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1 f inflammation and fibrosis of the kidney in salt-sensitive hypertension.
2  model observed for variants associated with salt-sensitive hypertension.
3 ute volume expansion, and the development of salt-sensitive hypertension.
4 -2 (COX-2) activity can induce or exacerbate 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 t in sodium handling and the pathogenesis of salt-sensitive hypertension.
8 unction mutations in the human channel cause salt-sensitive hypertension.
9 nterstitium sequesters excess Na+ and Cl- in salt-sensitive hypertension.
10 ed Na+, Cl-, and water retention in skin and salt-sensitive hypertension.
11 y, led to skin Cl- accumulation, and induced salt-sensitive hypertension.
12 ary prostaglandin E2 excretion and developed salt-sensitive hypertension.
13 dies indicate that oxidative stress mediates salt-sensitive hypertension.
14  relevant for kidney sodium reabsorption and salt-sensitive hypertension.
15 al gene expression dataset in a rat model of salt-sensitive hypertension.
16 oss of EP2 or IP receptor is associated with salt-sensitive hypertension.
17 ssociated with renal sodium reabsorption and salt-sensitive hypertension.
18 ncreases NO and cGMP production and prevents salt-sensitive hypertension.
19  (ENaC) is implicated in the pathogenesis of salt-sensitive hypertension.
20 a novel single-locus genetic model of severe salt-sensitive hypertension.
21 egation of the alpha1 Na,K-ATPase locus with salt-sensitive hypertension.
22 ransporter NCC, p-NCC and the development of salt-sensitive hypertension.
23 lume expansion and the clinical phenotype of salt-sensitive hypertension.
24 veral forms of high blood pressure including salt-sensitive hypertension.
25  inflammasome via IsoLG formation leading to salt-sensitive hypertension.
26 ) activity in the distal nephron and develop salt-sensitive hypertension.
27 ient diets impact the regular development of salt-sensitive hypertension.
28 n improved therapeutic approach for treating salt-sensitive hypertension.
29 h might be a potential therapeutic target in salt-sensitive hypertension.
30 tial therapeutic target for the treatment of salt-sensitive hypertension.
31 hanisms in the immune system contributing to salt-sensitive hypertension.
32 fects the regulation of acid-base balance in salt-sensitive hypertension.
33 with increased renal sodium reabsorption and salt-sensitive hypertension.
34 y cytokines to activate T cells and modulate salt-sensitive hypertension.
35 2)-derived superoxide in the pathogenesis of salt-sensitive hypertension.
36 hage polarization is blunted resulting in no salt-sensitive hypertension.
37 lack of a Cyp2c44 epoxygenase causes dietary salt-sensitive hypertension, a common form of the human
38 f exons 6-8 of Nedd4L in mice both result in salt-sensitive hypertension and elevated ENaC activity (
39 udohypoaldosteronism type II, a disease with salt-sensitive hypertension and hyperkalemia.
40            In several experimental models of salt-sensitive hypertension and in humans, blood pressur
41 on of the PGE2 type 4 (EP4) receptor induced salt-sensitive hypertension and increased phosphorylatio
42 In wild-type mice, the CNI tacrolimus caused salt-sensitive hypertension and increased the abundance
43 ted the hypothesis that the amplification of salt-sensitive hypertension and kidney damage in salt-se
44  (RhoGDIalpha) is involved in the control of salt-sensitive hypertension and renal injury via Rac1, w
45 tive (SS) rats, a widely used model of human salt-sensitive hypertension and renal injury.
46 and urinary excretion of uromodulin, causing salt-sensitive hypertension and renal lesions.
47 e EP2 receptor mediates arterial dilatation, salt-sensitive hypertension, and also plays an essential
48                Pcsk6-knockout mice developed salt-sensitive hypertension, and corin activation and pr
49 ter medulla between Dahl SS rats, a model of salt-sensitive hypertension, and salt-insensitive, conge
50                                The causes of salt-sensitive hypertension are extremely complex and ma
51  SGLT2 inhibition in a non-diabetic model of salt-sensitive hypertension blunts the development of sa
52  chronic caffeine administration antagonizes salt sensitive hypertension by promoting urinary sodium
53 he macula densa affects sodium excretion and salt-sensitive hypertension by decreasing tubuloglomerul
54  male, but not in female, db/db mice induces salt-sensitive hypertension by impairing ENaC downregula
55 xperimental autoimmune encephalomyelitis and salt-sensitive hypertension by modulating TH17 cells.
56 ribution of this gene to the pathogenesis of salt-sensitive hypertension by mutating Plekha7 in the D
57 se Liddle's syndrome, an autosomal dominant, salt-sensitive hypertension, by preventing the channel's
58  SGLT2 inhibition in a non-diabetic model of salt-sensitive hypertension, Dahl salt-sensitive (SS) ra
59                We used two common models for salt-sensitive hypertension: high salt and a deoxycortic
60 d to changes in sodium levels contributes to salt-sensitive hypertension in Cx30(-/-) mice.
61 ic susceptibility for arterial stiffness and salt-sensitive hypertension in Dahl rats based upon repo
62 epoxygenase activities and/or regulation and salt-sensitive hypertension in Dahl rats.
63                                              Salt-sensitive hypertension in male mice was associated
64 ay contribute to increased ENaC activity and salt-sensitive hypertension in mice with Cx30 deficiency
65 ceptor pathway in hematopoietic cells causes salt-sensitive hypertension in mice.
66 MP-elevating hormones, and may contribute to salt-sensitive hypertension in patients with endocrine d
67 a,K-ATPase gene as a susceptibility gene for salt-sensitive hypertension in the Dahl S rat model, and
68 , chronic obstructive pulmonary disease, and salt-sensitive hypertension induce a systemic proinflamm
69 anistic link between ENaC, inflammation, and salt-sensitive hypertension involving NLRP3 inflammasome
70                    Our findings suggest that salt-sensitive hypertension is not due solely to renal d
71 lls contribute to renal sodium retention and salt-sensitive hypertension is unknown.
72       Salt sensitivity of arterial pressure (salt-sensitive hypertension) is a serious global health
73 ether EGF influences ENaC, perhaps mediating salt-sensitive hypertension, is not well understood.
74        Transgenic Dahl S rats exhibited less salt-sensitive hypertension, less hypertensive renal dis
75 of 11beta-HSD1 in fat is sufficient to cause salt-sensitive hypertension mediated by an activated RAS
76                          The pathogenesis of salt-sensitive hypertension remains poorly defined, but
77 tical model that does not limit the cause of salt-sensitive hypertension solely to primary renal dysf
78 els of ANP correlate with the development of salt-sensitive hypertension (SS-HTN).
79 geted disruption of the EP2 receptor exhibit salt-sensitive hypertension, suggesting that this recept
80       gamma-MSH deficiency results in marked salt-sensitive hypertension that is rapidly improved wit
81 caffeine intake prevented the development of salt-sensitive hypertension through promoting urinary so
82 pathogenesis of renal injury and fibrosis in salt-sensitive hypertension through regulation of bone m
83 luence salt and water retention and risk for salt-sensitive hypertension, was genotyped in >1,000 ind
84 ult renal tubules causes a new form of mild, salt-sensitive hypertension without hyperkalemia that is