ライフサイエンスコーパス: salt-sensitive hypertension

1 t in sodium handling and the pathogenesis of salt-sensitive hypertension.

2 ute volume expansion, and the development of salt-sensitive hypertension.

3 -2 (COX-2) activity can induce or exacerbate salt-sensitive hypertension.

4 relevant for kidney sodium reabsorption and salt-sensitive hypertension.

5 etic cells can result in a predisposition to salt-sensitive hypertension.

6 during adaption to high dietary salt causes salt-sensitive hypertension.

7 unction mutations in the human channel cause salt-sensitive hypertension.

8 nterstitium sequesters excess Na+ and Cl- in salt-sensitive hypertension.

9 ed Na+, Cl-, and water retention in skin and salt-sensitive hypertension.

10 y, led to skin Cl- accumulation, and induced salt-sensitive hypertension.

11 ary prostaglandin E2 excretion and developed salt-sensitive hypertension.

12 dies indicate that oxidative stress mediates salt-sensitive hypertension.

13 al gene expression dataset in a rat model of salt-sensitive hypertension.

14 ransporter NCC, p-NCC and the development of salt-sensitive hypertension.

15 oss of EP2 or IP receptor is associated with salt-sensitive hypertension.

16 ssociated with renal sodium reabsorption and salt-sensitive hypertension.

17 ncreases NO and cGMP production and prevents salt-sensitive hypertension.

18 (ENaC) is implicated in the pathogenesis of salt-sensitive hypertension.

19 a novel single-locus genetic model of severe salt-sensitive hypertension.

20 egation of the alpha1 Na,K-ATPase locus with salt-sensitive hypertension.

21 lume expansion and the clinical phenotype of salt-sensitive hypertension.

22 model observed for variants associated with salt-sensitive hypertension.

23 lack of a Cyp2c44 epoxygenase causes dietary salt-sensitive hypertension, a common form of the human

24 f exons 6-8 of Nedd4L in mice both result in salt-sensitive hypertension and elevated ENaC activity (

25 udohypoaldosteronism type II, a disease with salt-sensitive hypertension and hyperkalemia.

26 In several experimental models of salt-sensitive hypertension and in humans, blood pressur

27 on of the PGE2 type 4 (EP4) receptor induced salt-sensitive hypertension and increased phosphorylatio

28 In wild-type mice, the CNI tacrolimus caused salt-sensitive hypertension and increased the abundance

29 (RhoGDIalpha) is involved in the control of salt-sensitive hypertension and renal injury via Rac1, w

30 tive (SS) rats, a widely used model of human salt-sensitive hypertension and renal injury.

31 and urinary excretion of uromodulin, causing salt-sensitive hypertension and renal lesions.

32 e EP2 receptor mediates arterial dilatation, salt-sensitive hypertension, and also plays an essential

33 Pcsk6-knockout mice developed salt-sensitive hypertension, and corin activation and pr

34 ter medulla between Dahl SS rats, a model of salt-sensitive hypertension, and salt-insensitive, conge

35 The causes of salt-sensitive hypertension are extremely complex and ma

36 chronic caffeine administration antagonizes salt sensitive hypertension by promoting urinary sodium

37 he macula densa affects sodium excretion and salt-sensitive hypertension by decreasing tubuloglomerul

38 xperimental autoimmune encephalomyelitis and salt-sensitive hypertension by modulating TH17 cells.

39 ribution of this gene to the pathogenesis of salt-sensitive hypertension by mutating Plekha7 in the D

40 se Liddle's syndrome, an autosomal dominant, salt-sensitive hypertension, by preventing the channel's

41 d to changes in sodium levels contributes to salt-sensitive hypertension in Cx30(-/-) mice.

42 ic susceptibility for arterial stiffness and salt-sensitive hypertension in Dahl rats based upon repo

43 epoxygenase activities and/or regulation and salt-sensitive hypertension in Dahl rats.

44 ceptor pathway in hematopoietic cells causes salt-sensitive hypertension in mice.

45 a,K-ATPase gene as a susceptibility gene for salt-sensitive hypertension in the Dahl S rat model, and

46 , chronic obstructive pulmonary disease, and salt-sensitive hypertension induce a systemic proinflamm

47 Our findings suggest that salt-sensitive hypertension is not due solely to renal d

48 lls contribute to renal sodium retention and salt-sensitive hypertension is unknown.

49 Salt sensitivity of arterial pressure (salt-sensitive hypertension) is a serious global health

50 ether EGF influences ENaC, perhaps mediating salt-sensitive hypertension, is not well understood.

51 Transgenic Dahl S rats exhibited less salt-sensitive hypertension, less hypertensive renal dis

52 of 11beta-HSD1 in fat is sufficient to cause salt-sensitive hypertension mediated by an activated RAS

53 The pathogenesis of salt-sensitive hypertension remains poorly defined, but

54 tical model that does not limit the cause of salt-sensitive hypertension solely to primary renal dysf

55 geted disruption of the EP2 receptor exhibit salt-sensitive hypertension, suggesting that this recept

56 gamma-MSH deficiency results in marked salt-sensitive hypertension that is rapidly improved wit

57 caffeine intake prevented the development of salt-sensitive hypertension through promoting urinary so

58 pathogenesis of renal injury and fibrosis in salt-sensitive hypertension through regulation of bone m

59 luence salt and water retention and risk for salt-sensitive hypertension, was genotyped in >1,000 ind

60 ult renal tubules causes a new form of mild, salt-sensitive hypertension without hyperkalemia that is