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1 0.9 versus 1.6 +/- 0.5 mmHg with intravenous ouabain).
2 /K(+) -ATPase (l-NMMA + ketorolac + BaCl2 + ouabain).
3 ) channels and Na(+) /K(+) -ATPase (BaCl2 + ouabain).
4 before or after administration of BaCl2 plus ouabain.
5 ively inhibiting alpha2 enzyme activity with ouabain.
6 e measured with and without NKA inhibited by ouabain.
7 ensitive to the Na+/K+-ATPase pump inhibitor ouabain.
8 of Na/K-ATPase, like the pumping pump, binds ouabain.
9 umps were silenced by continuous exposure to ouabain.
10 /K pump and the site of its interaction with ouabain.
11 ent arteriole to contract in the presence of ouabain.
12 n ADPKD cells exhibits a higher affinity for ouabain.
13 ked by a saturating concentration of dihydro-ouabain.
14 nal Na+/K+-ATPases induced by the binding of ouabain.
15 ibition of FGF2 secretion in the presence of ouabain.
16 of action potential fall in the presence of ouabain.
17 zation of the pump or affect the response to ouabain.
18 TPase with subtoxic doses of gramicidin A or ouabain.
19 by comparison with digoxin, digoxigenin, or ouabain.
20 c; and L-NMMA plus ketorolac plus BaCl2 plus ouabain.
21 podocyte primary cell cultures with low-dose ouabain.
22 s of these experiments showed that 20 microM ouabain, 0.3 microM ionomycin, or their combination incr
26 urve) was attenuated by BaCl2 (-61+/-3%) and ouabain (-44+/-12%) alone, and this effect was enhanced
27 unction of Na(+),K(+)-ATPase is activated by ouabain, a mammalian steroid hormone, at far lower conce
31 bition of the NKA alpha2 isoform by low dose ouabain abolished the ability of low Ko to reduce NKA cu
34 two mutants caused significant inhibition of ouabain-activated signal transduction and cell growth.
36 ptor function as evidenced by the failure of ouabain administration to induce the activation of Src a
38 loop, known to make a major contribution to ouabain affinity, strongly influenced conductance of sin
39 d astrocytes express Na(+) pumps with a high-ouabain-affinity catalytic subunit (alpha3 and alpha2, r
40 brain as a result of its actions on the high-ouabain-affinity Na(+) pumps in both neurones and astroc
41 Treatment of hTMC with sodium fluoride or ouabain, agents shown to cause morphological changes to
46 ns, resulting from intravitreal injection of ouabain, also exhibited increased TNFalpha expression th
48 ibitor of cytochrome-P450 enzymes or dihydro-ouabain, an inhibitor of Na+,K+-ATPase blocked the effec
50 onensin, a Na(+) ionophore, with and without ouabain, an NKA inhibitor, in suspensions of human eryth
51 vity to the electrolyte transport inhibitors ouabain and bumetanide, as well as bath Cl(-) and HCO(3)
54 veral cardiotonic steroids (CTSs), including ouabain and digoxin, increased RGS2 but not RGS4 protein
55 extracellular K(+) did not reduce p53 as did ouabain and digoxin, it did potentiate both digoxin- and
57 mally sensitive to the Na+/K+ pump inhibitor ouabain and exhibited age-dependent changes, including d
59 ies, we used the Na(+)/K(+) ATPase inhibitor ouabain and found conditions in which SD was always prev
66 demonstrated by reduction of the current by ouabain and the K(+) channel blockers Ba(2+), XE991, and
67 d by the beta-surface of the steroid core of ouabain and the side chains of alphaM1, alphaM2, and alp
68 e, or combined NO, PGs, Na(+) /K(+) -ATPase (ouabain) and KIR channel inhibition (n = 6; Protocol 2).
69 were cardiac glycosides, including digoxin, ouabain, and proscillaridin A, which inhibited HIF-1alph
70 n carbonylation is reversed after removal of ouabain, and this reversibility is largely independent o
71 -interacting pool of Src and act as a potent ouabain antagonist in cultured cells: 1) pNaKtide, unlik
73 that intraperitoneal administration of anti-ouabain antibodies to pregnant mice resulted in a >80% d
74 Consistently, exposure of intact cells to ouabain apparently increased the distance between the Na
77 and ouabain-resistant mutation of the alpha2 ouabain binding site (alpha2(R/R) mice) confers resistan
78 he CTS binding pocket of [Mg]E2P allows deep ouabain binding with possible long-range interactions be
81 cardiotonic steroids, which act through the ouabain-binding site and are important in cardiovascular
86 triggered by a conformational change of the ouabain-bound Na(+)/K(+)-ATPase molecule or more general
88 T inhibitors and the Na+/K+-ATPase inhibitor ouabain, but not 5-HT2 and 5-HT1B/1D receptor inhibitors
89 ht: prolonged subcutaneous administration of ouabain, but not digoxin, induces hypertension, and digo
91 Taken together, these results suggest that ouabain can protect the kidney from the apoptotic effect
94 iotonic steroids, most notably the digitalis/ouabain class of compounds, which have been used for cen
95 g kinetics with the previously described E2P-ouabain complex to derive specific details and the gener
96 g(2+) is bound in site II of the digoxin and ouabain complexes, whereas both sites are occupied by K(
97 sh retina by intravitreal injection of a low ouabain concentration to rapidly damage the ganglion cel
99 of the sensitivity of the alpha2 isoform to ouabain, conferring ouabain sensitivity to alpha1 augmen
100 resistant mice were inhibited by intravenous ouabain (control stop-flow pressure = 9.7 +/- 0.9 versus
101 nse light and recovered for up to 8 weeks or ouabain-damaged retinas that recovered for up to 3 weeks
102 rate at detecting the inner nuclear layer in ouabain-damaged retinas, but accurately detected the und
104 ents, loop of Henle perfusion with 50 microM ouabain decreased TGF responses (control stop-flow press
108 ing various cardiac glycoside compounds like ouabain, digoxin, digitoxin, and gitoxin with their agly
109 eyes that were injected intracamerally with ouabain, disodium 4,4'-diisothiocyanatostilbene-2,2'-dis
111 Pre-incubation (0.5-10 min) with 1-10 nm ouabain (EC50 < 1 nm) augmented Glu- and CCh-evoked sign
112 tion and cell proliferation, suggesting that ouabain effect is mediated through the MEK-ERK pathway.
114 reased by inhibition of the Na(+)/K(+) pump (ouabain), ENaC (amiloride), CF transmembrane conductance
116 one another in both assays: For example, the ouabain-evoked (3 nm) increases in MT70 and neuronal Ca2
118 NaKtide may be used as a novel antagonist of ouabain for probing the physiological and pathological s
119 , a digoxigenin derivative that displaces 3H-ouabain from Na+, K+ -ATPase, and attenuates some forms
121 3 compounds in the cardiac glycoside family, ouabain, gitoxigenin, and digitoxin, that inhibit placen
125 related to the presence of plants containing ouabain in the geographic locations where both inversion
126 ated the involvement of maternal circulating ouabain in the regulation of fetal growth and organ deve
127 tubular cells, cardiotonic steroids such as ouabain in vitro signal through Na/K-ATPase, which resul
128 ut was evoked using dorsal-root stimulation, ouabain increased burst frequency and extended locomotor
132 aft model of retinoblastoma, the cardenolide ouabain induced complete tumor regression in the treated
134 cal inhibition of the Na(+)/K(+)-ATPase with ouabain induced neurite degeneration, which was attenuat
136 -K(+) ATPase antagonists (ouabain or dihydro-ouabain) induced either a membrane depolarization in cur
137 ly, both Src and caveolin-1 are required for ouabain-induced activation of Akt and up-regulation of N
142 fish alpha1a.1 or rat alpha1 mRNA, while the ouabain-induced defect was rescued by expression of ouab
143 kinase kinase (MEK) inhibitor U0126 blocked ouabain-induced ERK activation and cell proliferation, s
144 /mTOR pathway by rapamycin completely blocks ouabain-induced expression of Na/K-ATPase and converts o
145 duced expression of Na/K-ATPase and converts ouabain-induced growth stimulation to growth inhibition
146 Na(+)] was increased to 20 mm or more (using ouabain-induced inhibition of the Na(+),K(+)-ATPase or t
148 nlike previous studies in other systems, the ouabain-induced internalization was insensitive to Src o
155 pproximately 85% in both cell types, whereas ouabain inhibited K(+)-hyperpolarization differently in
158 ility of digoxin-like CTSs to reactivate the ouabain-inhibited complex can be explained by de-oligome
159 st to NHK cells, the dose-response curve for ouabain inhibition of Na,K-ATPase activity indicated tha
166 rgeted mouse (alpha2(R/R)) which expresses a ouabain-insensitive alpha2 isoform of the Na,K-ATPase to
173 nd Ser(16), respectively, the latter because ouabain itself increased Ser(16) phosphorylation; thus,
175 After the reduction in maternal circulating ouabain, kidney expression of cyclin D1 was reduced and
176 /K(+)-ATPase, NO, and prostaglandins (BaCl2, ouabain, L-NMMA [N(G)-monomethyl-L-arginine] and ketorol
177 ng human pregnancy, the circulating maternal ouabain level increased and the highest concentration of
182 n each group, the CTSs were synergistic, but ouabain-like and digoxin-like CTSs antagonized one anoth
183 hronic salt retention elevates an endogenous ouabain-like compound (EOLC) and induces salt-dependent
184 train has a 10-fold increase in hypothalamic ouabain-like compound that is linked to the pathogenesis
189 in a feed-forward mechanism of regulation of ouabain-mediated renal proximal tubule Na/K-ATPase signa
190 Bcl-xL, an inhibitor of Bax, suggesting that ouabain might protect renal cells from Stx2-triggered ap
191 w and high levels of the specific NKA ligand ouabain modulate the endocytosis and total expression of
192 Using a systematic approach, we applied ouabain (Na(+)/K(+)-ATPase inhibitor), bumetanide (Na(+)
197 enal parameters in rats and the influence of ouabain on podocyte proteins both "in vivo" and "in vitr
198 rolonged elevations of circulating exogenous ouabain on renal parameters in rats and the influence of
200 G and a similar Na(+)/K(+)-ATPase inhibitor, ouabain, on the phosphorylation status of Jnk, p38, and
201 perfusion of Na(+)-K(+) ATPase antagonists (ouabain or dihydro-ouabain) induced either a membrane de
204 lace-cell-train-induced AHPs were blocked by ouabain or removal of extracellular potassium, but not b
205 a1 and alpha3 isoforms of Na(+)/K(+)-ATPase, ouabain or strophanthidin, inhibited this Na(+) current.
207 hate-buffered saline (PBS, vehicle) or PBS + ouabain, or after intraperitoneal injection of sodium io
208 r calcium, but were blocked by tetrodotoxin, ouabain, or the removal of extracellular potassium.
218 ally, in the rat model, elevated circulating ouabain reduced creatinine clearance (-18%, p < 0.05), i
219 rat model of pregnancy-induced hypertension, ouabain reduced mean arterial pressure and enhanced plac
220 arities in the Atpalpha variants, conferring ouabain resistance in both arrangements, may be the resu
222 lpha1 isoform of mice and rats is relatively ouabain resistant, gene-targeting strategies were used t
224 eloped mice in which the naturally occurring ouabain-resistant alpha1 isoform was made ouabain-sensit
227 opus alpha1beta3 Na/K pumps, which were made ouabain-resistant by point mutation, after expressing th
228 nfusion induces hypertension in rodents, and ouabain-resistant mutation of the alpha2 ouabain binding
229 Na/K pumps from ventricular myocytes and in ouabain-resistant pumps expressed in Xenopus oocytes.
230 -induced defect was rescued by expression of ouabain-resistant zebrafish alpha1a.1 or rat alpha1 mRNA
231 lpha1 is ouabain-sensitive and NKA-alpha2 is ouabain-resistant, we assessed the effects of PLM phosph
232 IR channels and Na(+)/K(+)-ATPase (BaCl2 and ouabain, respectively), and combined inhibition of KIR c
233 low concentration of the cardiac glycoside, ouabain, resulted in a modest increase in intracellular
234 Furthermore, in vivo, administration of ouabain reversed the imbalance between Bax and Bcl-xL in
236 mitochondrial depolarization observed before ouabain-SD was abolished by L-type channel block, and Zn
238 ncreases were observed in CA1 neurons before ouabain-SD, and L-type channel block prevented the intra
242 diotonic steroids (CTSs) such as digoxin and ouabain selectively inhibit Na+, K+ -ATPase (the Na+ pum
245 fragment, the sodium excretion rates in the ouabain-sensitive alpha1 isoform mice were equivalent to
248 wild-type mice and mice where NKA-alpha1 is ouabain-sensitive and NKA-alpha2 is ouabain-resistant, w
250 sgenic mice also exhibited a 36% decrease in ouabain-sensitive sodium reabsorption and a significantl
251 pNBTEA concentration and V(M) dependence of ouabain-sensitive transient charge movements in whole-ce
252 ep changes in V(M) elicited pNBTEA-activated ouabain-sensitive transient currents that had similariti
253 ximately 60 s), activity-dependent, TTX- and ouabain-sensitive, hyperpolarization ( approximately 5 m
257 Currently, the basis for the differences in ouabain sensitivity of NHK and ADPKD cells is unknown.
258 by micropuncture in mutant mice with altered ouabain sensitivity of the alpha1 and alpha2 Na,K-ATPase
259 of the alpha2 isoform to ouabain, conferring ouabain sensitivity to alpha1 augmented the natriuretic
263 t was found that nanomolar concentrations of ouabain, similar to those circulating in blood, induced
266 he antioxidant N-acetyl-L-cysteine prevented ouabain-stimulated Na/K-ATPase.c-Src signaling, protein
272 mparison with the low-affinity [K2]E2-MgF(x)-ouabain structure shows that the CTS binding pocket of [
273 reveal that SSA78 binding is antagonized by ouabain, supporting the interaction of SSA78 at one of t
276 by bath application of low concentrations of ouabain that selectively inhibit NKAalpha3 while alpha-m
280 Src kinase and inhibit its activity, whereas ouabain, the specific Na,K-ATPase inhibitor, binds and s
282 nses of the alpha1 and/or alpha2 isoforms to ouabain to assess for altered natriuretic responses to a
286 a receptor for cardiotonic steroids, such as ouabain, to regulate cellular protein kinase cascades.
288 ) current was fully inhibited by basolateral ouabain treatment, suggesting that the Na(+),K(+)-ATPase
289 ression analysis, the circulating endogenous ouabain value before surgery was the strongest predictor
295 nergy transfer distances measured with bound ouabain, we carried out molecular dynamics simulations w
300 diac glycosides (CGs) digoxin, digitoxin and ouabain, which directly inhibit ATP1A1 function, exhibit
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