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1 um channel openers (KCO; e.g., diazoxide and pinacidil).
2 >100-fold less sensitive than WT vessels to pinacidil.
3 impaired lymphatic contractile responses to pinacidil.
4 ly sensitive to the K(ATP) channel activator pinacidil.
5 xide, whereas SUR2 channels are sensitive to pinacidil.
6 so by levcromakalim, and not depolarized by pinacidil.
7 elaxation induced by the KATP channel opener pinacidil.
8 nclamide, and responds to both diazoxide and pinacidil.
9 nsitive potassium (K(ATP)) channel activator pinacidil.
10 P current activated by the K+ channel opener pinacidil.
11 cker nisoldipine and the K(+) channel opener pinacidil.
12 s including high K(+), ACh, nitric oxide and pinacidil.
13 ually by 100 microM diazoxide and 100 microM pinacidil.
14 K+ ATP channel activation with intracoronary pinacidil (0.2-5.0 microgram/kg per min) increased flow
15 s control=25%, flunarizine=24% (P=0.44), and pinacidil=0.1% (P<0.001) and the percent of time stable
17 -fold by diazoxide (340 microM), 1.4-fold by pinacidil (1 mM) and unaffected by cromakalim (0.5 mM).
18 eplacement of the N-cyanoguanidine moiety of pinacidil (1, Figure 1) with a diaminocyclobutenedione t
20 In these cells, the potassium channel opener pinacidil (10 micromol/L) did not prevent Ca2+ loading (
21 cellular phenotype that, in the presence of pinacidil (10 micromol/L), expressed K+ current and gain
22 d ones, and the density of current evoked by pinacidil (100 microM), a K(ATP) channel opener, was sig
25 ardium but not endocardium after exposure to pinacidil (2 to 5 micromol/L), a K(+) channel opener, or
27 sus CHx+IPC; P:<0.01) but not the effects of pinacidil (27+/-2% versus 29+/-3%, PIN versus CHx+PIN; P
28 h the K(+)(ATP) channel openers diazoxide or pinacidil 48 h prior to lethal ischemia protected hippoc
29 In contrast, these inhibitors did not alter pinacidil (5 microM)-induced dilation in SUR2(+/+) arter
30 with either Krebs-Henseleit solution (K-H), pinacidil (50 micromol/L in K-H), or hyperkalemic St.
33 rcentage recovery of developed pressure with pinacidil (60.3%+/-3.1%) was not statistically different
35 infarcts was mapped during administration of pinacidil, a K(ATP) channel activator, directly into the
39 s, the K(ATP) channel agonists diazoxide and pinacidil activated channels, and both compounds inhibit
40 nhibition and RNAi knockdown showed that the pinacidil activated KATP channels trigger signaling thro
41 e still functional in 10 mm d-glucose, since pinacidil-activated ATP-dependent K(+) (K(ATP)) currents
42 al K(ATP) currents by over 85% after 2 days (pinacidil-activated current densities were: vector alone
45 ATP-sensitive potassium (KATP) activation (pinacidil) amplified the pulse-flow response 3-fold, alt
46 Ht31 reduced K(ATP) current activated by pinacidil and also prevented its inhibition by Rp-cAMPS,
47 (+) currents were augmented by minoxidil and pinacidil and attenuated by glibenclamide as well as tet
49 n rabbit ventricular myocytes, we found that pinacidil and diazoxide open mitoK(ATP) channels, but P-
51 ic rats were 5- to 15-fold less sensitive to pinacidil and levcromakalim than were control arteries (
52 than were control arteries (EC50 values for pinacidil and levcromakalim were 1.4 and 0.6 mumol/L, re
56 ronary arterioles to the KATP-channel opener pinacidil and to the endothelium-independent vasodilator
57 We studied the effects of 10 and 25 mumol/L pinacidil, and ATP-sensitive K channel opener that provi
59 nels were sensitive to azide, diazoxide, and pinacidil, and their single-channel burst duration was 2
60 tive effects of diazoxide were reproduced by pinacidil, another mitoK(ATP) agonist, and blocked by th
61 tassium channel openers (PCOs) aprikalim and pinacidil are effective cardioplegic agents but exhibit
64 onal restoration was determined by recording pinacidil-based KATP current by whole cell voltage clamp
66 hannels are activated potently by 100 microM pinacidil but only weakly by 100 microM diazoxide; in ad
68 lphosphonium cation) and openers (diazoxide, pinacidil, chromakalim, minoxidil, testosterone) of the
69 [K+]e during ischemia, both before and after pinacidil, correlated with the time that the action pote
70 isolated cardiac mitochondria, diazoxide and pinacidil decreased the rate and magnitude of Ca2+ uptak
72 o not form functional cardiac KATP channels, pinacidil did not protect against hypoxia-reoxygenation.
73 e, 10(-4) M sodium nitroprusside or 10(-5) M pinacidil directly to capillaries initiated remote arter
74 , and KATP blocker profiling showed that the pinacidil DMR is due to the activation of SUR2/Kir6.2 KA
76 main peptide (SDP) also caused inhibition of pinacidil-evoked native whole-cell K(ATP) currents, indi
78 4.7% inhibition (mean +/- S.E.M.; n = 7) of pinacidil-evoked whole-cell KATP currents recorded in is
81 O2 was significantly (P<.05) elevated in the pinacidil group (0.77+/-0.12) compared with the St Thoma
82 l)-2-nitroethene-1,1-diamin e (Bay X 9228) > pinacidil > (-)-cromakalim > N-(4-benzoyl phenyl)-3,3,3-
83 exhibited a rank order of potency of P1075 > pinacidil > levcromakalim = BMS-180448 > nicorandil > di
85 channels preactivated by the channel opener pinacidil in rabbit ventricular myocytes, through reduci
86 2 channels were stimulated by cromakalim and pinacidil in the presence of ATP and Mg2+ but were insen
88 channel openers (minoxidil, cromakalim, and pinacidil) increased cellular DNA synthesis, whereas K(A
89 that treatment with the KATP channel agonist pinacidil increases survival of bees while decreasing vi
91 molecular mechanisms by which diazoxide and pinacidil induce vasodilation by studying diameter regul
95 with the DN Kir6.2 virus for 72 h suppressed pinacidil-inducible K(ATP) current density measured by w
101 ner (PCO)-induced hyperpolarized arrest with pinacidil minimizes cellular energy requirements during
102 sensitive to potassium channel opener drugs (pinacidil, minoxidil) in both chambers of the heart and
103 sensitive to potassium channel opener drugs (pinacidil, minoxidil) in both chambers of the heart and
104 was repeated with the K(ATP) channel opener pinacidil (n=6) and the calcium channel blocker flunariz
105 for ATP, measured by its ability to slow the pinacidil off-rate, was also approximately 20 times high
106 nitol abolished the effects of diazoxide and pinacidil on mitochondrial Ca2+, while the K+ ionophore
108 ned with the ATP-sensitive K current agonist pinacidil or I(Ca,L) blocker verapamil to maintain AP du
109 only at reperfusion, the K(+) channel opener pinacidil or the antioxidants 2-mercaptopropionylglycine
113 (to 10-15%) by the K(ATP) channel activator pinacidil (PIN) but were absent in Ca(v)3 DKO vessels.
114 mia/5 minutes of reperfusion, n=6) or PPC by pinacidil (PIN, 10 micromol/L; n=6), an ATP-sensitive po
115 ion of NO donors, exogenous H2O2 potentiated pinacidil-preactivated sarcKATP channel activity in inta
116 conjunction with the KATP channel activator pinacidil, prevented intracellular Ca2+ loading irrespec
118 levocromakalim (LCC), and to a lesser extent pinacidil, protect cultured rat hippocampal neurons agai
120 plegic arrest and preconditioning induced by pinacidil provided superior recovery of contractile func
121 nticipated lessening of the rise in [K+]e by pinacidil reflects the balance of its effects on these s
123 In the presence of MgATP, the response to pinacidil reversed approximately 14 times more slowly wi
124 In hearts with an initially excitable EBZ, pinacidil shortened the effective refractory period and
126 izing ATP-sensitive potassium channel opener pinacidil, the protein kinase C activator 4 beta-phorbol
130 ell phenotypic agonist profiling showed that pinacidil triggered characteristically similar dynamic m
135 A, did not affect KATP currents activated by pinacidil when the intracellular solution contained 0.1
136 he benzopyran, cromakalim, and the pyridine, pinacidil, whereas an SUR1 segment which includes TMD6-1
138 y the SUR2-specific K(ATP) channel activator pinacidil, which hyperpolarized both mouse and human lym