ライフサイエンスコーパス: potassium concentration

1 nscription induced by lowering extracellular potassium concentration.

2 ion for controlling blood pressure and serum potassium concentration.

3 ian manner with changes in the extracellular potassium concentration.

4 bsorbance and fluorescence) according to the potassium concentration.

5 rnstian manner with changes in extracellular potassium concentration.

6 of membrane potential and the extracellular potassium concentration.

7 ous infections leads to an increase in serum potassium concentration.

8 C is mediated by secondary changes in plasma potassium concentration.

9 rough repetitive elevations of extracellular potassium concentration.

10 assium transport, and unresponsive to plasma potassium concentration.

11 e cochlea, they promptly die due to the high potassium concentration.

12 anes, and (iii) a reduction in intracellular potassium concentration.

13 lar Ca(2+) and depended on the extracellular potassium concentration.

14 space, and an increase in the extracellular potassium concentration.

15 therapy was independent of the initial serum potassium concentration.

16 iety of medications that can alter the serum potassium concentration.

17 ructural heart disease and an abnormal serum potassium concentration.

18 of binding was demonstrated with increasing potassium concentrations.

19 ertension are now known to have normal serum potassium concentrations.

20 l non-haemolysed blood samples showed normal potassium concentrations.

21 sium induced by CA, Ucn2 cotreatment reduced potassium concentrations.

22 e for doing so effectively across a range of potassium concentrations.

23 The diarrheal fluid had a very high potassium concentration (130-170 mEq/L) and a very low s

24 Serum potassium concentration, 3-d food records, and 24-h urin

25 nts with diabetes had a slightly higher peak potassium concentration (5.14 +/- 0.45 mmol/L [CI, 4.93

26 (1.2 mg/dL) or more developed a higher peak potassium concentration (5.37 +/- 0.59 mmol/L [CI, 5.15

27 The elevated potassium concentration also depolarized the postsynapti

28 associated with an increase in extracellular potassium concentration and neuronal depolarization bloc

29 otassium buffering, increasing extracellular potassium concentration and overactivating the Na(+)-K(+

30 that KinC responds to lowered intracellular potassium concentration and that this is a quorum-sensin

31 (TBI) can be predicted by the extracellular potassium concentration and the change in energy homeost

32 Potassium concentration and transmembrane potential reco

33 e mechanisms by which DCT cells sense plasma potassium concentration and transmit the information to

34 atment and control groups had the same serum potassium concentrations and did not receive different a

35 iments performed under different calcium and potassium concentrations and in the presence of dextran

36 roximations, the transient solutions for the potassium concentrations and the corresponding membrane

37 which ictal activity was induced by elevated potassium concentrations and the fractional decrease in

38 population, there is no correlation between potassium concentrations and the occurrence of premature

39 hanism, inhibition was dependent on voltage, potassium concentration, and a histidine in the first P

40 duces no or only trivial reductions in serum potassium concentration, and because this therapy is unp

41 uch as mean predialysis serum phosphorus and potassium concentration, and behavioral compliance were

42 ll clinical scenario when choosing dialysate potassium concentrations, and an effective change in pra

43 changes in intracellular sodium or external potassium concentrations, and did not reflect a change i

44 imbalances, such as increased magnesium and potassium concentrations, and to cold shock, but increas

45 when extracellular sodium and intracellular potassium concentrations are within physiological ranges

46 lyte abnormalities, including abnormal serum potassium concentrations, are considered a correctable c

47 The increase in the extracellular potassium concentration associated with that wave leads

48 one, rats in the POL group had higher plasma potassium concentrations at 2 wk.

49 onse of the ECL intensity to the logarithmic potassium concentration between 10 mum and 10 mM was fou

50 Insulin administration lowers plasma potassium concentration by augmenting intracellular upta

51 the liver, that buffer the changes in plasma potassium concentration by means of transcellular potass

52 es are thought to regulate the extracellular potassium concentration by mechanisms involving both vol

53 ontrast, treatment with an elevated external potassium concentration caused only a moderate increase

54 None of the regimens reduced serum potassium concentrations, compared with baseline levels.

55 Mean serum potassium concentrations decreased from 4.9 mmol/L to 4.

56 of renal potassium conservation when plasma potassium concentration decreases.

57 The range of potassium concentrations detected by an RNA G-quadruplex

58 sed potassium intake in the HKD group, serum potassium concentrations did not significantly increase

59 y, the effects of an increased extracellular potassium concentration diffusing in space-that support

60 Changes in the sample potassium concentration directly modulate the potential

61 ith a stimulus-induced rise in extracellular potassium concentration during stimulation.

62 e at rat carotid bodies superfused with high potassium concentrations, during normoxic hypercapnia, a

63 The steady-state serum potassium concentration frequently changes during a card

64 eactions were slowed with an increase in the potassium concentration from 100 to 500 mM, via replacem

65 tamate inside the cell, raising the external potassium concentration generated an outward current att

66 A peak serum potassium concentration greater than 5.0 mmol/L develope

67 of patients; severe hyperkalemia (peak serum potassium concentration > or = 5.5 mmol/L) occurred in 2

68 may increase the risk of hyperkalemia (serum potassium concentration >5 mmol/L) in the setting of inc

69 s is mandated to avoid serious hyperkalemia (potassium concentration >5.5 mEq/L) and its attendant ri

70 tic, but the effect of such therapy on serum potassium concentration has not been established.

71 depolarized by ACh and by high extracellular potassium concentration (high K(+)).

72 ese fluctuations would abruptly alter plasma potassium concentration if not for rapid mechanisms, pri

73 ect of increasing dietary potassium on serum potassium concentration in hypertensive individuals with

74 In conclusion, each drug increases plasma potassium concentration in patients with GS.

75 critical for the buffering of extracellular potassium concentration in retina.

76 ave attempted to screen charge by increasing potassium concentration in single-channel experiments.

77 tion between PK and U was independent of the potassium concentration in the bolus over the range of 2

78 Increased potassium concentration in the cleft maintained the hair

79 The serum potassium concentration in the control group was 4.33 +/

80 , a process necessary to maintain an optimal potassium concentration in the extracellular environment

81 he graphite (used as starting material), the potassium concentration in the intercalation compound, a

82 sugar, pH, conductivity, calcium, sodium and potassium concentration in the juice were also evaluated

83 The serum potassium concentration in the treatment group (mean +/-

84 Low serum potassium concentrations in African Americans may contri

85 Whether interventions to increase serum potassium concentrations in African Americans might redu

86 Sodium and potassium concentrations in CSF were found higher in HS

87 uggest that the measurement of intracellular potassium concentrations in red blood cells (RBC-K) can

88 that the presence of abnormal extracellular potassium concentrations in tumors suppresses the immune

89 f the GTP-FtsZ polymers decreased with lower potassium concentration, in contrast with the increase i

90 Extracellular potassium concentration increased during the cortical sp

91 Serum potassium concentration increased from 3.0 mmol/L to 4.3

92 On placebo therapy, the average serum potassium concentration increased slightly (0.4 mEq/L) d

93 g tetrad formation inside the cell where the potassium concentration is higher.

94 ensor for measuring extracellular changes in potassium concentration is selectivity against the compe

95 potassium intake is sensed, even when plasma potassium concentration is still within the normal range

96 vity filter of KcsA as a function of ambient potassium concentration is studied with solid-state NMR.

97 l stage, but that depolarization by elevated potassium concentrations is without effect.

98 reversal potential was dependent on external potassium concentration; it was blocked by barium in the

99 ium (Kir) channels participate in regulating potassium concentration (K(+)) in the central nervous sy

100 e further enhanced by lowering extracellular potassium concentration ([K(+)](o)) from 5.4 to 3.6 mm.

101 is sensitive to changes in the extracellular potassium concentration ([K(+)](o)).

102 Blood potassium concentration ([K(+)]) influences the electroc

103 Elevation of the extracellular potassium concentration ([K(+)]e) impairs T cell recepto

104 fects of depolarizing rises in extracellular potassium concentration ([K+](o)) on synapses, we depola

105 ar and extracellular pH evoked extracellular potassium concentration ([K+]o were recorded.

106 together with measurements of extracellular potassium concentration ([K+]o) and a transmural ECG.

107 The effects of raising extracellular potassium concentration ([K+]o) from 3.0 to 5.3, 9.5 or

108 ts such as I(Kr) or I(Kl) when extracellular potassium concentration ([K+]o) is increased.

109 In slice preparations, external potassium concentration ([K+]o) is typically elevated fr

110 essed by moderate rises in the extracellular potassium concentration ([K+]o).

111 During neuronal activity, extracellular potassium concentration ([K+]out) becomes elevated and,

112 nductance was dependent on the extracellular potassium concentration ([K]o).

113 tracellular) and erythrocyte (intracellular) potassium concentrations ([K+]e and [K+]i) were determin

114 membrane depolarization induced by increased potassium concentration [K(+)] increased medium concentr

115 creases (0.5 to 2.0 mM) in the extracellular potassium concentration [K+]o.

116 s coincide with an increase in extracellular potassium concentrations [K(+)](e) yet little informatio

117 e is insensitive to changes in extracellular potassium concentration, [K+]o, because of the absence o

118 . Isolyte S 117 +/- 7 [p < .02]) and a lower potassium concentration (mEq/L: normal values 3.5 to 5.0

119 e exhibited less urinary flow, higher plasma potassium concentration, more fluid retention, and signi

120 e, mutant plants grew poorly on media with a potassium concentration of 100 micromolar or less.

121 r auditory hair cell function by maintaining potassium concentration of the scala media.

122 I) of incident diabetes for those with serum potassium concentrations of <4.0, 4.0-4.4, and 4.5-4.9 m

123 study, when clinically indicated, for serum potassium concentrations of 3.5 mmol/L or serum magnesiu

124 .5-4.9 mEq/L, compared with those with serum potassium concentrations of 5.0-5.5 mEq/L (referent), we

125 effect of light-evoked changes in subretinal potassium concentration on the transepithelial transport

126 the authors investigated the effects of high potassium concentrations on extracellular levels of gluc

127 with KGlu and was observed over an extended potassium concentration range.

128 cluding plasma urea, creatinine, sodium, and potassium concentrations) remained within normal ranges

129 rrent was not altered by changes in external potassium concentration, replacing external cations with

130 thermore, maintaining a normal intracellular potassium concentration represses the cell death process

131 nd 0.001 for SBP and aldosterone and urinary potassium concentrations, respectively).

132 Potassium concentrations showed larger increases in sens

133 were associated with a slight rise in serum potassium concentrations (similar to placebo); this may

134 Plasma potassium concentration strongly and negatively correlat

135 detection of both conformers at low ambient potassium concentration suggests that the high-K(+) and

136 panediol linkers and its lower dependency on potassium concentration suggests that this complex conta

137 esponds rapidly and reversibly to changes in potassium concentrations typical of whole blood samples.

138 The measured potassium concentration (uncorrected for fat fraction) o

139 Baseline plasma potassium concentration was 2.8+/-0.4 mmol/L and increas

140 the combination group; the highest recorded potassium concentration was 5.8 mmol/L in a patient in t

141 f GTP, became larger and polydisperse as the potassium concentration was decreased.

142 ine transport was also assessed after apical potassium concentration was lowered from 6.0 to 2.2 mM t

143 Interstitial potassium concentration was regulated by both K+-pump an

144 applications of forskolin, dopamine, or high-potassium concentration, we image an increase in cAMP le

145 Fecal potassium output and serum potassium concentration were measured for 12 h.

146 ldosterone, urinary aldosterone, and urinary potassium concentrations were also significantly higher

147 Serum bicarbonate and potassium concentrations were drawn every 6 hrs for 72 h

148 Mean serum potassium concentrations were lower in African Americans

149 al potential differences and transepithelial potassium concentrations were measured in anaesthetized

150 11), whereas changes in serum phosphorus and potassium concentrations were not different from the pla

151 d we review data linking serum and dialysate potassium concentrations with arrhythmias, cardiovascula

152 -h urinary potassium excretion [UKV; urinary potassium concentration x volume], the gold standard for