipid molecules predominate.
49        The ryanodine receptor (RyR) blockers tetracaine and Mg(2+) transiently suppressed the frequen
50 perchlorate also reversed the action of 2 mM tetracaine and restored delayed q gamma transients to an
51  Ca(2+) waves and this effect was blocked by tetracaine and ryanodine but not 2-aminoethoxydiphenyl b
52 d with the pan-RyR inhibitors dantrolene and tetracaine and the antiarrhythmic drug flecainide.
53 l to the SLBs decreased the affinity between tetracaine and the bilayers, while this interaction tigh
54                  These results indicate that tetracaine and TID bind in a mutually exclusive manner t
55                                     Although tetracaine and TID bind to the same site, the amine NCAs
56                                         Only tetracaine and tkP3BzPB, the two agents that had effects
57 s (reducing flux as seen experimentally with tetracaine) and sufficiently rapid intra-SR Ca diffusion
58 receptor (RyR)-specific agents ryanodine and tetracaine, and potentiated by caffeine.
59 from the cell during the burst on removal of tetracaine, and to estimates of the extra calcium gained
60 ]TID analog photoincorporation by NCAs (e.g. tetracaine) as well as identification of the sites of [(
61 (dimethylamino)ethyl 4-(butylamino)benzoate (tetracaine), as well as three large slowly reversible an
62         The SR Ca2+ content was increased by tetracaine, as shown by the integral of the caffeine-evo
63  This may be due to either direct effects of tetracaine at the acetylcholine binding site or preferen
64 This Ca2+ release was initially abolished by tetracaine before returning at a lower frequency, but gr
65 no derivatives inhibiting [(3)H]TCP or [(3)H]tetracaine binding to the resting AChR.
66 ues establishes that the high-affinity [(3)H]tetracaine-binding site is located within the lumen of t
67  photolabeling is at the high-affinity [(3)H]tetracaine-binding site.
68                                        [(3)H]Tetracaine binds at equilibrium to a single site with a
69 the ion channel, interact competitively with tetracaine but allosterically with TID.
70 phaM2-10 (alphaSer-252) was not inhibited by tetracaine but was enhanced 10-fold by proadifen or phen
71                       Before the addition of tetracaine, calculated Ca2+ influx and efflux across the
72          It is concluded that the effects of tetracaine can be accounted for by depression of calcium
73 rmeabilized cat ventricular myocytes, 0.7 mM tetracaine caused almost complete Ca spark inhibition fo
74        At low concentrations (0.25-1.25 mM), tetracaine caused an initial inhibition of spontaneous r
75 olabeling as well as its dependence on [(3)H]tetracaine concentration establish that the observed pho
76          The plots of maximum charge against tetracaine concentration suggested a saturable 1:1 drug
77  kinetics, even the micromolar (0.05-0.2 mM) tetracaine concentrations that failed to markedly alter
78                               The micromolar tetracaine concentrations that were hitherto reported to
79 sation of the SR Ca2+ release mechanism with tetracaine decreased the frequency of spontaneous releas
80                              Infusions of 2% tetracaine did not impair acquisition of the response or
81 nsiently less than influx and, on removal of tetracaine, efflux was greater than influx.
82                                    On adding tetracaine, efflux was transiently less than influx and,
83 stingly, the potency of the local anesthetic tetracaine for the inhibition of alpha3beta4 and alpha3b
84 ditioned response was notably reduced in the tetracaine group (M = 0.40, SEM +/- 0.216) relative to t
85 e channels incorporated into lipid bilayers, tetracaine (&gt; 0.25 mM) induced a steady inhibition of ch
86  receive either topical anesthesia with 0.5% tetracaine hydrochloride and subconjunctival balanced sa
87 ion sessions, an artificial tear solution or tetracaine hydrochloride was administered to the cornea
88 red saline nasal spray bilaterally, or (2) a tetracaine hydrochloride-oxymetazoline hydrochloride nas
89                                              Tetracaine hydrochloride-oxymetazoline nasal spray appea
90 50 = 4 muM) than in the resting state ([(3)H]tetracaine; IC50 = 60 muM), whereas it bound with only v
91 eviously abolished by the addition of 2.0 mM tetracaine in common with previous results of using ryan
92 revented by injection of a local anesthetic (tetracaine) in the cloacal region prior to courtship and
93                       As expected, bilateral tetracaine inactivation of the hippocampus disrupted spa
94  times and burst durations, mecamylamine and tetracaine induced unique subconductance states.
95                                          The tetracaine-induced decline in [Ca2+]i and increase total
96                   The low affinity inhibitor tetracaine induces a decrease in the extent of release t
97 bsence of agonist (resting state), there was tetracaine-inhibitable photolabeling of amino acids in t
98                                              Tetracaine inhibited [(125)I]TID labeling of M2-9 and M2
99                                Spermidine or tetracaine inhibited cleavage of bacterial membranes by
100                               Spermidine and tetracaine inhibited PLA2 activity and spermidine protec
101 olecule motility assay, the local anesthetic tetracaine inhibited the motility of individual kinesin
102 ne receptor (RyR) antagonists (ryanodine and tetracaine) inhibited both sparks and waves but increase
103  adequate to alter the voltage dependence of tetracaine inhibition, both point mutations are required
104 ChR is mediated by a steric mechanism; (iii) tetracaine inhibits CrV binding to the resting AChR, pro
105 ggest that the highly charged moiety of APPA-tetracaine interacts strongly with the negative charge c
106 ults in specific photoincorporation of [(3)H]tetracaine into each nAChR subunit.
107          We propose that the partitioning of tetracaine into solid-gel membranes is determined primar
108                    Microinjection of GABA or tetracaine into the medullary nucleus gigantocellularis
109                              Infusions of 2% tetracaine into the prelimbic-infralimbic areas did not
110                              Infusions of 2% tetracaine into the prelimbic-infralimbic or dorsal ante
111                                 Amethocaine, tetracaine, iontophoresis, and the S-caine patch, a prod
112                                        [(3)H]Tetracaine is a noncompetitive antagonist of the Torpedo
113 n of release by submaximal concentrations of tetracaine is caused by a gradual increase in SR Ca2+ lo
114 gated ion channels, and the local anesthetic tetracaine is known to block CNG channels in a manner th
115 ibition of alpha3beta4(6'F10'T) receptors by tetracaine is unaffected by membrane voltage, and at con
116 ction, demonstrated through the synthesis of tetracaine, is easily achieved, delivering the C-N cross
117 h that maximally effective concentrations of tetracaine isolate a single distinct species of conserve
118 c effect was also negated by coinfusion with tetracaine, molecular and pharmacologic inhibition of NR
119                                              Tetracaine (N,N-dimethylaminoethyl-4-butylaminobenzoate)
120  and cocaine and lidocaine, epinephrine, and tetracaine offers the advantage of replacing lidocaine i
121 separate kinetic and steady-state effects of tetracaine on intramembrane charge movements, at micromo
122 fluorometry was used to study the effects of tetracaine on spontaneous Ca2+ release from the sarcopla
123 icked the transient and sustained effects of tetracaine on spontaneous Ca2+ release.
124       We conclude that the primary effect of tetracaine on SR Ca(2+)-release channels is inhibition o
125      The effects of graded concentrations of tetracaine on the steady-state and kinetic properties of
126     Caffeine also antagonized the actions of tetracaine on the total available qgamma charge, but did
127                          We suggest that, in tetracaine or acidosis, the initial phase of the Ca2+ tr
128  were attenuated by microinjection of either tetracaine or cobalt into sites near the A7 cell group n
129                        Similar injections of tetracaine or cobalt more than 500 microm from the A7 ne
130  depressing RyR open probability (P(o)) with tetracaine or intracellular acidification.
131 onic acid or caffeine but were unaffected by tetracaine or nifedipine.
132 urate analogs inhibited the binding of [(3)H]tetracaine or photoincorporation of 3-trifluoromethyl-3-
133 in a junctional cluster (which is reduced by tetracaine or ruthenium red) and other SR Ca handling pr
134 of ryanodine receptors (RyRs) are blocked by tetracaine or ruthenium red, Ca sparks lasting hundreds
135 ty labeled by [(125)I]TID in the presence of tetracaine, PCP, or HTX.
136                                   Removal of tetracaine produced a transient overshoot of contraction
137  significant block of Na(+) channels by APPA-tetracaine required concentrations of hundreds of nanomo
138 1 drug binding that spared a fixed amount of tetracaine-resistant (q beta) charge but inhibited a dis
139 ained at the reduced values expected for the tetracaine-resistant qbeta charge.
140                  Exposure of the myocytes to tetracaine resulted in a gradual increase in the SR Ca2+
141 nAChR-rich membranes equilibrated with [(3)H]tetracaine resulted in covalent incorporation with simil
142 ut recovery after incubation with 300 microM tetracaine resulted in SR Ca(2+) release with no coheren
143 positive charge at the tertiary amine end of tetracaine results in higher potency and voltage depende
144 nAChR-rich membranes equilibrated with [(3)H]tetracaine results in specific photoincorporation of [(3
145                                              Tetracaine reversed the effects of caffeine but not of r
146                                              Tetracaine's effective pK(a) was reduced by 0.3-0.4 pH u
147                                              Tetracaine's location in the membrane placed the drug's
148                                              Tetracaine's location within the membrane (as indicated
149 nteractions are the critical determinants of tetracaine's location.
150 arget ryanodine receptors (RyR1: dantrolene, tetracaine, S107) and L-type Ca(2+) channels (LTCCs: nif
151     Nevertheless, a complete inhibition of a tetracaine-sensitive (q gamma) charge movement by 2 mM t
152 nd substantial I(K1), but no temperature- or tetracaine-sensitive K(+) currents.
153              Abrupt block of SR Ca2+ leak by tetracaine shifts Ca2+ from the cytosol to SR.
154  and was the same for neutral and protonated tetracaine, showing that the dipole-dipole and hydrophob
155 With all four subunits contributing to [(3)H]tetracaine site, the site in the closed channel state of
156 he isolated peptides demonstrated that [(3)H]tetracaine specifically labeled two sets of homologous h
157 ug (P407-CM-T) in which the local anesthetic tetracaine (T) is attached to the polymer poloxamer 407
158 R subunit specifically photolabeled by [(3)H]tetracaine that contribute to the high-affinity binding
159            These parallel earlier effects of tetracaine that have been reported upon the transient an
160 -sensitive (q gamma) charge movement by 2 mM tetracaine that left only q beta charge, sharply altered
161 yl]oxy]ethyl )propan-1-aminium acetate (APPA-tetracaine), that contains three positively charged amin
162 hifts of fluorescence emission at high lipid:tetracaine, the corresponding increases in fluorescence
163                                On removal of tetracaine there was an increase of the Na+-Ca2+ exchang
164                                On removal of tetracaine, there was a burst of spontaneous Ca2+ releas
165 cell, allowing for various concentrations of tetracaine to be introduced over the surface in a buffer
166 ) was still observed after pretreatment with tetracaine to block Ca(2+) release from ryanodine recept
167                           In the presence of tetracaine to eliminate Ca(2+) release from ryanodine re
168 binding of the noncompetitive antagonist [3H]tetracaine to nAChR-rich membranes (IC50 = 150 microM).
169                               The ability of tetracaine to reduce spark magnitude suggests that these
170 xposed to 0 Na+, 0 Ca2+ solution +/-1 mmol/L tetracaine (to block resting leak).
171                                              Tetracaine-treated females had accumulation patterns sim
172  of fluorescence intensity of membrane-bound tetracaine (TTC) on solution pH.
173 n the similar burst on removal of 100 microM tetracaine v/sigma was higher than control (166 +/- 9 %,
174 ransient decrease of contraction produced by tetracaine was accompanied by a small transient increase
175      The q beta charge thus isolated by 2 mM tetracaine was conserved through a wide range of applied
176                In contrast, the RyR2 blocker tetracaine was equally efficacious in mutant Purkinje ce
177 e sarcoplasmic reticulum (SR) measured using tetracaine was significantly increased in diabetic myocy
178  by blocking ryanodine receptors (RyR2) with tetracaine, was approximately 50% higher in cAF versus c
179 SR Ca(2+) increased as [ATP] was reduced or [tetracaine] was increased.
180                               The effects of tetracaine were examined on rat ventricular myocytes.
181                               The effects of tetracaine were studied on voltage-clamped rat ventricul
182 nAChR-rich membranes photolabeled with [(3)H]tetracaine were subjected to enzymatic digestion, and pe
183 tifungal (tolnaftate), and local anesthetic (tetracaine), were examined.
184          Co-infusion of the local anesthetic tetracaine with duodenal lipids abolished the lipid-indu
185         Interactions of the local anesthetic tetracaine with unilamellar vesicles made of dimyristoyl

 
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