ライフサイエンスコーパス: pinacidil

1 um channel openers (KCO; e.g., diazoxide and pinacidil).

2 elaxation induced by the KATP channel opener pinacidil.

3 xide, whereas SUR2 channels are sensitive to pinacidil.

4 so by levcromakalim, and not depolarized by pinacidil.

5 nclamide, and responds to both diazoxide and pinacidil.

6 nsitive potassium (K(ATP)) channel activator pinacidil.

7 P current activated by the K+ channel opener pinacidil.

8 cker nisoldipine and the K(+) channel opener pinacidil.

9 s including high K(+), ACh, nitric oxide and pinacidil.

10 ually by 100 microM diazoxide and 100 microM pinacidil.

11 K+ ATP channel activation with intracoronary pinacidil (0.2-5.0 microgram/kg per min) increased flow

12 s control=25%, flunarizine=24% (P=0.44), and pinacidil=0.1% (P<0.001) and the percent of time stable

13 Pinacidil (1 microM) also activated an inwardly rectifyi

14 -fold by diazoxide (340 microM), 1.4-fold by pinacidil (1 mM) and unaffected by cromakalim (0.5 mM).

15 eplacement of the N-cyanoguanidine moiety of pinacidil (1, Figure 1) with a diaminocyclobutenedione t

16 Pinacidil 10 mumol/L had no effect in the rabbit and onl

17 In these cells, the potassium channel opener pinacidil (10 micromol/L) did not prevent Ca2+ loading (

18 cellular phenotype that, in the presence of pinacidil (10 micromol/L), expressed K+ current and gain

19 d ones, and the density of current evoked by pinacidil (100 microM), a K(ATP) channel opener, was sig

20 Responses to pinacidil (100 to 400 micromol/L), an opener of K(ATP) c

21 At a basic cycle length of 2000 ms, pinacidil (2 to 3 mumol/L) abbreviated the QT interval f

22 ardium but not endocardium after exposure to pinacidil (2 to 5 micromol/L), a K(+) channel opener, or

23 Pinacidil 25 mumol/L unexpectedly lessened the rise in [

24 sus CHx+IPC; P:<0.01) but not the effects of pinacidil (27+/-2% versus 29+/-3%, PIN versus CHx+PIN; P

25 h the K(+)(ATP) channel openers diazoxide or pinacidil 48 h prior to lethal ischemia protected hippoc

26 In contrast, these inhibitors did not alter pinacidil (5 microM)-induced dilation in SUR2(+/+) arter

27 with either Krebs-Henseleit solution (K-H), pinacidil (50 micromol/L in K-H), or hyperkalemic St.

28 probability (NP(o)) by 486 +/- 120% whereas pinacidil (500 microM) had no effect.

29 control=71%, flunarizine=48% (P<0.001), and pinacidil=56% (P<0.001).

30 rcentage recovery of developed pressure with pinacidil (60.3%+/-3.1%) was not statistically different

31 In both groups of rats, pinacidil (a cyanoguanidine K(ATP) agonist; 0.3 to 300 m

32 infarcts was mapped during administration of pinacidil, a K(ATP) channel activator, directly into the

33 Intrathecal injection of pinacidil, a KATP channel opener, significantly increase

34 pendent vasoconstriction that was relaxed by pinacidil, a selective K(ATP) channel opener.

35 vity was totally abolished by treatment with pinacidil, a specific opener of KATP channels.

36 s, the K(ATP) channel agonists diazoxide and pinacidil activated channels, and both compounds inhibit

37 nhibition and RNAi knockdown showed that the pinacidil activated KATP channels trigger signaling thro

38 e still functional in 10 mm d-glucose, since pinacidil-activated ATP-dependent K(+) (K(ATP)) currents

39 al K(ATP) currents by over 85% after 2 days (pinacidil-activated current densities were: vector alone

40 The kinetics of pinacidil amide formation by CYP3A4 yielded an apparent

41 followed by cleavage of the O-O bond to give pinacidil amide.

42 ATP-sensitive potassium (KATP) activation (pinacidil) amplified the pulse-flow response 3-fold, alt

43 Ht31 reduced K(ATP) current activated by pinacidil and also prevented its inhibition by Rp-cAMPS,

44 (+) currents were augmented by minoxidil and pinacidil and attenuated by glibenclamide as well as tet

45 ide, activated the NCCa-ATP channel, whereas pinacidil and cromakalin did not.

46 n rabbit ventricular myocytes, we found that pinacidil and diazoxide open mitoK(ATP) channels, but P-

47 KATP modulators (pinacidil and glibenclamide) or the specific Kir6.2-siRN

48 ic rats were 5- to 15-fold less sensitive to pinacidil and levcromakalim than were control arteries (

49 than were control arteries (EC50 values for pinacidil and levcromakalim were 1.4 and 0.6 mumol/L, re

50 ations to the synthetic KATP channel openers pinacidil and levcromakalim.

51 In the absence of nucleotide, pinacidil and P1075 activated Kir6.2/SUR2B and Kir6.2/SU

52 t for K(ATP)-channel openers (KCOs), such as pinacidil and P1075.

53 ronary arterioles to the KATP-channel opener pinacidil and to the endothelium-independent vasodilator

54 We studied the effects of 10 and 25 mumol/L pinacidil, and ATP-sensitive K channel opener that provi

55 KCl (5 to 20 mmol/L), bradykinin, adenosine, pinacidil, and sodium nitroprusside.

56 nels were sensitive to azide, diazoxide, and pinacidil, and their single-channel burst duration was 2

57 tive effects of diazoxide were reproduced by pinacidil, another mitoK(ATP) agonist, and blocked by th

58 tassium channel openers (PCOs) aprikalim and pinacidil are effective cardioplegic agents but exhibit

59 ene expression of selected M1 markers, while pinacidil augmented M1 markers.

60 onal restoration was determined by recording pinacidil-based KATP current by whole cell voltage clamp

61 Moreover, pinacidil, bradykinin, methacholine, and morphine failed

62 hannels are activated potently by 100 microM pinacidil but only weakly by 100 microM diazoxide; in ad

63 Pinacidil caused loss of action potential dome in male,

64 lphosphonium cation) and openers (diazoxide, pinacidil, chromakalim, minoxidil, testosterone) of the

65 [K+]e during ischemia, both before and after pinacidil, correlated with the time that the action pote

66 isolated cardiac mitochondria, diazoxide and pinacidil decreased the rate and magnitude of Ca2+ uptak

67 Hearts treated with pinacidil demonstrated a rapid recovery of a coordinated

68 o not form functional cardiac KATP channels, pinacidil did not protect against hypoxia-reoxygenation.

69 e, 10(-4) M sodium nitroprusside or 10(-5) M pinacidil directly to capillaries initiated remote arter

70 , and KATP blocker profiling showed that the pinacidil DMR is due to the activation of SUR2/Kir6.2 KA

71 Terfenadine, verapamil, and pinacidil each induced all-or-none repolarization at som

72 main peptide (SDP) also caused inhibition of pinacidil-evoked native whole-cell K(ATP) currents, indi

73 Pinacidil-evoked recombinant whole-cell Kir6.1/SUR2B cur

74 4.7% inhibition (mean +/- S.E.M.; n = 7) of pinacidil-evoked whole-cell KATP currents recorded in is

75 Pinacidil failed to activate current and the inward curr

76 uced by azide) plus a KCO (diazoxide for T1, pinacidil for T2).

77 O2 was significantly (P<.05) elevated in the pinacidil group (0.77+/-0.12) compared with the St Thoma

78 l)-2-nitroethene-1,1-diamin e (Bay X 9228) > pinacidil > (-)-cromakalim > N-(4-benzoyl phenyl)-3,3,3-

79 exhibited a rank order of potency of P1075 > pinacidil > levcromakalim = BMS-180448 > nicorandil > di

80 perpolarization and enhanced the response to pinacidil in arteries from diabetic animals.

81 channels preactivated by the channel opener pinacidil in rabbit ventricular myocytes, through reduci

82 2 channels were stimulated by cromakalim and pinacidil in the presence of ATP and Mg2+ but were insen

83 Diazoxide and pinacidil, in a concentration-dependent manner, also act

84 channel openers (minoxidil, cromakalim, and pinacidil) increased cellular DNA synthesis, whereas K(A

85 that treatment with the KATP channel agonist pinacidil increases survival of bees while decreasing vi

86 The response to pinacidil indicates that K(ATP) channels in the EBZ rema

87 molecular mechanisms by which diazoxide and pinacidil induce vasodilation by studying diameter regul

88 In summary, data indicate that pinacidil-induced vasodilation requires SUR2B, whereas d

89 In SUR2(-/-) arteries, pinacidil-induced vasodilation was 10% of that in SUR2(+

90 Atpenin also attenuated diazoxide-, but not pinacidil-induced vasodilation.

91 with the DN Kir6.2 virus for 72 h suppressed pinacidil-inducible K(ATP) current density measured by w

92 Although pinacidil is a nonselective activator of expressed sK(AT

93 Some rats were pretreated with pinacidil (K+(ATP)channel opener), bradykinin, methachol

94 Glibenclamide (KATP blocker) and pinacidil (KATP opener) treatment not only affect macrop

95 mm extracellular glucose) but insensitive to pinacidil (< or =500 microM).

96 atment also increased the phorbol ester- and pinacidil-mediated early preconditioning effect.

97 ner (PCO)-induced hyperpolarized arrest with pinacidil minimizes cellular energy requirements during

98 was repeated with the K(ATP) channel opener pinacidil (n=6) and the calcium channel blocker flunariz

99 for ATP, measured by its ability to slow the pinacidil off-rate, was also approximately 20 times high

100 nitol abolished the effects of diazoxide and pinacidil on mitochondrial Ca2+, while the K+ ionophore

101 activation increases the I(KATP) Induced by pinacidil or by MI.

102 ned with the ATP-sensitive K current agonist pinacidil or I(Ca,L) blocker verapamil to maintain AP du

103 only at reperfusion, the K(+) channel opener pinacidil or the antioxidants 2-mercaptopropionylglycine

104 ATP-sensitive K+ channel openers cromakalim, pinacidil, or diazoxide.

105 to KCl and bradykinin but not to adenosine, pinacidil, or nitroprusside.

106 mia/5 minutes of reperfusion, n=6) or PPC by pinacidil (PIN, 10 micromol/L; n=6), an ATP-sensitive po

107 ion of NO donors, exogenous H2O2 potentiated pinacidil-preactivated sarcKATP channel activity in inta

108 conjunction with the KATP channel activator pinacidil, prevented intracellular Ca2+ loading irrespec

109 Unlike DZX, pinacidil promoted ischemia-mediated arrhythmias in both

110 levocromakalim (LCC), and to a lesser extent pinacidil, protect cultured rat hippocampal neurons agai

111 Pinacidil provided superior protection versus K-H (44.4%

112 plegic arrest and preconditioning induced by pinacidil provided superior recovery of contractile func

113 nticipated lessening of the rise in [K+]e by pinacidil reflects the balance of its effects on these s

114 Pinacidil restored conduction and excitability when the

115 In the presence of MgATP, the response to pinacidil reversed approximately 14 times more slowly wi

116 In hearts with an initially excitable EBZ, pinacidil shortened the effective refractory period and

117 Following channel activation by pinacidil, the catalytic fragment of PKC inhibited the K

118 izing ATP-sensitive potassium channel opener pinacidil, the protein kinase C activator 4 beta-phorbol

119 adine or verapamil to inhibit INa and ICa or pinacidil to activate IK-ATP.

120 ble for the conversion of the cyano group of pinacidil to the corresponding amide.

121 Cell shortening was enhanced in pinacidil-treated myocytes, but depressed in verapamil-t

122 ell phenotypic agonist profiling showed that pinacidil triggered characteristically similar dynamic m

123 l versus beta-cell channels to cromakalim or pinacidil versus diazoxide.

124 In all stages of injury, the effect of pinacidil was inhibited by the selective antagonist of K

125 The effects of pinacidil were completely reversed by glybenclamide (10

126 A, did not affect KATP currents activated by pinacidil when the intracellular solution contained 0.1

127 he benzopyran, cromakalim, and the pyridine, pinacidil, whereas an SUR1 segment which includes TMD6-1

128 >60%, but did not alter dilations induced by pinacidil, which did not elevate ROS.

129 blocker, glibenclamide, and was mimicked by pinacidil, which is a K(ATP) channel opener.

130 Incubation of pinacidil with CYP3A4 in the presence of (18)O(2) or H(2

131 Incubations of pinacidil with recombinant CYP enzymes confirm that CYP3