ライフサイエンスコーパス: isoprenaline

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 5 microM thapsigargin (TG) or stimulated by isoprenaline.

16 d, intermediate in control and shortest with isoprenaline.

17 re equivalent to that of the highest dose of isoprenaline.

18 ntagonized the response to the highest doses isoprenaline.

19 plx2-/- mice using the noradrenergic agonist isoprenaline.

20 as the most efficacious dilator, followed by isoprenaline.

21 tent but less efficacious than carbachol and isoprenaline.

22 cubation of rat neonatal cardiomyocytes with isoprenaline.

23 In canine atrial myocytes, isoprenaline (1 microM) consistently reduced ICl,vol in

24 Forskolin (10 microM) or isoprenaline (1 microM) exerted multiple effects.

25 The beta-adrenergic receptor agonist isoprenaline (1 microM) had no effect on Ito.

26 dministration of the beta-adrenergic agonist isoprenaline (1 microM) or the membrane-permeable 8-brom

27 f decline, of the Ca2+ transient produced by isoprenaline (1.0 mumol l-1) was not significantly diffe

28 The beta-adrenergic agonist isoprenaline (10 microM) also activated a glibenclamide-

29 Basolateral application of isoprenaline (10 microM) did not affect ISC in cells mai

30 We studied the contractile response to isoprenaline (10 nm) in isolated hearts and isolated car

31 th control (21.6 +/- 1.5 ms) and faster with isoprenaline (14.5 +/- 0.9 ms), but in all cases was muc

32 ly inhibited by noradrenaline (10 microM) or isoprenaline (2-5 microM), and completely prevented by 8

33 current clamp, beta-adrenergic stimulation (isoprenaline, 30 nm) increased both the Ca2+ transient a

34 nM) was not changed by TG (270 +/- 21 nM) or isoprenaline (302 +/- 10 nM).

35 o stimulated by shrinkage and isoproteronol (isoprenaline, 5 microgr;M).

36 a-AR stimulation (intravenous isoproterenol (isoprenaline): 6, 12 and 24 ng (kg fat-free mass)-1 min-

37 O-methyl-cAMP, an Epac-selective agonist, or isoprenaline, a non-selective beta-adrenergic receptor a

38 a-adrenergic stimulation with isoproterenol (isoprenaline) accelerated spark amplitude recovery and d

39 a-adrenergic stimulation with isoproterenol (isoprenaline) accelerated spark amplitude recovery and d

40 Isoprenaline also promoted translocation of NDPK-C to th

41 nities were 10-fold lower in the presence of isoprenaline and adrenaline than when salbutamol or terb

42 Isoprenaline and adrenaline were more efficacious in fun

43 cked the inhibitory response to forskolin or isoprenaline and all cells responded with a monophasic s

44 Agonist responses to isoprenaline and CGP 12177 had different sensitivities t

45 o discriminate between responses elicited by isoprenaline and CGP 12177.

46 tiple washout experiments, cAMP responses to isoprenaline and formoterol waned with increasing number

47 bular salivary gland (adrenaline, carbachol, isoprenaline and forskolin) mobilized Ca2+ from internal

48 ed ducts showed that all agonists, including isoprenaline and forskolin, mobilized Ca2+ exclusively f

49 ncreased by beta-adrenergic stimulation with isoprenaline and increased in a saturating manner with i

50 In the presence of isoprenaline and nifedipine, the amplitude of the Ca2+ t

51 .08, n = 22, and -9.68 +/- 0.07, n = 17, for isoprenaline and salbutamol-induced responses, respectiv

52 3) bound to the full agonists carmoterol and isoprenaline and the partial agonists salbutamol and dob

53 ker, was markedly reduced in the presence of isoprenaline and the region of negative slope was absent

54 in response to the beta-adrenoceptor agonist isoprenaline and to 8-bromo-cAMP, an analogue of cAMP, t

55 ent on myocardial sensitivity to adrenergic (isoprenaline) and muscarinic cholinergic (carbachol) sti

56 ine, bradykinin, substance P, isoproterenol (isoprenaline) and sodium nitroprusside were measured by

57 urrent amplitude was increased 47 +/- 12% by isoprenaline, and 73 +/- 13% by forskolin.

58 Both the isoprenaline- and forskolin-induced increases in IKr wer

59 Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or exposure to hypoxia/reo

60 The effect of isoprenaline became persistent if cells were pretreated

61 e the nonselective beta-adrenoceptor agonist isoprenaline, behaved as a potent, full agonist at beta

62 ectively, and 34% of the maximal response of isoprenaline (beta1)).

63 Isoproterenol (isoprenaline; betaAR agonist) dilated 1A, 2A and 3A near

64 ly reduced in hypertrophic hearts induced by isoprenaline but not in those induced by swimming exerci

65 Ih was potentiated by both noradrenaline and isoprenaline by a mechanism consistent with a shift in t

66 ked only 81 +/- 5% of IKr in the presence of isoprenaline compared to 100 +/- 0% in control.

67 Isoprenaline decreased left ventricular end-systolic vol

68 nergic stimulation with 1 muM isoproterenol (isoprenaline)) decreased the latency period and increase

69 However, isoprenaline did elicit cAMP accumulation in these cells

70 Further experiments showed that isoprenaline did increase I(SC) in cells treated (24 h)

71 ly, the FBF response to incremental doses of isoprenaline did not differ between genotype groups befo

72 Paradoxically, it is often stated that isoprenaline does not activate IK,ACh.

73 In NGF tissue, isoprenaline elicited a significantly smaller response t

74 tor (betaAR) agonists such as isoproterenol (isoprenaline), even though both stimulate the same signa

75 embrane's Na(+) conductance (G(Na)), whereas isoprenaline-evoked changes in apical Cl(-) conductance

76 ed that these hormones are essential for the isoprenaline-evoked increase in the apical membrane's Na

77 current was increased by the application of isoprenaline (expected to increase the underlying Ca2+ t

78 Irrespective of P(O2), isoprenaline failed to elicit a discernible change in I(

79 10 mM or addition of 3 microM isoproterenol (isoprenaline) failed to normalize the frequency of spont

80 e beta-AR-coupled adenylyl cyclase system to isoprenaline, Gpp(NH)p and forskolin was studied by meas

81 Maximum doses of either carbachol or isoprenaline had no effect on coronary perfusate distrib

82 Isoprenaline had no effect on dialysate lactate, which w

83 Isoprenaline had no effect on Na+ pump capacity at PO2 l

84 Pre-treatment with isoprenaline in vitro increased MF-LTP by 125% (P<0.001)

85 2+) release +/- 1 microm isoproterenol (ISO; isoprenaline) in voltage-clamped ventricular myocytes of

86 Isoprenaline increased ICl,ATP pre-activated by ATPgamma

87 olutions with weak Ca2+i buffering, however, isoprenaline increased net macroscopic Cl- currents.

88 Likewise, isoprenaline increased stroke work in control hearts (14

89 isometric contractions during SR inhibition, isoprenaline increased the force but did not alter the t

90 Isoprenaline increased the integral of the subsequent ri

91 Similarly, isoprenaline increased the spontaneous firing frequency

92 ith the beta-receptor agonist isoproterenol (isoprenaline) increased RyR1 PKA phosphorylation, twitch

93 However, isoprenaline induced a similar rise in intracellular Ca(

94 In contrast, introduction of 100 nM isoprenaline induced arrhythmogenicity in both KCNE1-/-

95 Impaired acetylcholine- (P < 0.01) and isoprenaline-induced (P < 0.05) vasodilatation in isolat

96 cAMP levels and sensitized cardiomyocytes to isoprenaline-induced augmentation of contractility, wher

97 Adenoviral infection unmasked a 1 microM isoprenaline-induced IK,ACh which was prevented by propr

98 tal to adenylyl cyclase were not involved in isoprenaline-induced IK,ACh.

99 The isoprenaline-induced increase in ICa was significantly s

100 selective PKA inhibitor KT5720 prevented the isoprenaline-induced increase in IKr only when the incre

101 The forskolin- and isoprenaline-induced increases in IKr were inhibited by

102 onal responses to incremental isoproterenol (isoprenaline) infusion (2, 4 and 6 microg kg min-1) were

103 ally with 5.4 mM K+o, noradrenaline (NA) and isoprenaline (Iso) (1-50 microM) stimulated Ip by 40-45%

104 enoreceptor (beta1-AR) by the catecholamines isoprenaline (Iso) and adrenaline (Adr) is regulated by

105 ic infusion of the nonselective beta-agonist isoprenaline (ISO) and compared this with cold-activated

106 nses to the beta-adrenergic receptor agonist isoprenaline (Iso) in CA1 pyramidal cells, suggesting th

107 beta-AR stimulation with isoprenaline (ISO) increased Ca2+ transient amplitude, I

108 as used to study effects of the beta agonist isoprenaline (Iso) on the current-voltage (I-V) relation

109 oncentrations of the cAMP-producing agonists isoprenaline (Iso) or histamine.

110 e slow afterhyperpolarization (sAHP) such as isoprenaline (ISO) or noradrenaline (NA) reduced the hyp

111 Isoprenaline (ISO) prolonged APDs and triggered EADs in

112 tivity of ICa to the beta-adrenergic agonist isoprenaline (Iso) was studied in both WT and NOS3-KO mo

113 nt stimulated by the beta-adrenergic agonist isoprenaline (Iso), and washout of ACh revealed a stimul

114 However, under isoprenaline (ISO), both the application of JNJ-303 and

115 the absence and presence of the beta-agonist isoprenaline (Iso).

116 ly stimulated by the beta-adrenergic agonist isoprenaline (Iso).

117 Isoproterenol (isoprenaline; ISO) increased the amplitude of the inward

118 ath application of 0.5 microM isoproterenol (isoprenaline; ISO) when measured using the whole-cell pa

119 oestrogen and weight loss to isoproterenol (isoprenaline; Iso)-induced Fos immunoreactivity (IR) and

120 f the beta-adrenergic agonist isoproterenol (isoprenaline; ISO).

121 Isoproterenol (isoprenaline; ISO; 0.01 microM), a non-selective beta-AR

122 thysmography) responses to administration of isoprenaline (isoproterenol) before and after NO inhibit

123 In vivo administration of isoprenaline (isoproterenol) predisposes I Ks channel tr

124 of beta-adrenergic receptors with 10 microM isoprenaline (isoproterenol, ISO) enhanced INa by 68.4 +

125 ted by activation of beta 1-adrenoceptors by isoprenaline (Kp = 1.6 microM), indicating that salmeter

126 ion with a zero chloride solution containing isoprenaline led to a significant change in potential di

127 h-clamp analysis demonstrated expression and isoprenaline-mediated regulation of I Ks in atrial myocy

128 hat persisted even in the presence of 100 nM isoprenaline (n = 6).

129 Isoprenaline occasionally activated IK,ACh in uninfected

130 The effects of forskolin or isoprenaline on I(Cl,swelling) were inhibited by intrace

131 kinase 1 (50 microM) prevented the effect of isoprenaline on IK,ACh.

132 gargin (2.5 mumol l-1) reduced the effect of isoprenaline on the amplitude of the Ca2+ transient.

133 TP pre-activated by ATPgammaS or PDBu, while isoprenaline or forskolin alone failed to activate any C

134 Activation of protein kinase A (PKA) by isoprenaline or forskolin caused an increase in IKr tail

135 with a cAMP-mediated agonist (isoproterenol (isoprenaline) or vasoactive intestinal peptide) in the p

136 on of the beta-receptor (with isoproterenol (isoprenaline)) or at the post-receptor level (with forsk

137 The inhibitory effect of AA on the isoprenaline- or cAMP-stimulated ICa,L is largely reduce

138 ventricular (LV) contractile function or on isoprenaline- or preload-induced increase in cardiac con

139 s in vitro to vasodilators acetylcholine and isoprenaline (P < 0.05).

140 e, RV developed pressure and HR responses to isoprenaline (P < 0.05).

141 n was achieved by 0.01 microm isoproterenol (isoprenaline) plus 0.1 microm ICI 118551, a selective be

142 ttached patch recording, bath application of isoprenaline produced a pronounced inhibition of SOC act

143 beta-Adrenoceptor stimulation (with 5 microM isoprenaline) produced marked increases in net work, pow

144 We show that the adrenergic agonist isoprenaline promotes receptor and G protein activation

145 Isoprenaline rapidly stimulated cardiac CCK gene express

146 ding the selective beta-adrenoceptor agonist isoprenaline reduced the current evoked by cyclopiazonic

147 a-Adrenergic stimulation with isoproterenol (isoprenaline) reversed electromechanical alternans, sugg

148 This may explain the enhanced sensitivity to isoprenaline seen under these slightly hyperoxic conditi

149 Isoprenaline sensitivity was blocked by hyperpolarizatio

150 Within a minute, full agonists (e.g., isoprenaline) stimulated large increases in intracellula

151 olute magnitude, of basal and isoproterenol (isoprenaline)-stimulated Ca2+ current (ICa) was decrease

152 c acid (MA), had no inhibitory effect on the isoprenaline-stimulated Ca2+ current, whereas, in the sa

153 Isoprenaline-stimulated difference currents were not out

154 ynoic acid (ETYA), was without effect on the isoprenaline-stimulated ICa,L.

155 e of contraction and a higher sensitivity to isoprenaline-stimulated inotropy compared with control s

156 utant, termed beta2AR(SSS), showed increased isoprenaline-stimulated phosphorylation and differences

157 end-stage human HF, in rats after long-term isoprenaline stimulation through osmotic minipumps, and

158 cerbated cardiac remodeling during long-term isoprenaline stimulation.

159 ratio) when subjected to increasing doses of isoprenaline stress under baseline and pressure-overload

160 or displayed higher affinity for the agonist isoprenaline than the wild-type receptor but not for the

161 In the presence of isoprenaline, the amplitude of both ICa and the Ca2+ tra

162 containing 5 mM Ca2+-1 microM isoproterenol (isoprenaline) they produced Ca2+ sparks spontaneously.

163 ic pressure-volume relation was increased by isoprenaline to a greater extent in control than transge

164 the unused donor group were desensitized to isoprenaline to a similar degree as those from the faili

165 .v.) and shifted the dose-response curve for isoprenaline to higher agonist concentrations without al

166 However, the positive inotropic response to isoprenaline was also blunted in ssTnI hearts.

167 The effect of isoprenaline was blocked by the antagonist propranolol.

168 line (ACh) and the beta-adrenoceptor agonist isoprenaline was decreased in the PR group, while there

169 the hearts of the NGF mice, the response to isoprenaline was diminished, and this was due to an unco

170 any given cell, the response to forskolin or isoprenaline was qualitatively similar suggesting that a

171 As expected, the lusitropic effect of isoprenaline was significantly blunted in ssTnI hearts.

172 nditioning pulse duration in the presence of isoprenaline was used to reduce the amplitude of the Ca2

173 by the finding that IKr, in the presence of isoprenaline, was somewhat less sensitive to block.

174 of the PKA pathway activator isoproterenol (isoprenaline) were unchanged compared to I-1((-/-)) aort

175 atheter for forearm vasodilator responses to isoprenaline with plethysmography.

176 l cardiomyocytes responded to isoproterenol (isoprenaline) with a decrease in cell size, mature cardi

177 51 substantially reduced the HVC response to isoprenaline without affecting HR responses.