ライフサイエンスコーパス: natriuretic

1 ic acid, which has both vasoconstrictive and natriuretic actions.

2 ested the hypothesis that attenuation of the natriuretic effect of dopamine D1-like receptors during

3 tion of enalapril to fenoldopam restored the natriuretic effect of fenoldopam and its inhibitory effe

4 al tubule sodium transport, neutralizing the natriuretic effect of fenoldopam.

5 more important are the osmotic diuretic and natriuretic effects contributing to plasma volume contra

6 accumulation of the endocytic tracer atrial natriuretic factor-red fluorescent protein at early stag

7 Atrial natriuretic factor-VEGF-B167 expression was low in norma

8 rrespondent renal water reabsorption, limits natriuretic osmotic diuresis, and results in concurrent

9 ysteine <10 micromol/L, N-terminal pro-brain natriuretic peptide <100 pg/mL, no microalbuminuria, no

10 dy), high-sensitivity troponin I, and B-type natriuretic peptide ( Table 1 ).

11 nin T (0.05 ng/ml) and N-terminal pro-B-type natriuretic peptide (3,000 pg/ml).

12 f reduced survival were elevated serum brain natriuretic peptide (482 +/- 337 pg/mL) and uric acid (8

13 ; P = 0.001), and serum N-terminal pro-brain natriuretic peptide (647 +/- 1,127 pg/ml vs. 1,578 +/- 2

14 e cardiac natriuretic peptides (NPs), atrial natriuretic peptide (ANP) and B-type natriuretic peptide

15 1-regulated cardioprotective peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide

16 Cardiomyocytes secrete atrial natriuretic peptide (ANP) and B-type natriuretic peptide

17 Atrial natriuretic peptide (ANP) has a central role in regulati

18 Atrial natriuretic peptide (ANP) influences glucose homeostasis

19 Multivariable regression revealed that brain natriuretic peptide (beta=-0.250; P<0.001) and receptor

20 e determined whether plasma levels of B-type natriuretic peptide (BNP) and cardiac troponin I are ass

21 of activated T cells -c3 (NFATc3), and brain natriuretic peptide (BNP) compared to controls.

22 atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in heart tissue may also contr

23 atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in response to mechanical stre

24 B-type natriuretic peptide (BNP) is a guanylyl cyclase A (GC-A)

25 at risk" for HFpEF given elevated brain-type natriuretic peptide (BNP) level; 160 had HFpEF by docume

26 Studies suggesting that B-type natriuretic peptide (BNP) may predict outcomes of mitral

27 Brain natriuretic peptide (BNP) serum concentration has been s

28 odium calcium exchanger (Ncx1) and the brain natriuretic peptide (Bnp) whose hypertrophic upregulatio

29 Circulating RBP4, TTR, B-type natriuretic peptide (BNP), and troponin I (TnI) concentr

30 atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), have central roles in sodium

31 eft ventricular ejection fraction and b-type natriuretic peptide (BNP).

32 rtality in addition to N-terminal pro-B-type natriuretic peptide (C-statistic: 0.59 versus 0.63) and

33 ivating mutations in the receptor for C-type natriuretic peptide (CNP), guanylyl cyclase B (GC-B, als

34 andidate therapy employs an analog of C-type natriuretic peptide (CNP), which antagonizes the mitogen

35 left atrium dimension, E/e', and pro B-type natriuretic peptide (hazard ratio, 1.05; 95% confidence

36 p = 0.040), as well as N-terminal pro-brain natriuretic peptide (hazard ratio: 1.655; p < 0.001) and

37 g as that obtained for N-terminal pro-B-type natriuretic peptide (multivariable HR for a 1-SD higher

38 s the increased cardiac expression of atrial natriuretic peptide (NP) and B-type NP, with their plasm

39 ion between the renal sympathetic nerves and natriuretic peptide (NP) metabolism.

40 e association between achieving predischarge natriuretic peptide (NP) thresholds and mortality and re

41 e association between achieving predischarge natriuretic peptide (NP) thresholds and mortality and re

42 determinants of plasma N-terminal proatrial natriuretic peptide (NT-proANP) in the general community

43 N-terminal pro-brain natriuretic peptide (NT-proBNP) and high-sensitivity car

44 ether the N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) and high-sensitivity tro

45 Hokusai-VTE study used N-terminal pro-brain natriuretic peptide (NT-proBNP) and right to left ventri

46 Combining abnormal N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin T with live

47 Increased N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentration predicts p

48 N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a strong predictor of

49 whether a reduction in N-terminal pro-B-type natriuretic peptide (NT-proBNP) is associated with impro

50 Serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) is considered a marker t

51 .001); and had higher N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels (P < .001), large

52 tone and usual care on N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels compared with usu

53 ST2 and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were measured in

54 walk distance, plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, and health statu

55 patients with elevated N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, reduces the inci

56 s associated with lower N-terminal pro-brain natriuretic peptide (NT-proBNP) levels.

57 n those with available N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels.

58 kers (such as N-terminal prohormone of brain natriuretic peptide (NT-proBNP)) and a measure of functi

59 ied the association of N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitive troponin

60 ortant biomarkers were N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity cardia

61 ercent change in serum N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity tropon

62 he association between N-terminal pro-B-type natriuretic peptide (NT-proBNP), which is a marker of he

63 termine whether an amino-terminal pro-B-type natriuretic peptide (NT-proBNP)-guided treatment strateg

64 distance, and levels of N-terminal pro-brain natriuretic peptide (NT-proBNP).

65 g-transformed level of N-terminal pro-B-type natriuretic peptide (NT-proBNP).

66 tional class, N-terminal prohormone of brain natriuretic peptide (NT-proBNP)concentrations, Borg dysp

67 +/- 0.04, P = .01) and N-terminal pro-brain natriuretic peptide (NT-proBNP; 191 +/- 261 vs 33 +/- 33

68 mass index (p = 0.002), N-terminal pro-brain natriuretic peptide (p < 0.001), early mitral inflow vel

69 nd had higher levels of N-terminal pro-brain natriuretic peptide (p = 0.001) compared with less sympt

70 exercise capacity, and N-terminal pro-brain natriuretic peptide (P>0.30 for all).

71 rrelated with N-terminal prohormone of brain natriuretic peptide (P<0.001), 6-minute walk distance (P

72 tance [6MWD], N-terminal prohormone of brain natriuretic peptide [NT-proBNP] concentration, and WHO f

73 nins I and T, N-terminal prohormone of brain natriuretic peptide [NT-proBNP]) to predict baseline sus

74 (that is stage III with N-terminal pro-brain natriuretic peptide [NTproBNP] >8500 pg/mL) disease, VWF

75 e and soluble epoxide hydrolase, agonists of natriuretic peptide A and vasoactive intestinal peptide

76 C-type natriuretic peptide activation of guanylyl cyclase B (GC

77 centric left ventricular remodeling, greater natriuretic peptide activation, higher filling pressures

78 dest improvement over a model without B-type natriuretic peptide and ankle-brachial index (C statisti

79 s had echocardiograms and measures of B-type natriuretic peptide and C-reactive protein before the pr

80 V mass and DeltaLV mass, N-terminal probrain natriuretic peptide and change in N-terminal probrain na

81 signaling by extracellular peptides (C-type natriuretic peptide and EGF receptor ligands) maintain t

82 Circulating N-terminal pro-B-type natriuretic peptide and high-sensitivity cardiac troponi

83 sma concentrations of N- terminal pro-B-type natriuretic peptide and high-sensitivity cardiac troponi

84 age, biomarkers (N-terminal fragment B-type natriuretic peptide and high-sensitivity cardiac troponi

85 obustly associated with N-terminal pro-brain natriuretic peptide and incident HF or death.

86 on who underwent mitral valve surgery, brain natriuretic peptide and LV-GLS provided synergistic risk

87 To further investigate the local action of natriuretic peptide and p38 MAPK in podocytes, we genera

88 size) with concomitant N-terminal pro-brain natriuretic peptide and subsequent HF hospitalization or

89 Elevated brain natriuretic peptide and uric acid, decreased left ventri

90 of soluble ST2 and amino-terminal pro-B-type natriuretic peptide at 12 hours added value to CardShock

91 mRNA expression of the cardiac stress marker natriuretic peptide B is also observed in the right vent

92 mRNA expression of myosin heavy chain 7 and natriuretic peptide B is up-regulated in both ventricles

93 sus 40), higher median N-terminal pro-B-type natriuretic peptide concentration (403 versus 320 pg/mL;

94 o -0.8, p=0.0070), and N-terminal pro B-type natriuretic peptide concentration in plasma -970 pg/mL (

95 se without LVSD, plasma N-terminal pro-brain natriuretic peptide concentration was greater than 400 p

96 e effects of genetic variants on circulating natriuretic peptide concentrations and compared the impa

97 extensive adjustments, N-terminal pro-B-type natriuretic peptide concentrations predicted ICU or 90-d

98 Short-term mechanical circulatory support, natriuretic peptide decile, glomerular filtration rate,

99 urin measurements, and N-terminal pro-B-type natriuretic peptide did not improve patient classificati

100 in mice revealed that this unexpected atrial natriuretic peptide effect is brought about by spatial r

101 These results indicate that natriuretic peptide exerts a renoprotective effect via i

102 rotein kinase IIdelta phosphorylation, brain natriuretic peptide expression, and sustained capillariz

103 stolic dysfunction and had higher myocardial natriuretic peptide expression.

104 The concept of natriuretic peptide guidance has been extensively studie

105 When including B-type natriuretic peptide in the model, only a decreasing myoc

106 55 +/- 10%; p < 0.001; n = 259), and B-type natriuretic peptide increased (median [interquartile ran

107 In HF-CON, n-terminal pro-brain natriuretic peptide increased by 88 +/- 120 pg/mL during

108 Finally, we revealed that atrial natriuretic peptide increased phosphorylation of MAPK ph

109 proportional change in N-terminal pro-B-type natriuretic peptide level from baseline to 180 days.

110 ), a 10-year risk of CVD < 20%, and a B-type natriuretic peptide level greater than their gender-spec

111 [IQR, 19%-33%]; median N-terminal pro-B-type natriuretic peptide level of 2049 pg/mL [IQR, 1054-4235

112 blem list, inpatient loop diuretic, or brain natriuretic peptide level of 500 pg/mL or higher; (3) lo

113 igns and symptoms of congestion and elevated natriuretic peptide level requiring hospitalization or o

114 iastolic diameter; serum troponin level; and natriuretic peptide level) in each individual.

115 e HR for a 1-SD higher N-terminal pro-B-type natriuretic peptide level, 1.15; 95% CI, 1.04-1.26), int

116 troponin T level, log N-terminal pro-B-type natriuretic peptide level, fibroblast growth factor 23 l

117 Age, B-type natriuretic peptide level, renal dysfunction, 24-h AHI,

118 apy but fewer comorbidities and lower B-type natriuretic peptide level.

119 have evaluated adjusting HF therapy based on natriuretic peptide levels ("guided therapy") with incon

120 55-2.44), and abnormal N-terminal pro-B-type natriuretic peptide levels (defined as >400 pg/mL; odds

121 e rates in addition to an increase in B-type natriuretic peptide levels (P=0.01), C-reactive protein

122 N-terminal pro-B-type natriuretic peptide levels decreased similarly in both g

123 N-terminal prohormone brain natriuretic peptide levels did not increase significantl

124 roBNP levels of 1000 pg/mL or more or B-type natriuretic peptide levels of 250 pg/mL or more, regardl

125 Brain natriuretic peptide levels on admission were lower (medi

126 N-terminal pro-B-type natriuretic peptide levels were abnormal in 97.4% of the

127 N-Terminal pro-B type natriuretic peptide levels were below the level consider

128 aride binding protein, troponin T, and brain natriuretic peptide levels were measured.

129 In contrast, N-terminal pro-B-type natriuretic peptide levels were not associated with mort

130 h HFrEF (ejection fraction </=40%), elevated natriuretic peptide levels within the prior 30 days, and

131 uality of life, higher N-terminal pro-B-type natriuretic peptide levels, and a poorer prognosis.

132 nd right ventricular structure and function, natriuretic peptide levels, and incident HF.

133 In Cox Proportional Hazard analyses, B-type natriuretic peptide levels, C-reactive protein levels, a

134 ity of life, incidence of arrhythmias, brain natriuretic peptide levels, left ventricular ejection fr

135 lation and diuretic use, n-terminal probrain natriuretic peptide levels, renal dysfunction, neurohumo

136 0.0001), despite lower N-terminal pro-B-type natriuretic peptide levels.

137 d significantly higher N-terminal pro-B-type natriuretic peptide levels; in addition, early rise in N

138 3, NAC+NaHCO3, ischemic preconditioning, and natriuretic peptide may have nephroprotective effects, t

139 cardiography and plasma N-terminal pro-brain natriuretic peptide measurement and were followed for up

140 Although natriuretic peptide measurements are widely used in prac

141 Circulating natriuretic peptide measurements have been used extensiv

142 Natriuretic peptide measurements have clearly revolution

143 Interpretation of natriuretic peptide measurements will depend on many fac

144 he reduced fat oxidation and elevated atrial natriuretic peptide message of cardiac hypertrophy.

145 n of nitric oxide-CAPON signalling and brain natriuretic peptide on cGMP and cAMP regulation of cardi

146 Y708C, R776W, and G959A) bound (125)I-C-type natriuretic peptide on the surface of cells but failed t

147 Early changes in N-terminal pro-B-type natriuretic peptide or high-sensitivity cardiac troponin

148 , and an elevated circulating level of brain natriuretic peptide or N-terminal pro-brain natriuretic

149 egulating liver X receptor alpha through the natriuretic peptide pathway.

150 lobal longitudinal strain (LV-GLS) and brain natriuretic peptide provided incremental prognostic util

151 or soluble ST2 and amino-terminal pro-B-type natriuretic peptide provides early risk assessment beyon

152 ferentiation via the guanylate cyclase NPR2 (natriuretic peptide receptor 2) and not the G-protein-co

153 e G-protein-coupled clearance receptor NPR3 (natriuretic peptide receptor 3).

154 ing at a low concentration by binding to its natriuretic peptide receptor A (NPRA) receptor and, in t

155 of guanylyl cyclase B (GC-B), also known as natriuretic peptide receptor B or NPR2, stimulates long

156 ecorded in atrial myocytes from wild-type or natriuretic peptide receptor C knockout (NPR-C(-/-)) mic

157 The ratio of the signaling receptor, natriuretic peptide receptor type A, to the clearance re

158 Guanylyl cyclase-A (GC-A) signaling, a natriuretic peptide receptor, exerts renoprotective effe

159 rdiomyocyte death, and N-terminal pro B-type natriuretic peptide release; all are classical hallmarks

160 The atrial natriuretic peptide secreted by atrial myocytes is a maj

161 of soluble ST2 and amino-terminal pro-B-type natriuretic peptide showed excellent discrimination for

162 Increased activation of natriuretic peptide signaling was seen in white AT of HF

163 kinase-1alpha (PKG1alpha) transduces NO and natriuretic peptide signaling; therefore, PKG1alpha acti

164 tatin C, syndecan-4, and N terminal-probrain natriuretic peptide than HF patients (all p </= 0.01).

165 essure and in levels of N-terminal pro-brain natriuretic peptide than the placebo group.

166 of soluble ST2 and amino-terminal pro-B-type natriuretic peptide to clinical parameters for risk stra

167 ft ventricles revealed three specific genes [natriuretic peptide type A (Nppa), sarcolipin (Sln), and

168 rdiac stage III patients (amino-terminal pro-natriuretic peptide type B >8500 ng/L) had lower respons

169 volumes, scar size, and N-terminal pro-brain natriuretic peptide values comparing the 2 treatment gro

170 ntricular ejection fraction, and lower brain natriuretic peptide values on admission.

171 Elevated N-terminal pro-B-type natriuretic peptide was also associated with an increase

172 ddition, early rise in N-terminal pro-B-type natriuretic peptide was associated with a better outcome

173 -week-old animals, and the PCH marker atrial natriuretic peptide was not different in young versus ol

174 Median levels of brain natriuretic peptide were 550 pg/mL in patients with a BM

175 nction, end-systolic volume index and B-type natriuretic peptide were most strongly associated with S

176 itivity troponin T and midregional proatrial natriuretic peptide were prospectively analyzed in 109 p

177 d potential mediators, including BNP (B-type natriuretic peptide) and endothelin-1.

178 natriuretic peptides (N-terminal pro-B type natriuretic peptide) and rest/exercise echocardiography

179 in primary (change in N-terminal pro B-type natriuretic peptide) and secondary (change in left atria

180 ciated with NT-proBNP (N-terminal pro-B-type natriuretic peptide) concentration (0.57 on a log scale

181 Importantly, proBNP (pro-brain natriuretic peptide) increased at 12 months in 20 millio

182 CNP (C-type natriuretic peptide) inhibits myofibrogenesis and osteog

183 ceptors and NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) levels were important across all ou

184 g levels of NT-proBNP (N-terminal pro-B-type natriuretic peptide) than HF patients without AF.

185 RI, and log NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) were retained (chi(2), 62.2; P<0.00

186 -pro-arginine vasopressin, and MR-pro-atrial natriuretic peptide), alone or as a panel, could be usef

187 LA volume, NT-proBNP (N-terminal pro-B-type natriuretic peptide), or left ventricular E/e' (all P<0.

188 circulating NT-proBNP (N-terminal pro-B-type natriuretic peptide), TNF-alpha, IL-6, IL-12, IL-17, mal

189 The effect of NT-proBNP (N-terminal probrain natriuretic peptide)-guided therapy in patients with acu

190 g/mL) serum NT-proBNP (N-terminal pro-B-type natriuretic peptide).

191 >/= 500 ng/mL and amino-terminal pro-B-type natriuretic peptide, >/= 4,500 ng/L) had higher 30-day m

192 oid hormone, prolactin, N-terminal pro-brain natriuretic peptide, 25-hydroxyvitamin D) and 2 nonhormo

193 ination of standard CVD risk factors, B-type natriuretic peptide, and ankle-brachial index (model 6)

194 aditional risk factors, N-terminal pro-brain natriuretic peptide, and baseline hs-cTnT level.

195 ic peptide and change in N-terminal probrain natriuretic peptide, and body mass index (P<0.05 for eac

196 entrations of glucose, N-terminal pro-B type natriuretic peptide, and cystatin C.

197 on cardiac troponin I, N-terminal pro-B-type natriuretic peptide, and d-dimer levels at baseline.

198 Cardiac troponin I, N-terminal pro-B-type natriuretic peptide, and d-dimer levels were measured at

199 e measured (troponin T, N-terminal pro-brain natriuretic peptide, and heart-type fatty acid binding p

200 ejection fraction with N-terminal pro-brain natriuretic peptide, and high-sensitive troponin was neg

201 ensitivity troponin T, N-terminal pro-B-type natriuretic peptide, and high-sensitivity C-reactive pro

202 n, D-dimer, troponin T, N-terminal pro-brain natriuretic peptide, and high-sensitivity C-reactive pro

203 iltration rate, higher N-terminal pro-B-type natriuretic peptide, and ischemic cause of heart failure

204 iotensin inhibition therapy, elevated B-type natriuretic peptide, and larger left ventricular end-dia

205 mer, homoarginine, and N-terminal pro B-type natriuretic peptide, and lower levels of low-density lip

206 chronic kidney disease, N-terminal-pro brain natriuretic peptide, and lymphocyte GRK2 protein levels

207 class or Ross class), N-terminal pro-B-type natriuretic peptide, and quality of life (QOL) were asse

208 ometry, measurement of N-terminal pro-B-type natriuretic peptide, and subjective health assessment.

209 duced fat oxidation to affect cardiac atrial natriuretic peptide, and thus, induce adipose lipolysis,

210 pericardial effusion, N-terminal pro-B-type natriuretic peptide, and troponin T.

211 iber direction increased expression of brain natriuretic peptide, but off-axis stretches (causing fib

212 reatine kinase, myoglobin, N-terminal B-type natriuretic peptide, C-reactive protein, and leukocyte c

213 ood samples were evaluated for cardiac brain natriuretic peptide, choline, and TMAO levels.

214 r expression of cardiac stress genes (B-type natriuretic peptide, collagen gene expression), less car

215 isease as indicated by N-terminal pro B-type natriuretic peptide, E/E', and left atrial volume.

216 er adjustment for age, N-terminal pro-B-type natriuretic peptide, ejection fraction, E/E', and left v

217 nt after adjustment for N-terminal pro-brain natriuretic peptide, ejection fraction, stroke volume in

218 Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol)

219 e 2 began with de Bold's discovery of atrial natriuretic peptide, followed by isolation of the enzyme

220 Exercise testing, echocardiography, B-type natriuretic peptide, functional health assessment, and m

221 tional class [WHO-FC], N-terminal-pro-B-type natriuretic peptide, hemodynamics) and lung-transplantat

222 ronary artery calcium, N-terminal pro B-type natriuretic peptide, high-sensitivity cardiac troponin T

223 Levels of N-terminal fragment B-type natriuretic peptide, high-sensitivity cardiac troponin T

224 ronary artery calcium, N-terminal pro B-type natriuretic peptide, high-sensitivity cardiac troponin T

225 Plasma levels of B-type natriuretic peptide, hs-TnI (high-sensitivity troponin I

226 oss, reduction in amino terminal, pro B-type natriuretic peptide, increased plasma renin activity, an

227 x metalloproteinase-3, N-terminal pro-B-type natriuretic peptide, interleukin-6, soluble CD40 ligand,

228 lthough LCZ696 reduced N-terminal pro B-type natriuretic peptide, levels of the other 4 biomarkers we

229 rular filtration rate, N-terminal pro-B-type natriuretic peptide, mineralocorticoid receptor antagoni

230 rminal pro-B-type natriuretic peptide/B-type natriuretic peptide, the 6-min walk test distance, and h

231 ection fraction, plasma n-terminal pro-brain natriuretic peptide, tumor necrosis factor-alpha, and C-

232 e found between any 2 time points for B-type natriuretic peptide, tumor necrosis factor-alpha, IL-1b,

233 de concentrations and compared the impact of natriuretic peptide-associated genetic variants on blood

234 C-reactive protein and N-terminal pro B-type natriuretic peptide.

235 perative end-systolic volume index or B-type natriuretic peptide.

236 unoassay protocol for the detection of brain natriuretic peptide.

237 s, and higher levels of N-terminal pro-brain natriuretic peptide.

238 further adjustment for N-terminal pro-B-type natriuretic peptide.

239 natriuretic peptide or N-terminal pro-brain natriuretic peptide.

240 asive hemodynamics, and N-terminal pro-brain natriuretic peptide.

241 cture and function, and N-terminal pro brain natriuretic peptide.

242 itional markers, such as N-terminal probrain natriuretic peptide.

243 nt, peripheral ischemic preconditioning, and natriuretic peptide.

244 ft ventricular ejection fraction, and B-type natriuretic peptide.

245 etic peptides, such as N-terminal pro-B-type natriuretic peptide/B-type natriuretic peptide, the 6-mi

246 med BNP and LV-GLS were 4.04 (absolute brain natriuretic peptide: 60 pg/dL) and -20.7%.

247 justed for age, sex, and N-terminal probrain natriuretic peptide: adrenomedullin (hazard ratio per lo

248 to LCZ696 for lowering N-terminal pro B-type natriuretic peptide; however, left atrial volume reducti

249 stance, and NT-proBNP (N-terminal pro-B-type natriuretic peptide; P<0.05 for all).

250 vity troponin and N-terminal fragment B-type natriuretic peptide], and clinical history of prior stro

251 troponins, NT-proBNP [N-terminal pro-B-type natriuretic peptide], and galectin-3).

252 me, including central venous pressure, brain-natriuretic-peptide concentration, and fractional urinar

253 r molecule that transduces nitric-oxide- and natriuretic-peptide-coupled signalling, stimulating phos

254 Current guidelines recommend use of natriuretic peptides (N-terminal pro-B type natriuretic

255 Natriuretic peptides (NP) have prognostic value in heart

256 tify musclin-a peptide with high homology to natriuretic peptides (NP)-as an exercise-responsive myok

257 Biologically active natriuretic peptides (NPs) are an integral part of cardi

258 The cardiac natriuretic peptides (NPs), atrial natriuretic peptide (

259 The cardiac natriuretic peptides (NPs), atrial NP and B-type NP, reg

260 The functional homologues of vertebrate natriuretic peptides (NPs), the plant natriuretic peptid

261 )-A, also known as NPR-A or NPR1, by cardiac natriuretic peptides (NPs).

262 ebrate natriuretic peptides (NPs), the plant natriuretic peptides (PNPs), are a novel class of peptid

263 "super"-induction of fetal genes, including natriuretic peptides A and B (Nppa/Nppb).

264 More recent evidence suggests that natriuretic peptides along with the next generation of b

265 Changes in insulin signaling, circulating natriuretic peptides and adipokines, and varied expressi

266 nzyme responsible for the degradation of the natriuretic peptides and many other vasoactive peptides.

267 The natriuretic peptides are biochemical markers of heart fa

268 ng, a 6-minute walk test, and measurement of natriuretic peptides before and 1 year after AVR.

269 d blocking angiotensin II signaling, augment natriuretic peptides by inhibiting their breakdown by ne

270 e still learning how complex the dynamics of natriuretic peptides can be in the interpretation of tes

271 Plasma concentrations of natriuretic peptides decline with obesity in patients wi

272 in exercise capacity, functional class, and natriuretic peptides from baseline to 12 months, but tre

273 r, cardiac expression of peptides other than natriuretic peptides has only been suggested using trans

274 BACKGROUND AND Natriuretic peptides have led the way as a diagnostic an

275 echocardiographic parameters and circulating natriuretic peptides that confound HFpEF diagnosis.

276 spnea, and elevated plasma concentrations of natriuretic peptides were randomized to receive a double

277 ed for known predictors, including age, sex, natriuretic peptides, and comorbidity.

278 ns with abnormal cardiac structure/function, natriuretic peptides, and incident heart failure (HF) is

279 ly used plasma biomarkers include troponins, natriuretic peptides, and lipoprotein particles, yet int

280 Increasing evidence behind the use of natriuretic peptides, emergence of novel biomarkers, and

281 encodes an enzyme that degrades circulating natriuretic peptides, showed the strongest differential

282 These include natriuretic peptides, soluble suppressor of tumorgenicit

283 rt the use of 3 such intermediate endpoints: natriuretic peptides, such as N-terminal pro-B-type natr

284 osterone system and decreased sensitivity to natriuretic peptides.

285 is a membrane-bound enzyme that breaks down natriuretic peptides.

286 lower circulating levels of atrial and brain natriuretic peptides.

287 th resistance to diuretics and to endogenous natriuretic peptides.

288 g/m(2); P<0.0001) and a smaller reduction in natriuretic peptides.

289 ntrations of troponin-T and N-terminal brain natriuretic propeptide, as well as with moderate-to-seve

290 Natriuretic regulation of extracellular fluid volume hom

291 P<0.001) and lesser ability to predict poor natriuretic response (area under the curve =0.76, 95% co

292 for acute decompensated heart failure, poor natriuretic response can be predicted soon after diureti

293 Poor natriuretic response could be accurately predicted with

294 the tubuloglomerular feedback response, the natriuretic response to acute volume expansion, and the

295 This prediction was confirmed by the natriuretic response to diuretics targeting the thick as

296 This prediction was confirmed by the natriuretic response to diuretics.

297 ordingly, ClC-K2 KO mice did not exhibit the natriuretic response to furosemide and exhibited a sever

298 Poor natriuretic response was defined as a cumulative sodium

299 bumetanide, 40% of the population had a poor natriuretic response.

300 This natriuretic-ureotelic, water-conserving principle relies