ライフサイエンスコーパス: ANP

1 ANP and cGMP inhibited TGF-beta1-induced myofibroblast t

2 ANP and mANP also had opposing effects on ICa,L in human

3 ANP augmented insulin secretion at the threshold glucose

4 ANP blocks vascular endothelial growth factor (VEGF) pro

5 ANP effects were mediated by the Rac1 GTPase effector PA

6 ANP greatly enhances the phosphorylation at Ser-239 of t

7 ANP increased AP upstroke velocity (Vmax), AP duration,

8 ANP increased haematocrit from 40.6% to 46.8%, correspon

9 ANP reduced the response of ARPE-19 cells to VEGF apical

10 ANP significantly reversed VEGF-induced BRB TEER reducti

11 ANP's TEER response was concentration but not time depen

12 ANP(1-28) remained unchanged, while NT-ANP(1-98) was red

13 ANP-induced cGMP production is selectively suppressed by

14 ovirus showed increased expression of Cav-3, ANP, and Akt phosphorylation.

15 or purified neutral endopeptidase to abolish ANP-dependent activation of NPR-A.

16 ed knockdown of GC-A, VASP, or PKG abolishes ANP-induced VASP Ser-239 phosphorylation, stress fiber f

17 e release of circulating biologically active ANP.

18 which is proteolytically converted to active ANP.

19 ets, before and after saline administration, ANP levels were up to 50% higher in AG individuals than

20 le and skin microvascular permeability after ANP.

21 Although ANP and BNP are well-characterized regulators of blood p

22 An ANP gradient was developed, allowing for the direct anal

23 NP (1 pM to 1 micromol/L), and/or isatin, an ANP receptor antagonist.

24 PDE-5 and ANP compartments were functionally separated, as inhibit

25 Because both ASK1 and ANP are associated with pathologic cardiac hypertrophy,

26 d higher in 293 compared with HeLa cells and ANP did not increase internalization of FLAG-GC-A.

27 These results indicate that corin and ANP are essential for physiological changes at the mater

28 erface, suggesting that defects in corin and ANP function may contribute to pre-eclampsia.

29 Here we identify a new function of corin and ANP in promoting trophoblast invasion and spiral artery

30 nocyte progenitors that express both MDR and ANP.

31 that the PDE4 inhibitor rolipram attenuates ANP-induced increases in vascular permeability after inf

32 ANPs containing trisubstituted nitrogen (aza-ANPs) has been synthesized.

33 The aza-acyclic nucleoside phosphonates (aza-ANPs) are good inhibitors of Plasmodium falciparum HGXPR

34 t that the different affinities of these aza-ANPs could be due to the flexibility of the loops surrou

35 Prodrugs of these aza-ANPs exhibit antimalarial activity against Pf lines with

36 y a candidate route of communication between ANP and its receptors on the external membrane of smooth

37 FLAG-GC-A bound ANP identically with wild-type GC-A and was internalized

38 n of particulate guanylate cyclase (GC-A) by ANP leads to a substantial, dose-dependent, rapid, and s

39 hances the stimulation of NPR-A and NPR-B by ANP and CNP, respectively.

40 ation intensity with high-level induction by ANP or cGMP signaling leading to apoptotic cell death ra

41 ioma cells through either stimulating pGC by ANP/BNP, or blocking PDE by 3-isobutyl-1-methylxanthine/

42 mechanism of vascular barrier protection by ANP via modulation of GEF-H1 function.

43 se in net apical-to-basal fluid transport by ANP (5 muM) that was inhibited completely by the ANP rec

44 ite: increased with SIL+ISO but unaltered by ANP+ISO.

45 ing enzyme (IDE) was found to rapidly cleave ANP, but the functional consequences of such cleavages i

46 IDE rapidly cleaves ANP and CNP, thus inactivating their ability to raise in

47 aneously demonstrated a lack of compensatory ANP elevation in advanced hypertension.

48 At low concentrations, ANP and beta-AR agonists additively enhanced expression

49 lation of secretory granules (SG) containing ANP propeptides (pro-ANP), a signature of maladaptive hy

50 After continuous ANP infusion for 60 min, the arterioles were dilated (10

51 In contrast, ANP elicited sustained submembrane elevations in [cGMP](

52 ors of PDE3A mimicked the effect of low-dose ANP on thrombin-induced permeability, and inhibition of

53 In pulmonary ECs, ANP suppressed thrombin-induced disassembly of periphera

54 nding to the mRNA of NPPA, the gene encoding ANP.

55 locus containing the adjacent genes encoding ANP and BNP harbored 4 independent cis variants with eff

56 e with selective deletion of the endothelial ANP receptor.

57 lar permeability after infusion of exogenous ANP and observations of elevated central venous pressure

58 detected in mice grafted with HSE expressing ANP from either keratinocytes or fibroblasts, and topica

59 These data indicate that the familial ANP mutation associated with atrial fibrillation has onl

60 ompanied by increased protein expression for ANP and BNP.

61 JCI performed a knockout of the receptor for ANP in vascular endothelia in order to distinguish the e

62 etion of the guanylyl cyclase-A receptor for ANP.

63 ost 30% of whole body clearance required for ANP to regulate plasma volume.

64 human and animal studies indicate a role for ANP as a regulator of blood pressure with conflicting re

65 GMP-dependent signaling cascade leading from ANP receptors to nuclear accumulation of both molecules.

66 Further, ANP and BNP elicit increases in blood microvessel permea

67 e.g., TNFalpha), hypertrophic factors (e.g., ANP), and profibrotic factors (e.g., TGFbeta1) from both

68 At 6 mmol/L glucose, ANP readily elicited Ca(2+) influx in control beta-cells

69 e aortic constriction coincident with higher ANP expression and smaller myocyte volume.

70 at failed to associate with pro-ANP hindered ANP-mediated protection against hypertrophy, which was r

71 lays a cross-reactivity for all NP hormones (ANP, BNP, and CNP), in contrast to other NPRs, which are

72 rmore, mice with HSE grafts expressing human ANP did not develop elevated blood pressure when fed a h

73 Mice with elevated plasma levels of human ANP showed lower renin levels and, correspondingly, had

74 Significant plasma levels of human ANP were detected in mice grafted with HSE expressing AN

75 scan for sequence variants within the human ANP gene, a mutation was identified that results in a 40

76 In 293 cells, (125)I-ANP and (125)I-IgG uptake curves were superimposable bec

77 HeLa cells endogenously express GC-A, (125)I-ANP binding and cross-linking studies only detected NPR-

78 n part, because previous studies used (125)I-ANP binding to track these receptors, which are expresse

79 n following 10 min of treatment with Ang II, ANP or 8-bromo-cGMP.

80 n mice results in dysmorphic LDCVs, impaired ANP secretion, and hypertension.

81 In ANP mixotrophic fermentation, the two molecules of CO2 a

82 (TRAP/HTV), which was further exacerbated in ANP(-/-) mice.

83 erse aortic constriction were exaggerated in ANP-null mice compared with wild-type controls.

84 n, a PI3K inhibitor, blocked the increase in ANP expression.

85 e, relative to the corresponding increase in ANP-induced renal water excretion.

86 challenge is associated with a reduction in ANP production.

87 ull-length PS1 (inactive gamma-secretase) in ANP.24 cells.

88 lacking functional KATP channels (SUR1-KO), ANP increased electrical activity, suggesting no involve

89 d 1660 and 1447 women who underwent MT and l-ANP, respectively.

90 or lumpectomy with an axillary procedure (L-ANP).

91 tomy carries higher complication rate than l-ANP with wound infection being the most common.

92 PDE2 mediates ANP/cGMP-induced decreases in aldosterone production.

93 In mice, ANP and mANP (10-100 nmol/L) had opposing effects on atr

94 that, in the extrasplenic microcirculation, ANP causes greater increases in post- than precapillary

95 helial (ARPE-19) cells with VEGF (10 ng/ml), ANP (1 pM to 1 micromol/L), and/or isatin, an ANP recept

96 Either modified ANP plasma levels or peptide structural alterations have

97 miR-155 and miR-105, were found to modulate ANP production in human cardiomyocytes and target geneti

98 Moreover, ANP potentiated the effect of glucagon-like peptide 1 (G

99 Increased expression of phospho-mTOR, ANP, and SERCA2a also suggests that T(3) promotes matura

100 owed that AQP1 current activation by 4.5 mum ANP decreases the normal basal-to-apical fluid transport

101 We have termed this peptide mutant ANP.

102 MD (P=0.001 and P=0.04, respectively), and N-ANP was inversely related to baseline mean flow velocity

103 easure (adjusting for known risk factors), N-ANP and renin were positively related to FMD (P=0.001 an

104 min-creatinine ratio), baseline mean flow (N-ANP, BNP, PAI-1, CRP, aldosterone), FMD (N-ANP, PAI-1, C

105 N-ANP, BNP, PAI-1, CRP, aldosterone), FMD (N-ANP, PAI-1, CRP, renin), and reactive hyperemia (BNP, PA

106 N-terminal pro-atrial natriuretic peptide [N-ANP], B-type natriuretic peptide [BNP], renin, aldostero

107 lar endothelial function identified plasma N-ANP as a key correlate of mean flow under basal conditio

108 ic or diuretic response with low-dose native ANP.

109 ults in a 40-AA peptide consisting of native ANP((1-28)) and a C-terminal extension of 12 AA.

110 nal blood flow enhancing actions than native ANP in vivo.

111 owering properties when compared with native ANP.

112 For FLAG-NPR-C, neither ANP, BNP, nor CNP increased its internalization in eithe

113 In contrast, neither ANP nor mANP had any effect on Na(+) current in mouse at

114 th human HGPRT have led to the design of new ANPs.

115 Akt phosphorylation was inhibited by 100 nm ANP.

116 ncreased by 4-fold in the presence of 100 nm ANP.

117 Notably, ANP abolished spontaneous contraction amplitude (P = 0.0

118 Notably, ANPs are also required for both the elicitor-induced oxi

119 rmined, three of these in complex with novel ANPs and one with GMP and pyrophosphate.

120 end toward lower levels of plasma atrial NP (ANP) and significantly smaller levels of cyclic guanosin

121 In human adipocytes, atrial NP (ANP) and ventricular NP (BNP) activated PPARgamma coacti

122 Three distinct NPs (ANP, BNP, and CNP) can selectively activate natriuretic

123 ANP(1-28) remained unchanged, while NT-ANP(1-98) was reduced in pre-hypertension (p < 0.05).

124 of IDE expression diminishes the ability of ANP and BNP to stimulate NPR-B.

125 rmeability may be critical to the ability of ANP to lower arterial blood pressure.

126 The action of ANP and rolipram to modify albumin clearances in duodenu

127 l contribution to the hypovolaemic action of ANP can be measured by the magnitude of the ANP-induced

128 ity from those of other endocrine actions of ANP in the regulation of plasma volume.

129 l molecular mechanism by which activation of ANP/cGMP/protein kinase G signaling disrupts TGF-beta1-i

130 The activity of ANP may in part be cGMP dependent, as 8-bromo-cGMP had s

131 activity-related musclin-dependent boost of ANP/cGMP signaling results in significantly lower maximu

132 In this review, we define the bounds of ANP mixotrophy, calculate the potential metabolic advant

133 Additionally, the cleavages of ANP and BNP by IDE render them active with NPR-B and a r

134 s affecting the circulating concentration of ANP associated with blood pressure, whereas those affect

135 le further evaluation of the contribution of ANP-dependent microvascular beds (such as gastro-intesti

136 entricular myocytes (RV), the lowest dose of ANP (0.003 nm) inhibited Ang II-stimulated BrdU uptake b

137 of forskolin was reversed at higher doses of ANP or NO.

138 on of permeability seen with higher doses of ANP.

139 ition of permeability caused by low doses of ANP.

140 ghting the blood pressure-lowering effect of ANP in the general population.

141 The protective effects of ANP against TRAP/HTV-induced lung injury were linked to

142 These effects of ANP and BNP on contractile function were examined furthe

143 etic and endothelial permeability effects of ANP cooperate in intravascular volume regulation.

144 The current study evaluated effects of ANP on beta-cell function by the use of a beta-cell-spec

145 ated by cAMP Epac pathways in the effects of ANP on beta-cell function; the latter seems to prevail.

146 more sensitive to the inhibitory effects of ANP than the LV (P < 0.0001).

147 Physiological effects of ANP, including decreased systolic blood pressure, increa

148 helia in order to distinguish the effects of ANP-dependent increases in vascular permeability from th

149 esults in the generation of a mutant form of ANP (mANP), was identified and shown to cause atrial fib

150 and assessment of different plasma forms of ANP and BNP.

151 Continuous infusion of ANP into the splenic artery (10 ng min(-1) for 60 min) o

152 rats treated with intravitreal injections of ANP, VEGF, or vehicle.

153 evels of pro-ANP but no detectable levels of ANP as compared with WT littermates.

154 ed HSE resulted in persistent high levels of ANP expression in vivo.

155 demonstrates a novel protective mechanism of ANP against pathologic hyperpermeability and suggests a

156 rt, we have discovered that the precursor of ANP, natriuretic peptide precursor (NPPA), physically in

157 s study identifies miR-425 as a regulator of ANP production, raising the possibility that miR-425 ant

158 acid 425 (miR-425), a negative regulator of ANP, were examined.

159 tools to identify novel miRNA regulators of ANP production that could be targeted to raise ANP level

160 nse of NPR-A and NPR-B to the stimulation of ANP, BNP, and CNP in cultured cells.

161 stone deacetylase 4 (HDAC4), upregulation of ANP and BNP in failing hearts did not require increased

162 Here, a novel class of ANPs containing trisubstituted nitrogen (aza-ANPs) has b

163 id foundation for the further development of ANPs as selective inhibitors of MtHGPRT and as antituber

164 tabilizing the endothelial barrier to offset ANP-induced increases in vascular permeability may be pa

165 nhanced the repressive effects of miR-425 on ANP production in human cardiomyocytes.

166 y of alcohol dependence via its influence on ANP and amygdala processing.

167 We show that pregnant corin- or ANP-deficient mice developed high blood pressure and pro

168 nopyrimidine (PMEO-DAPym) differs from other ANPs in that the aliphatic alkyloxy linker is bound to t

169 Aggregated nanogel particles (ANPs) were generated by aggregating GNPs to micron-size,

170 Atrial natriuretic peptide (ANP) acts acutely to reduce plasma volume by at least 3

171 tective peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in heart tissu

172 myocytes secrete atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in response to

173 peptides (NPs), atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), have central

174 uretic peptides, atrial natriuretic peptide (ANP) and B-type or brain natriuretic peptide (BNP), in t

175 nucleic acid for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were increased

176 ogram, including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), is a hallmark

177 hway in RPE with atrial natriuretic peptide (ANP) and with membrane-permeable analogs of cGMP would i

178 Atrial natriuretic peptide (ANP) binds guanylyl cyclase-A (GC-A) and natriuretic pep

179 Atrial natriuretic peptide (ANP) binds guanylyl cyclase-A/natriuretic peptide recept

180 acts as the pro-atrial natriuretic peptide (ANP) convertase.

181 t with increased atrial natriuretic peptide (ANP) expression that depended upon phosphatidylinositol-

182 impact of rs5065 atrial natriuretic peptide (ANP) gene variant on coronary artery disease (CAD) and i

183 c variant of the atrial natriuretic peptide (ANP) gene.

184 as 10 micromol/L atrial natriuretic peptide (ANP) had no effect.

185 Atrial natriuretic peptide (ANP) has a central role in regulating blood pressure in

186 The role of atrial natriuretic peptide (ANP) in regulating fetal cardiac growth is poorly unders

187 c oxide (NO) and atrial natriuretic peptide (ANP) induced synthesis of intracellular cGMP, [cGMP](i).

188 Atrial natriuretic peptide (ANP) influences glucose homeostasis and possibly acts as

189 cardiac hormone atrial natriuretic peptide (ANP) is a 28-amino acid (AA) peptide that consists of a

190 Atrial natriuretic peptide (ANP) is a hormone with diuretic, natriuretic, and vasodi

191 Atrial natriuretic peptide (ANP) is a hormone with numerous beneficial cardiovascula

192 Atrial natriuretic peptide (ANP) is an endogenous peptide hormone that is synthesize

193 dy the effect of atrial natriuretic peptide (ANP) on the extrasplenic microcirculation.

194 doses of either atrial natriuretic peptide (ANP) or NO donors potentiated the inhibitory effects of

195 ing initiated by atrial natriuretic peptide (ANP) stimulation leading to elevation of cGMP levels and

196 on of endogenous atrial natriuretic peptide (ANP) to increase vascular permeability to the plasma pro

197 Atrial natriuretic peptide (ANP) via its guanylyl cyclase-A (GC-A) receptor particip

198 ulating chimeric atrial natriuretic peptide (ANP) was detected in high concentration in subjects with

199 he C terminus of atrial natriuretic peptide (ANP) was recently genetically linked to patients with fa

200 e that activates atrial natriuretic peptide (ANP), a cardiac hormone that is important in regulating

201 on by expressing atrial natriuretic peptide (ANP), a hormone able to decrease blood pressure, in bioe

202 ces secretion of atrial natriuretic peptide (ANP), a regulator of blood pressure and natriuresis.

203 es of NPR-C with atrial natriuretic peptide (ANP), and with brain natriuretic peptide (BNP).

204 he gene encoding atrial natriuretic peptide (ANP), is associated with blood pressure.

205 meostasis by the atrial natriuretic peptide (ANP), making PDE2-type enzymes important targets for dru

206 The receptor for atrial natriuretic peptide (ANP), natriuretic peptide receptor A (NPRA), is expresse

207 y in response to atrial natriuretic peptide (ANP), which acts with the kidney to regulate plasma volu

208 protein in both atrial natriuretic peptide (ANP)-dependent and -independent manner.

209 oxide (NO)- and atrial natriuretic peptide (ANP)-initiated cGMP signaling cascades are important in

210 ial regulator of atrial natriuretic peptide (ANP)-mediated counterhypertrophic responses in cardiomyo

211 ar modulation of atrial natriuretic peptide (ANP)-stimulated activation of GC-A.

212 late cyclase for atrial natriuretic peptide (ANP).

213 eptides, such as atrial natriuretic peptide (ANP).

214 y treatment with atrial natriuretic peptide (ANP).

215 iption factor of atrial natriuretic peptide (ANP).

216 at activation of atrial natriuretic peptide (ANP)/cGMP/protein kinase G signaling inhibits transformi

217 served that the cardiac natriuretic peptides ANP and BNP and the guanylate cyclase-linked natriuretic

218 e species, the cardiac natriuretic peptides (ANP and BNP) are produced by cardiomyocytes in the devel

219 Atrial and brain natriuretic peptides (ANP and BNP, respectively) are cardiac hormones released

220 betaMHC), atrial/brain natriuretic peptides (ANP/BNP), and skeletal alpha-actin (sACT) was increased,

221 d and quantified under aqueous normal phase (ANP) conditions, using a Diamond Hydride (DH) column for

222 : reversed phase (RP), aqueous normal phase (ANP), and hydrophilic interaction (HILIC) for the analys

223 e acyclic pyrimidine nucleoside phosphonate (ANP) phosphonylmethoxyethoxydiaminopyrimidine (PMEO-DAPy

224 Acyclic nucleoside phosphonates (ANPs) are inhibitors of HG(X)PRT and arrest the growth o

225 synthesized acyclic nucleoside phosphonates (ANPs) have been shown to be competitive inhibitors of Mt

226 Acyclic nucleoside phosphonates (ANPs) that contain a 6-oxopurine base are good inhibitor

227 rocess called anaerobic, non-photosynthetic (ANP) mixotrophic fermentation.

228 eles are associated with higher human plasma ANP levels.

229 ooperative mechanism where Anxa6 potentiates ANP-dependent counterhypertrophic responses in cardiomyo

230 5I/Q568P had a reduced (38+/-7%, P<0.01) pro-ANP processing activity compared to that of wild type.

231 llular calcium (Ca(2+)) stimulated Anxa6-pro-ANP colocalization and membrane association.

232 utions occur, was required for efficient pro-ANP processing in functional assays.

233 There was no significant difference in pro-ANP levels between subjects with lone AF and control sub

234 Cor-/- mice have elevated levels of pro-ANP but no detectable levels of ANP as compared with WT

235 tes by facilitating regulated traffic of pro-ANP.

236 recursor, proatrial natriuretic peptide (pro-ANP), which is proteolytically converted to active ANP.

237 ata establish corin as the physiological pro-ANP convertase and indicate that corin deficiency may co

238 protease that has been shown to process pro-ANP in vitro, but its physiological importance had not b

239 h decreased corin activity in processing pro-ANP.

240 ranules (SG) containing ANP propeptides (pro-ANP), a signature of maladaptive hypertrophy having coun

241 It also rescued pro-ANP translocation in cells expressing an Anxa6 mutant (A

242 inant soluble corin transiently restores pro-ANP conversion, resulting in the release of circulating

243 a6 mutants that failed to associate with pro-ANP hindered ANP-mediated protection against hypertrophy

244 pted a dynamic association of Anxa6 with pro-ANP-SG, parallel to their participation in anterograde t

245 Prolonged ANP exposure concomitantly reduced surface and total GC-

246 se-dependent signaling cascade that promotes ANP expression, resulting in a unique combination of pro

247 P production that could be targeted to raise ANP levels, which may have applications for the treatmen

248 microRNA 425 (miR-425) was found to regulate ANP production by binding to the mRNA of NPPA, the gene

249 a specific ANP receptor antagonist, reversed ANP's effect.

250 ry syndrome [ACS]) were genotyped for rs5065 ANP gene variant.

251 The MA of rs5065 ANP gene variant associates with increased susceptibilit

252 The size of SANPs, ANPs and GNPs was analyzed using a Coulter counter and t

253 le because these cells only express a single ANP receptor.

254 ough some aspects of heart maturation (size, ANP expression) are independent of GR at these key sites

255 Isatin, a specific ANP receptor antagonist, reversed ANP's effect.

256 In sum, ANP is an effective inhibitor of VEGF-induced vascular l

257 cal mapping studies in mice demonstrate that ANP sped electric conduction in the atria, whereas mANP

258 fluid balance, we tested the hypothesis that ANP or BNP (100 nM) would likewise elevate lymphatic per

259 We hypothesized that ANP would suppress near-term fetal cardiomyocyte prolife

260 Taken together, our findings suggest that ANP-mediated cGMP signal transduction pathways regulate

261 A growing body of evidence suggests that ANP might be involved in the symptomology of alcohol dep

262 well as conditional triple mutants show that ANPs are required for elicitor-triggered defense respons

263 The ANP and B-type natriuretic peptide play an important rol

264 (5 muM) that was inhibited completely by the ANP receptor antagonist anantin and a 60% increase in ne

265 Recently, a mutation in the ANP gene, which results in the generation of a mutant fo

266 ed whether reactivity to alcohol cues in the ANP target region amygdala, a key area implicated in add

267 Moreover, the ANP-induced phosphorylation of VASP at Ser-239 is accomp

268 m the promoter region, and activation of the ANP gene.

269 NP73-102, the NH(2)-terminal peptide of the ANP prohormone, which down-regulates NPRA expression, al

270 use of a beta-cell-specific knockout of the ANP receptor with guanylate cyclase activity (betaGC-A-K

271 ally, suggesting polarized expression of the ANP receptors in these cells.

272 ANP can be measured by the magnitude of the ANP-induced increase in blood-to-tissue albumin transpor

273 hibitory effect of both serum and LPA on the ANP-stimulated generation of cGMP.

274 Consistent with this, the ANP potently stimulated human trophoblasts in invading M

275 n a second phosphonate group attached to the ANP scaffold.

276 Thus ANP-induced increases in endothelial permeability may be

277 tidrug resistance (MDR) type 1, is linked to ANP expression on a bicistronic vector and was coexpress

278 Skin microcirculation responded to ANP similarly.

279 Our findings point to ANPs as key transduction elements that coordinate damage

280 rameshift product (fsANP), but not wild-type ANP (wtANP), was elevated in the serum of affected patie

281 tive was to compare the effects of wild-type ANP and mANP on atrial electrophysiology in mice and hum

282 fibrillation and demonstrate that wild-type ANP is antiarrhythmic.

283 zed MT and inactivation of Rho signaling via ANP-induced, PAK1-dependent inhibitory phosphorylation o

284 In vivo, ANP attenuated lung injury caused by excessive mechanica

285 In vivo, ANP significantly reduced VEGF-induced BRB leakage and t

286 uman umbilical vein endothelial cells, where ANP substantially enhances intracellular cGMP content, p

287 lar Ca(2+) handling mechanisms through which ANP attenuates this sustained elevation in cytosolic Ca(

288 While ANP and BNP appear to adopt similar receptor-bound confo

289 and 2.7 +/- 0.8-fold (P = 0.07, n = 7) with ANP and BNP, respectively.

290 that skeletal muscle albumin clearance with ANP treatment accounts for at most 30% of whole body cle

291 d, in skin and skeletal muscle compared with ANP alone (500 ng kg(-1) min(-1)).

292 eurohumoral properties of mANP compared with ANP were assessed in vivo in normal dogs.

293 wn structures of human HGPRT in complex with ANP-based inhibitors suggests reasons for the variations

294 tle with SIL+ISO yet rose nearly 5-fold with ANP, whereas protein kinase G activation (vasodilator-st

295 rly in vivo following treatment of mice with ANP or cGMP.

296 is was not restorable by co-stimulation with ANP.

297 ed myoblasts only when applied together with ANP.

298 Confluent monolayers were treated with ANP or membrane-permeable cGMP analogs in the presence o

299 s in 62.5% of hearts, whereas treatment with ANP completely prevented the occurrence of arrhythmias.

300 in response to 100 nm Ang II with or without ANP (0.003-100 nm) or 1 microm 8-bromo-cGMP.