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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.
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
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
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
44 nities were 10-fold lower in the presence of isoprenaline and adrenaline than when salbutamol or terb
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
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
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
63 Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or exposure to hypoxia/reo
65 e the nonselective beta-adrenoceptor agonist isoprenaline, behaved as a potent, full agonist at beta
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
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
78 ly, the FBF response to incremental doses of isoprenaline did not differ between genotype groups befo
80 ainst isoprenaline-induced mortality, whilst isoprenaline elevated cGMP and protected myocardial ener
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
88 10 mM or addition of 3 microM isoproterenol (isoprenaline) failed to normalize the frequency of spont
90 inhibition primarily reduced the efficacy of isoprenaline for beta-arrestin2 translocation, whereas f
92 e beta-AR-coupled adenylyl cyclase system to isoprenaline, Gpp(NH)p and forskolin was studied by meas
98 2+) release +/- 1 microm isoproterenol (ISO; isoprenaline) in voltage-clamped ventricular myocytes of
100 olutions with weak Ca2+i buffering, however, isoprenaline increased net macroscopic Cl- currents.
102 isometric contractions during SR inhibition, isoprenaline increased the force but did not alter the t
105 ith the beta-receptor agonist isoproterenol (isoprenaline) increased RyR1 PKA phosphorylation, twitch
109 cAMP levels and sensitized cardiomyocytes to isoprenaline-induced augmentation of contractility, wher
111 Adenoviral infection unmasked a 1 microM isoprenaline-induced IK,ACh which was prevented by propr
114 selective PKA inhibitor KT5720 prevented the isoprenaline-induced increase in IKr only when the incre
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
123 as used to study effects of the beta agonist isoprenaline (Iso) on the current-voltage (I-V) relation
125 e slow afterhyperpolarization (sAHP) such as isoprenaline (ISO) or noradrenaline (NA) reduced the hyp
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
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
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
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
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
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
162 ventricular (LV) contractile function or on isoprenaline- or preload-induced increase in cardiac con
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
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
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
180 e of contraction and a higher sensitivity to isoprenaline-stimulated inotropy compared with control s
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
187 ratio) when subjected to increasing doses of isoprenaline stress under baseline and pressure-overload
189 or displayed higher affinity for the agonist isoprenaline than the wild-type receptor but not for the
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
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
205 nditioning pulse duration in the presence of isoprenaline was used to reduce the amplitude of the Ca2
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
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