ライフサイエンスコーパス: natriuresis

1 h intrarenal actions that influence pressure natriuresis.

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

3 and generates a metabolite that facilitates natriuresis.

4 ce without increasing heart rate and promote natriuresis.

5 al tubule sodium transport but did not cause natriuresis.

6 ated salt sensitivity, and impaired pressure natriuresis.

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

8 spite the assumption of pressure-independent natriuresis.

9 ical decrease in urinary cGMP and attenuated natriuresis.

10 -renal signaling which mediates postprandial natriuresis.

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

12 lasting and were associated with significant natriuresis.

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

14 not regulated by the hormones that regulate natriuresis.

15 renal link to coordinate salt ingestion with natriuresis.

16 is a link between increased arterial BP and natriuresis.

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

18 l nephron must be mainly responsible for the natriuresis.

19 sodium retention, and compensatory nocturnal natriuresis.

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

21 9% NaCl, 15% dextrose), KO mice had impaired natriuresis (37 +/- 10 versus 99 +/- 9 mmol of Na(+) per

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

23 Natriuresis accompanied by blockade of proximal glomerul

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

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

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

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

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

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

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

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

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

33 22 mmol/L) and manifested the expected early natriuresis and diuresis of vasopressin escape.

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

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

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

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

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

39 atriuretic peptide concentrations and causes natriuresis and diuresis.

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

41 ects, neurohormonal suppression and enhanced natriuresis and diuresis.

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

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

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

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

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

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

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

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

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

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

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

53 Since natriuresis as well as phosphaturia were observed in all

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 The natriuresis induced by amiloride was significantly great

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

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

84 Natriuresis is effectively induced by both furosemide an

85 Pressure natriuresis is impaired in hypertension and mechanistic

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

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

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

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

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

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

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

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

94 compensate for genetically impaired pressure-natriuresis mechanisms.

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

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

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

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

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

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

101 A brisk natriuresis precedes the escape from this antidiuresis.

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

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

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

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

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

107 ng observed haemodynamic changes or pressure-natriuresis relationships.

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

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

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

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

112 Biochemical indices of natriuresis showed bendroflumethiazide to be less effect

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

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

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

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

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

118 mpathoinhibitory response and attenuated the natriuresis to VE.

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

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

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

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

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

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

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

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

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

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

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

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

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

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