ライフサイエンスコーパス: natriuresis

1 not regulated by the hormones that regulate natriuresis.

2 renal link to coordinate salt ingestion with natriuresis.

3 is a link between increased arterial BP and natriuresis.

4 DS (n=5) increased MBG and OLC excretion and natriuresis.

5 l nephron must be mainly responsible for the natriuresis.

6 sodium retention, and compensatory nocturnal natriuresis.

7 h intrarenal actions that influence pressure natriuresis.

8 h the increase in BP, likely due to pressure-natriuresis.

9 and generates a metabolite that facilitates natriuresis.

10 ce without increasing heart rate and promote natriuresis.

11 ide:10 mg oral torsemide resulted in similar natriuresis.

12 nce of approximately 4:1 resulted in similar natriuresis.

13 ease in UNa and 115 mmol (32%) greater total natriuresis.

14 l NCC (tNCC), and augmented thiazide-induced natriuresis.

15 predicted a larger post-diuretic spontaneous natriuresis.

16 ngest predictor of post-diuretic spontaneous natriuresis.

17 redicted both a higher UNa and greater total natriuresis.

18 res, without obvious changes in diuresis and natriuresis.

19 o C-21-activated AT(2)Rs during induction of natriuresis.

20 o C-21-activated AT(2)Rs during induction of natriuresis.

21 renal blood flow, and promoted diuresis and natriuresis.

22 cGMP can bind to NKA and thereby mediate natriuresis.

23 tidiuresis while oxytocin secretion promotes natriuresis.

24 tion, where it stimulates vasodilatation and natriuresis.

25 otensin II, and a leftward shift in pressure natriuresis.

26 al tubule sodium transport but did not cause natriuresis.

27 ated salt sensitivity, and impaired pressure natriuresis.

28 spite the assumption of pressure-independent natriuresis.

29 ical decrease in urinary cGMP and attenuated natriuresis.

30 -renal signaling which mediates postprandial natriuresis.

31 ic peptide receptor (NPR-A), and dehydration natriuresis.

32 lasting and were associated with significant natriuresis.

33 ide (ANP), a regulator of blood pressure and natriuresis.

34 ant increases in diuresis volume and 24-hour natriuresis (0.08 +/- 0.02 mmol/100g in CCl(4) vehicle v

35 9% NaCl, 15% dextrose), KO mice had impaired natriuresis (37 +/- 10 versus 99 +/- 9 mmol of Na(+) per

36 mals exhibited marked anti-diuresis and anti-natriuresis (40 and 47%), which peaked at 1-3 weeks.

37 Natriuresis accompanied by blockade of proximal glomerul

38 sults indicate that blunted volume expansion natriuresis accompanied by cellular resistance to ANP in

39 bservations suggesting that proximal tubular natriuresis activates renal tubuloglomerular feedback th

40 strated a substantial impairment of pressure natriuresis: acute increases in blood pressure did not i

41 The natriuresis after 1 day was significantly higher in the

42 The primary end point was natriuresis after 1 day.

43 Low natriuresis after an FST identified patients at a higher

44 e or dapagliflozin showed markedly increased natriuresis after thiazide challenge.

45 n similar increases in both urinary cGMP and natriuresis among healthy normal, PSD, and PDD subjects.

46 of BNP resulted in significant diuresis and natriuresis and an increase in GFR.

47 ds; two distinct control mechanisms for both natriuresis and arterial resistances can be implemented,

48 ibitor, marinobufagenin (MBG), in regulating natriuresis and blood pressure (BP) responses to sustain

49 t vascular responses in the kidney to effect natriuresis and BP control.

50 e could exert reno-protective effects beyond natriuresis and BP reduction.

51 Secondary end points included cumulative natriuresis and diuresis after 2 days of treatment, leng

52 ction with more pronounced effects regarding natriuresis and diuresis in patients with a lower eGFR.

53 on of nephron sodium transporters, decreased natriuresis and diuresis in response to l-dihydroxypheny

54 R phosphorylation and restored ETBR-mediated natriuresis and diuresis in SHRs.

55 that infusion of ANP results in substantial natriuresis and diuresis in wild-type mice but fails to

56 22 mmol/L) and manifested the expected early natriuresis and diuresis of vasopressin escape.

57 Overall, natriuresis and diuresis were higher with acetazolamide,

58 BR was hyperphosphorylated and ETBR-mediated natriuresis and diuresis were not evident.

59 and loop diuretic is effective in maximizing natriuresis and diuresis while preserving renal function

60 The actions of both peptides include natriuresis and diuresis, a decrease in systemic blood p

61 pressure, improve cardiac output, stimulate natriuresis and diuresis, and rapidly induce symptomatic

62 e was feasible, safe, and resulted in higher natriuresis and diuresis, as well as a shorter length of

63 Ang II infusion normally promotes natriuresis and diuresis, but COX2 deficiency blocked th

64 ceptor ligand, preserved furosemide-mediated natriuresis and diuresis, while reducing cardiac preload

65 ects, neurohormonal suppression and enhanced natriuresis and diuresis.

66 reduces NaCl and water absorption, promoting natriuresis and diuresis.

67 atriuretic peptide concentrations and causes natriuresis and diuresis.

68 plasma renin and angiotensin, while inducing natriuresis and diuresis.

69 ein phosphatase PP2A reduced AT(2)R-mediated natriuresis and evaluated changes in PP2A activity and l

70 and raised renal perfusion pressure induced natriuresis and increased phosphorylated Src(Tyr416) and

71 The natriuresis and increased urinary cGMP excretion (U(cGMP

72 Predictors of natriuresis and its relationship with the main trial end

73 ckout (KO) mice had higher amiloride-induced natriuresis and lower plasma [K(+) ] at baseline.

74 Natriuretic peptides (NPs) control natriuresis and normalize changes in blood pressure.

75 SGLT2 inhibition promotes natriuresis and osmotic diuresis, leading to plasma volu

76 rption decreased significantly, resulting in natriuresis and osmotic diuresis.

77 tubular sodium reabsorption impairs pressure natriuresis and plays an important role in initiating ob

78 exerts renoprotective effects by stimulating natriuresis and reducing blood pressure.

79 Blunted volume expansion (VE) natriuresis and renal resistance to atrial natriuretic p

80 e measured by higher cumulative diuresis and natriuresis and shortened length of stay without treatme

81 d but did not completely reverse the blunted natriuresis, and ANP resistance persisted in IMCD cells

82 , 2 (MK-7145), demonstrated robust diuresis, natriuresis, and blood pressure lowering in preclinical

83 he main endpoints of decongestion, diuresis, natriuresis, and clinical outcomes are assessed accordin

84 ion rate (GFR), effective renal plasma flow, natriuresis, and diuresis.

85 l collecting ducts, higher amiloride-induced natriuresis, and enhanced sodium chloride co-transporter

86 nin-angiotensin-aldosterone system, pressure natriuresis, and reduced renal nerve activity, actions t

87 Next, proteins involved in vasodilation/natriuresis are discussed with emphasis on natriuretic p

88 dy found that the ETBR-mediated diuresis and natriuresis are impaired in hypertension with unknown me

89 actions of SGLT2 inhibition, glycosuria and natriuresis, are pivotal in enhancing glucose control, p

90 Since natriuresis as well as phosphaturia were observed in all

91 d had significantly blunted thiazide-induced natriuresis as well as renal potassium wasting and hypok

92 ers reveal that dopamine causes diuresis and natriuresis, as well as some degree of renal vasodilatat

93 Intra-renal DNP resulted in marked natriuresis associated with increased urinary cyclic gua

94 , including that of SGK1, caused substantial natriuresis, but not kaliuresis, in WT mice, which indic

95 Thus, on a high NaCl diet fenoldopam causes natriuresis by inhibiting renal proximal and distal tubu

96 michannels have an integral role in pressure natriuresis by releasing ATP into the tubular fluid, whi

97 pelin-13 increased renal blood flow by ~15%, natriuresis by ~20% and free water clearance by ~10%, co

98 ffeine intake produces moderate diuresis and natriuresis, caffeine increases the blood pressure (BP)

99 stance, defined as an inadequate quantity of natriuresis despite an adequate diuretic regimen, is a m

100 s) are cardiac-derived hormones that promote natriuresis, diuresis, and vasodilation.

101 eased levels of cGMP decrease BP by inducing natriuresis, diuresis, and vasodilation.

102 ution containing 4% BSA resulted in a marked natriuresis/diuresis in wild-type mice but no response i

103 K-2Cl cotransporter are major factors in the natriuresis/diuresis that is one of the hallmarks of isc

104 n, the physiologic effects of NPs on GFR and natriuresis do not involve podocytes.

105 The resulting natriuresis-driven diuretic water loss is assumed to con

106 The lower arterial pressure and enhanced natriuresis during high salt loading in Pkd1 knockout mi

107 enal function while simultaneously promoting natriuresis during treatment for heart failure.

108 ated with higher cumulative urine output and natriuresis, findings consistent with better diuretic ef

109 response prediction equation (NRPE) predicts natriuresis following a loop diuretic dose using a urine

110 responses evoked by peripheral ang II and to natriuresis following volume expansion.

111 e wave velocity, glomerular filtration rate, natriuresis, free water clearance and urinary protein ex

112 The greater natriuresis from higher diuretic doses in the torsemide

113 e feasibility and efficacy of a standardized natriuresis-guided diuretic protocol in patients with ac

114 A standardized natriuresis-guided diuretic protocol to guide decongesti

115 Poor natriuresis has been associated with a poorer response t

116 This process, known as dehydration natriuresis, helps prevent further accentuation of hyper

117 effects include transient volume expansion, natriuresis, hemodilution, immunomodulation, and improve

118 on and augmented hydrochlorothiazide-induced natriuresis; high sodium intake had opposite effects.

119 s pleiotropic, influencing body composition, natriuresis, immune function, and entrainment of circadi

120 receptor A (NPRA) and cause vasodilation and natriuresis important in the regulation of blood pressur

121 ) exchanger-3 and Na(+)/K(+)ATPase, inducing natriuresis in a bradykinin-nitric oxide-cGMP-dependent

122 o investigate the effect of acetazolamide on natriuresis in ADHF and its relationship with outcomes.

123 Here we describe the role of pressure natriuresis in blood pressure control and outline the ca

124 ed mice with amiloride resulted in a blunted natriuresis in both wild-type mice (FE(Na) = 1.10 +/- 0.

125 DPSPX induced a natriuresis in control rats (from 0.40 +/- 0.11 to 5.97

126 Stimulation of ETBR by BQ3020-induced natriuresis in human (h) GRK4gamma wild-type (WT) mice.

127 e of both diuretic-induced and post-diuretic natriuresis in hypervolemic ADHF.

128 ose) dopamine to furosemide therapy enhances natriuresis in patients with compensated congestive hear

129 caused substantial and sustained (1- to 2-h) natriuresis in rats and no or minimal concomitant potass

130 to hypertension, renal vasoconstriction, and natriuresis in rats with intact renal nerves.

131 er renal angiotensin II levels, and enhanced natriuresis in response to L-NAME.

132 MP activation, which contributes to impaired natriuresis in response to VE.

133 Early intervention to restore pressure natriuresis in T1DM may complement reductions in cardiov

134 lar volume expansion resulted in significant natriuresis in wild-type (7.0 +/- 0.8 microl min(-1), N

135 ed and low intake augmented thiazide-induced natriuresis in wild-type but not in Kcnj16(-/-) mice.

136 ry cyclic guanosine monophosphate (cGMP) and natriuresis increased after VE.

137 iuretic therapies, the mean diuretic-induced natriuresis increased three-fold.

138 , mice had reduced BP, enhanced salt-induced natriuresis, increased urinary nitrite and nitrate (NOx)

139 The natriuresis induced by amiloride was significantly great

140 t a simplified Guyton-Coleman model in which natriuresis is a function of arterial pressure via the p

141 Pressure natriuresis is an important physiological regulator of B

142 on, in the standard version of our new model natriuresis is assumed to be independent of arterial pre

143 Natriuresis is effectively induced by both furosemide an

144 Pressure natriuresis is impaired in hypertension and mechanistic

145 late cyclase, the receptor subtype mediating natriuresis is less well defined.

146 Increased natriuresis is strongly related to successful decongesti

147 ich target extracellular cGMP acts to induce natriuresis is unknown.

148 clude that one mechanism by which DA induces natriuresis is via protein kinase A-mediated phosphoryla

149 TMAO-treated rats showed higher diuresis and natriuresis, lower arterial pressure and plasma NT-proBN

150 (NPR1) to affect vasodilation, diuresis and natriuresis, lowering venous pressures and relieving ven

151 diuretic response was defined as cumulative natriuresis < 50 mmol over the study visit.

152 scular resistance and associated substantial natriuresis make this a potentially attractive therapeut

153 In contrast, diuretic-induced natriuresis may be associated with reduced GFR and RAAS

154 aired activation of urinary cGMP and reduced natriuresis may contribute to volume overload and the pr

155 failure of fava bean consumption to provoke natriuresis may indicate that dopa concentrations in com

156 point can only be sustained if the pressure natriuresis mechanism is impaired, suggesting that hyper

157 nction of arterial pressure via the pressure-natriuresis mechanism, and arterial resistances are cont

158 compensate for genetically impaired pressure-natriuresis mechanisms.

159 tion (CPDSR) following loop diuretic-induced natriuresis, minimizing sodium excretion and producing a

160 This restored natriuresis, Na(+) transporter internalization/inactivat

161 No significant additional increment in natriuresis occurred when dopamine and furosemide were a

162 he effect of aliskiren, we found significant natriuresis on both diets.

163 nce, new pharmaceutical strategies to induce natriuresis or aquaresis, and the physiological basis an

164 8-bromo-cAMP administration had no effect on natriuresis or AT(2)R recruitment in SHR.

165 Only the parent 2 induced natriuresis over a range of doses without accompanying k

166 longer duration of kidney drug delivery and natriuresis (P <= 0.004 for both).

167 was associated with improved median 24-hour natriuresis (P = 0.03) and urine output (P = 0.005), exp

168 centrations relative to control (P=0.024), a natriuresis (P=0.046), and a tendency for creatinine exc

169 Empagliflozin causes significant natriuresis, particularly when combined with loop diuret

170 pot urine sample, then 6-h (diuretic-induced natriuresis period) and 18-h (post-diuretic period) urin

171 al sodium reabsorption and impaired pressure natriuresis play key roles.

172 A brisk natriuresis precedes the escape from this antidiuresis.

173 ontrary to CPDSR, a greater diuretic-induced natriuresis predicted a larger post-diuretic spontaneous

174 t to the substantial decrease in spontaneous natriuresis predicted by CPDSR, no change in post-diuret

175 ) are associated with increased diuresis and natriuresis, preserved glomerular filtration rate (GFR),

176 peripheral angiotensin II (ang II), and the natriuresis produced by extracellular fluid volume expan

177 d with larger 18-h post-diuretic spontaneous natriuresis (r = 0.7, P < 0.001).

178 nt results demonstrated that NaPi2a-mediated natriuresis, rather than decreases in serum FGF23 levels

179 rtension amplifies this risk, while pressure natriuresis regulates long-term blood pressure.

180 athway may lead to resetting of the pressure-natriuresis relation in the kidney, sodium retention, an

181 as a reduction in the slope of the pressure-natriuresis relation.

182 antly, the new model reproduces the pressure-natriuresis relationship--the correlation between arteri

183 ng observed haemodynamic changes or pressure-natriuresis relationships.

184 After 2 days, the natriuresis remained higher in the protocol arm (538 ver

185 Diuresis, natriuresis, renal excretion, and tissue levels of MBG a

186 This acute pressure natriuresis response is a uniquely powerful means of sta

187 e in diabetic rats, and rescued the pressure natriuresis response without influencing lithium clearan

188 CA and Ucn2 infusion produced a diuresis and natriuresis, responses with Ucn2 and Ucn+CA were 2- to 3

189 kg per minute) or were subjected to pressure-natriuresis+/-rostafuroxin infusion.

190 We further propose that the diuresis and natriuresis seen during air breathing were mediated by t

191 Biochemical indices of natriuresis showed bendroflumethiazide to be less effect

192 SGLT2 inhibitors and clinical correlates of natriuresis, such as the impact on blood pressure, heart

193 roperties such as blood pressure regulation, natriuresis, suppression of adverse remodeling, inhibiti

194 a+ transporter genes might contribute to the natriuresis that follows ischemic acute renal failure, t

195 tion of NKA-mediated ion transport decreases natriuresis through activation of basolateral (NKA) and

196 e caused a slight nonsignificant increase in natriuresis to 36.7 +/- 8.5 mEq/3 h.

197 F+V and F+T increased diuresis and natriuresis to a similar extent during drug administrati

198 y and local inflammation can impair pressure natriuresis to cause hypertension.

199 mpathoinhibitory response and attenuated the natriuresis to VE.

200 AngII shifts pressure natriuresis toward higher BP primarily by increasing tub

201 Four days postpartum, volume expansion natriuresis, U(cGMP)V, and PDE5 protein levels in IMCD c

202 ol littermates did not differ in BP, GFR, or natriuresis under baseline conditions.

203 DA induces natriuresis via acute inhibition of the renal proximal t

204 talis-like sodium pump ligands (SPLs) effect natriuresis via inhibition of renal tubular Na(+),K(+)-A

205 After 14 days of empagliflozin, natriuresis waned due to increased reabsorption in the P

206 a was 92 +/- 25 mmol/L on average, and total natriuresis was 425 +/- 234 mmol.

207 sodium excretion by 10-fold (P<0.0001); this natriuresis was abolished by direct renal interstitial i

208 C-21-induced natriuresis was accompanied by an increase in renal inte

209 on on the RPT as acute systemic C-21-induced natriuresis was additive to that induced by chlorothiazi

210 Paradoxically, greater 6-h diuretic-induced natriuresis was associated with larger 18-h post-diureti

211 On the high NaCl diet, fenoldopam-induced natriuresis was associated with the inhibition of renal

212 After 3 weeks, pressure natriuresis was induced by serial arterial ligation.

213 sodium excretion compared with placebo, and natriuresis was maintained over 10 days with little kali

214 This natriuresis was not, however, associated with evidence o

215 PDSR, no change in post-diuretic spontaneous natriuresis was observed (P = 0.47).

216 esponse (n=98), outpatient and inpatient OOD natriuresis was poorly correlated (r=0.26).

217 horylated NCC/total NCC and thiazide-induced natriuresis were significantly increased in the Nedd4-2

218 , Npr1-/- mice were resistant to dehydration natriuresis, which suggests that Sgk1-dependent activati

219 olamide strongly and independently predicted natriuresis with a 16 mmol/L (19%) increase in UNa and 1

220 Early natriuresis with a reduction in plasma volume, a consequ

221 Stronger natriuresis with better decongestion translated into a s

222 at the renal concentration mechanism couples natriuresis with correspondent renal water reabsorption,

223 ence of a large acute or chronic diuresis or natriuresis with these agents, either when given alone o

224 hron, resulting in the observed modest acute natriuresis with these agents.

225 se doses resulted in a substantially greater natriuresis with torsemide (P < 0.001).

226 ared with controls, the RYGB group had brisk natriuresis, with significantly lower tmax for urine sod

227 A1 adenosine receptor, is proposed to cause natriuresis without causing a decline in renal function.

228 duced hypertension by causing glucosuria and natriuresis without changes in the Renin-Angiotensin-Ald

229 We hypothesised that pressure natriuresis would be impaired, and BP increased, in the