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1 adrenergic stimulation (70 nM isoproterenol (isoprenaline)).
2  determined by application of isoproterenol (isoprenaline).
3 oplasmic reticulum and a blunted response to isoprenaline.
4 reversal potential of IKr in the presence of isoprenaline.
5 thus allows the Na+ pump to be controlled by isoprenaline.
6  both at baseline and after stimulation with isoprenaline.
7 yocytes at baseline and after treatment with isoprenaline.
8  of shortening in response to treatment with isoprenaline.
9  did not prevent the activation of IK,ACh by isoprenaline.
10  Ca2+ transient amplitude in the presence of isoprenaline.
11 nt increased as ICa increased in response to isoprenaline.
12  ml-1 overnight) did not block the effect of isoprenaline.
13 stimulation of the L-type calcium current by isoprenaline.
14 e responses to the more efficacious agonist, isoprenaline.
15 cubation of rat neonatal cardiomyocytes with isoprenaline.
16  5 microM thapsigargin (TG) or stimulated by isoprenaline.
17 d, intermediate in control and shortest with isoprenaline.
18 ined the ECT contractile kinetic response to isoprenaline.
19 ding in assisting displacement of nadolol to isoprenaline.
20 that this was preserved in Px rats receiving isoprenaline.
21 re equivalent to that of the highest dose of isoprenaline.
22 ntagonized the response to the highest doses isoprenaline.
23 plx2-/- mice using the noradrenergic agonist isoprenaline.
24 as the most efficacious dilator, followed by isoprenaline.
25 tent but less efficacious than carbachol and isoprenaline.
26                   In canine atrial myocytes, isoprenaline (1 microM) consistently reduced ICl,vol in
27                     Forskolin (10 microM) or isoprenaline (1 microM) exerted multiple effects.
28         The beta-adrenergic receptor agonist isoprenaline (1 microM) had no effect on Ito.
29 dministration of the beta-adrenergic agonist isoprenaline (1 microM) or the membrane-permeable 8-brom
30 f decline, of the Ca2+ transient produced by isoprenaline (1.0 mumol l-1) was not significantly diffe
31                  The beta-adrenergic agonist isoprenaline (10 microM) also activated a glibenclamide-
32                   Basolateral application of isoprenaline (10 microM) did not affect ISC in cells mai
33       We studied the contractile response to isoprenaline (10 nm) in isolated hearts and isolated car
34 th control (21.6 +/- 1.5 ms) and faster with isoprenaline (14.5 +/- 0.9 ms), but in all cases was muc
35 ly inhibited by noradrenaline (10 microM) or isoprenaline (2-5 microM), and completely prevented by 8
36  current clamp, beta-adrenergic stimulation (isoprenaline, 30 nm) increased both the Ca2+ transient a
37 nM) was not changed by TG (270 +/- 21 nM) or isoprenaline (302 +/- 10 nM).
38 o stimulated by shrinkage and isoproteronol (isoprenaline, 5 microgr;M).
39 a-AR stimulation (intravenous isoproterenol (isoprenaline): 6, 12 and 24 ng (kg fat-free mass)-1 min-
40 O-methyl-cAMP, an Epac-selective agonist, or isoprenaline, a non-selective beta-adrenergic receptor a
41 a-adrenergic stimulation with isoproterenol (isoprenaline) accelerated spark amplitude recovery and d
42 a-adrenergic stimulation with isoproterenol (isoprenaline) accelerated spark amplitude recovery and d
43                                              Isoprenaline also promoted translocation of NDPK-C to th
44 nities were 10-fold lower in the presence of isoprenaline and adrenaline than when salbutamol or terb
45                                              Isoprenaline and adrenaline were more efficacious in fun
46 cked the inhibitory response to forskolin or isoprenaline and all cells responded with a monophasic s
47  Starting from the beta-adrenoceptor agonist isoprenaline and beta-blocker carvedilol, we designed an
48                         Agonist responses to isoprenaline and CGP 12177 had different sensitivities t
49 o discriminate between responses elicited by isoprenaline and CGP 12177.
50 tiple washout experiments, cAMP responses to isoprenaline and formoterol waned with increasing number
51 bular salivary gland (adrenaline, carbachol, isoprenaline and forskolin) mobilized Ca2+ from internal
52 ed ducts showed that all agonists, including isoprenaline and forskolin, mobilized Ca2+ exclusively f
53 ncreased by beta-adrenergic stimulation with isoprenaline and increased in a saturating manner with i
54                           In the presence of isoprenaline and nifedipine, the amplitude of the Ca2+ t
55 .08, n = 22, and -9.68 +/- 0.07, n = 17, for isoprenaline and salbutamol-induced responses, respectiv
56 3) bound to the full agonists carmoterol and isoprenaline and the partial agonists salbutamol and dob
57 ker, was markedly reduced in the presence of isoprenaline and the region of negative slope was absent
58 in response to the beta-adrenoceptor agonist isoprenaline and to 8-bromo-cAMP, an analogue of cAMP, t
59 ent on myocardial sensitivity to adrenergic (isoprenaline) and muscarinic cholinergic (carbachol) sti
60 ine, bradykinin, substance P, isoproterenol (isoprenaline) and sodium nitroprusside were measured by
61 urrent amplitude was increased 47 +/- 12% by isoprenaline, and 73 +/- 13% by forskolin.
62                                     Both the isoprenaline- and forskolin-induced increases in IKr wer
63     Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or exposure to hypoxia/reo
64                                The effect of isoprenaline became persistent if cells were pretreated
65 e the nonselective beta-adrenoceptor agonist isoprenaline, behaved as a potent, full agonist at beta
66 ectively, and 34% of the maximal response of isoprenaline (beta1)).
67                               Isoproterenol (isoprenaline; betaAR agonist) dilated 1A, 2A and 3A near
68 ly reduced in hypertrophic hearts induced by isoprenaline but not in those induced by swimming exerci
69 Ih was potentiated by both noradrenaline and isoprenaline by a mechanism consistent with a shift in t
70                      Digoxin, dobutamine and isoprenaline caused a significant increase in power outp
71 ked only 81 +/- 5% of IKr in the presence of isoprenaline compared to 100 +/- 0% in control.
72                                              Isoprenaline decreased left ventricular end-systolic vol
73 nergic stimulation with 1 muM isoproterenol (isoprenaline)) decreased the latency period and increase
74  systematic changes in 14 ligands, including isoprenaline derivatives, full and partial agonists, and
75                                     However, isoprenaline did elicit cAMP accumulation in these cells
76              Further experiments showed that isoprenaline did increase I(SC) in cells treated (24 h)
77                                              Isoprenaline did not change the contraction profile on e
78 ly, the FBF response to incremental doses of isoprenaline did not differ between genotype groups befo
79       Paradoxically, it is often stated that isoprenaline does not activate IK,ACh.
80 ainst isoprenaline-induced mortality, whilst isoprenaline elevated cGMP and protected myocardial ener
81                               In NGF tissue, isoprenaline elicited a significantly smaller response t
82 n to the PM occurred to similar extents with isoprenaline, epinephrine, and norepinephrine, kinase in
83 tor (betaAR) agonists such as isoproterenol (isoprenaline), even though both stimulate the same signa
84 embrane's Na(+) conductance (G(Na)), whereas isoprenaline-evoked changes in apical Cl(-) conductance
85 ed that these hormones are essential for the isoprenaline-evoked increase in the apical membrane's Na
86  current was increased by the application of isoprenaline (expected to increase the underlying Ca2+ t
87                       Irrespective of P(O2), isoprenaline failed to elicit a discernible change in I(
88 10 mM or addition of 3 microM isoproterenol (isoprenaline) failed to normalize the frequency of spont
89  inotropes were tested: digoxin, dobutamine, isoprenaline, flecainide, verapamil and atenolol.
90 inhibition primarily reduced the efficacy of isoprenaline for beta-arrestin2 translocation, whereas f
91                                              Isoprenaline further shortened RyR refractoriness in DKI
92 e beta-AR-coupled adenylyl cyclase system to isoprenaline, Gpp(NH)p and forskolin was studied by meas
93                                       Px and isoprenaline had contrasting effects on cardiac substrat
94         Maximum doses of either carbachol or isoprenaline had no effect on coronary perfusate distrib
95                                              Isoprenaline had no effect on dialysate lactate, which w
96                                              Isoprenaline had no effect on Na+ pump capacity at PO2 l
97                           Pre-treatment with isoprenaline in vitro increased MF-LTP by 125% (P<0.001)
98 2+) release +/- 1 microm isoproterenol (ISO; isoprenaline) in voltage-clamped ventricular myocytes of
99                                              Isoprenaline increased ICl,ATP pre-activated by ATPgamma
100 olutions with weak Ca2+i buffering, however, isoprenaline increased net macroscopic Cl- currents.
101                                    Likewise, isoprenaline increased stroke work in control hearts (14
102 isometric contractions during SR inhibition, isoprenaline increased the force but did not alter the t
103                                              Isoprenaline increased the integral of the subsequent ri
104                                   Similarly, isoprenaline increased the spontaneous firing frequency
105 ith the beta-receptor agonist isoproterenol (isoprenaline) increased RyR1 PKA phosphorylation, twitch
106                                     However, isoprenaline induced a similar rise in intracellular Ca(
107          In contrast, introduction of 100 nM isoprenaline induced arrhythmogenicity in both KCNE1-/-
108       Impaired acetylcholine- (P < 0.01) and isoprenaline-induced (P < 0.05) vasodilatation in isolat
109 cAMP levels and sensitized cardiomyocytes to isoprenaline-induced augmentation of contractility, wher
110                 Therefore, we propose higher isoprenaline-induced Ca(2+) spark frequencies might faci
111     Adenoviral infection unmasked a 1 microM isoprenaline-induced IK,ACh which was prevented by propr
112 tal to adenylyl cyclase were not involved in isoprenaline-induced IK,ACh.
113                                          The isoprenaline-induced increase in ICa was significantly s
114 selective PKA inhibitor KT5720 prevented the isoprenaline-induced increase in IKr only when the incre
115                           The forskolin- and isoprenaline-induced increases in IKr were inhibited by
116     Moreover, Px rats were protected against isoprenaline-induced mortality, whilst isoprenaline elev
117 onal responses to incremental isoproterenol (isoprenaline) infusion (2, 4 and 6 microg kg min-1) were
118 ally with 5.4 mM K+o, noradrenaline (NA) and isoprenaline (Iso) (1-50 microM) stimulated Ip by 40-45%
119 enoreceptor (beta1-AR) by the catecholamines isoprenaline (Iso) and adrenaline (Adr) is regulated by
120 ic infusion of the nonselective beta-agonist isoprenaline (ISO) and compared this with cold-activated
121 nses to the beta-adrenergic receptor agonist isoprenaline (Iso) in CA1 pyramidal cells, suggesting th
122                     beta-AR stimulation with isoprenaline (ISO) increased Ca2+ transient amplitude, I
123 as used to study effects of the beta agonist isoprenaline (Iso) on the current-voltage (I-V) relation
124 oncentrations of the cAMP-producing agonists isoprenaline (Iso) or histamine.
125 e slow afterhyperpolarization (sAHP) such as isoprenaline (ISO) or noradrenaline (NA) reduced the hyp
126                                              Isoprenaline (ISO) prolonged APDs and triggered EADs in
127 zed a PEG-Iso molecule by covalently linking isoprenaline (Iso) to a 5000 Da PolyEthylene-Glycol (PEG
128 tivity of ICa to the beta-adrenergic agonist isoprenaline (Iso) was studied in both WT and NOS3-KO mo
129 nt stimulated by the beta-adrenergic agonist isoprenaline (Iso), and washout of ACh revealed a stimul
130                               However, under isoprenaline (ISO), both the application of JNJ-303 and
131 gated protective effects of canagliflozin in isoprenaline (ISO)-induced cardiac oxidative damage-a mo
132 e effects of green tea leaves powder against isoprenaline (ISO)-induced myocardial infarction in rats
133 we investigated if canagliflozin can reverse isoprenaline (ISO)-induced renal oxidative damage in rat
134 the absence and presence of the beta-agonist isoprenaline (Iso).
135 ly stimulated by the beta-adrenergic agonist isoprenaline (Iso).
136                                              Isoprenaline (Iso, 1 mg/kg, sc., 10 days) was administer
137                               Isoproterenol (isoprenaline; ISO) increased the amplitude of the inward
138 ath application of 0.5 microM isoproterenol (isoprenaline; ISO) when measured using the whole-cell pa
139  oestrogen and weight loss to isoproterenol (isoprenaline; Iso)-induced Fos immunoreactivity (IR) and
140 f the beta-adrenergic agonist isoproterenol (isoprenaline; ISO).
141 g adrenergic stimulation with isoproterenol (isoprenaline; ISO).
142                               Isoproterenol (isoprenaline; ISO; 0.01 microM), a non-selective beta-AR
143 thysmography) responses to administration of isoprenaline (isoproterenol) before and after NO inhibit
144 drenergic stimulation of HFpEF myocytes with isoprenaline (isoproterenol) failed to elicit robust inc
145                    In vivo administration of isoprenaline (isoproterenol) predisposes I Ks channel tr
146  of beta-adrenergic receptors with 10 microM isoprenaline (isoproterenol, ISO) enhanced INa by 68.4 +
147 ted by activation of beta 1-adrenoceptors by isoprenaline (Kp = 1.6 microM), indicating that salmeter
148 ion with a zero chloride solution containing isoprenaline led to a significant change in potential di
149  sought to understand the impact of repeated isoprenaline-mediated beta-stimulation upon cardiac mito
150 h-clamp analysis demonstrated expression and isoprenaline-mediated regulation of I Ks in atrial myocy
151 hat persisted even in the presence of 100 nM isoprenaline (n = 6).
152                                              Isoprenaline occasionally activated IK,ACh in uninfected
153                               The effects of isoprenaline on contraction were compared between rigid
154                  The effects of forskolin or isoprenaline on I(Cl,swelling) were inhibited by intrace
155 kinase 1 (50 microM) prevented the effect of isoprenaline on IK,ACh.
156 gargin (2.5 mumol l-1) reduced the effect of isoprenaline on the amplitude of the Ca2+ transient.
157 TP pre-activated by ATPgammaS or PDBu, while isoprenaline or forskolin alone failed to activate any C
158      Activation of protein kinase A (PKA) by isoprenaline or forskolin caused an increase in IKr tail
159 with a cAMP-mediated agonist (isoproterenol (isoprenaline) or vasoactive intestinal peptide) in the p
160 on of the beta-receptor (with isoproterenol (isoprenaline)) or at the post-receptor level (with forsk
161           The inhibitory effect of AA on the isoprenaline- or cAMP-stimulated ICa,L is largely reduce
162  ventricular (LV) contractile function or on isoprenaline- or preload-induced increase in cardiac con
163 s in vitro to vasodilators acetylcholine and isoprenaline (P < 0.05).
164 e, RV developed pressure and HR responses to isoprenaline (P < 0.05).
165 n was achieved by 0.01 microm isoproterenol (isoprenaline) plus 0.1 microm ICI 118551, a selective be
166 ttached patch recording, bath application of isoprenaline produced a pronounced inhibition of SOC act
167 beta-Adrenoceptor stimulation (with 5 microM isoprenaline) produced marked increases in net work, pow
168          We show that the adrenergic agonist isoprenaline promotes receptor and G protein activation
169                                              Isoprenaline rapidly stimulated cardiac CCK gene express
170 ding the selective beta-adrenoceptor agonist isoprenaline reduced the current evoked by cyclopiazonic
171 a-Adrenergic stimulation with isoproterenol (isoprenaline) reversed electromechanical alternans, sugg
172 This may explain the enhanced sensitivity to isoprenaline seen under these slightly hyperoxic conditi
173                                              Isoprenaline sensitivity was blocked by hyperpolarizatio
174                               Whereas Px and isoprenaline separately produced clinical endpoints rela
175        Within a minute, full agonists (e.g., isoprenaline) stimulated large increases in intracellula
176 olute magnitude, of basal and isoproterenol (isoprenaline)-stimulated Ca2+ current (ICa) was decrease
177 c acid (MA), had no inhibitory effect on the isoprenaline-stimulated Ca2+ current, whereas, in the sa
178                                              Isoprenaline-stimulated difference currents were not out
179 ynoic acid (ETYA), was without effect on the isoprenaline-stimulated ICa,L.
180 e of contraction and a higher sensitivity to isoprenaline-stimulated inotropy compared with control s
181 psy for the determination of spontaneous and isoprenaline-stimulated lipolysis in adipocytes.
182 data from the recent GWAS of spontaneous and isoprenaline-stimulated lipolysis in the unique GENetics
183 utant, termed beta2AR(SSS), showed increased isoprenaline-stimulated phosphorylation and differences
184  end-stage human HF, in rats after long-term isoprenaline stimulation through osmotic minipumps, and
185                                         Upon isoprenaline stimulation, GRKs strongly influenced beta-
186 cerbated cardiac remodeling during long-term isoprenaline stimulation.
187 ratio) when subjected to increasing doses of isoprenaline stress under baseline and pressure-overload
188       We found that individually both Px and isoprenaline suppressed cardiac mitochondrial respiratio
189 or displayed higher affinity for the agonist isoprenaline than the wild-type receptor but not for the
190                           In the presence of isoprenaline, the amplitude of both ICa and the Ca2+ tra
191 hat the DKI cells present a full response to isoprenaline, the data suggest that phosphorylation of S
192 containing 5 mM Ca2+-1 microM isoproterenol (isoprenaline) they produced Ca2+ sparks spontaneously.
193 ic pressure-volume relation was increased by isoprenaline to a greater extent in control than transge
194  the unused donor group were desensitized to isoprenaline to a similar degree as those from the faili
195 .v.) and shifted the dose-response curve for isoprenaline to higher agonist concentrations without al
196 apacity for glucose uptake and metabolism in isoprenaline-treated rats.
197                                              Isoprenaline treatment, but not Px, decreased ejection f
198  However, the positive inotropic response to isoprenaline was also blunted in ssTnI hearts.
199              In addition, the application of isoprenaline was associated with unchanged L-type Ca(2+)
200                                The effect of isoprenaline was blocked by the antagonist propranolol.
201 line (ACh) and the beta-adrenoceptor agonist isoprenaline was decreased in the PR group, while there
202  the hearts of the NGF mice, the response to isoprenaline was diminished, and this was due to an unco
203 any given cell, the response to forskolin or isoprenaline was qualitatively similar suggesting that a
204        As expected, the lusitropic effect of isoprenaline was significantly blunted in ssTnI hearts.
205 nditioning pulse duration in the presence of isoprenaline was used to reduce the amplitude of the Ca2
206                                              Isoprenaline was used to stimulate beta-ARs.
207  by the finding that IKr, in the presence of isoprenaline, was somewhat less sensitive to block.
208  of the PKA pathway activator isoproterenol (isoprenaline) were unchanged compared to I-1((-/-)) aort
209  the intracellular loop 3 in the presence of isoprenaline, which is capable of acting as a biased ago
210 atheter for forearm vasodilator responses to isoprenaline with plethysmography.
211 ompared the effects of the synthetic agonist isoprenaline with the endogenous catecholamines: epineph
212 l cardiomyocytes responded to isoproterenol (isoprenaline) with a decrease in cell size, mature cardi
213 51 substantially reduced the HVC response to isoprenaline without affecting HR responses.

 
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