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1 induction of edn1 mRNA occurred in cortical, outer medullary, and inner medullary collecting duct cel
4 embrane of acid-secreting cells in the renal outer medullary collecting duct (OMCD) and in gastric pa
8 ells: The A-intercalated cells in the kidney outer medullary collecting duct and the gastric parietal
10 LC26A7 in enhanced bicarbonate absorption in outer medullary collecting duct in hypokalemia and in ac
13 cting segment, cortical collecting duct, and outer medullary collecting duct, whereas NaHCO(3) loadin
14 dney and lung and specifically to the kidney outer medullary collecting ducts by in situ hybridizatio
15 ng limbs of Henle's loop was strong, whereas outer medullary collecting ducts were weakly stained.
16 ing limb, distal nephron segments (inner and outer medullary collecting ducts), and macula densa-cont
17 d by in vitro microperfusion of cortical and outer medullary collecting ducts, was unaffected in muta
21 test the hypothesis that vasoconstriction of outer medullary descending vasa recta (OMDVR) is modulat
23 rdly rectifying K channels such as the renal outer medullary K (ROMK) channel (also called Kir1.1 and
25 WNK4 normally induces clearance of the renal outer medullary K(+) channel (ROMK) from the cell surfac
27 osterone-independent activation of the renal outer medullary K(+) channel and ENaC, to which angioten
28 K(+) diets induced upregulation of the renal outer medullary K(+) channel in AS(-/-) mice, whereas up
29 CaR had no comparable effect on the renal outer medullary K(+) channel, an apical membrane distal
30 expression of betaENaC, gammaENaC, the renal outer medullary K+ channel (ROMK), and total and phospho
31 Na+ reabsorption and K+ secretion via renal outer medullary K+ channel and now suggest that WNK4 is
32 ntly to mutations in an ATP-sensitive, renal outer medullary K+channel, ROMK, and earlier to mutation
35 but not by acid/base perturbations and that outer medullary NHE3 protein abundance is increased by c
38 inhibition of the potassium-excretory renal outer medullary potassium (ROMK) channel have also been
39 syndrome is caused by mutations in the renal outer medullary potassium (ROMK) channel, but the molecu
41 egulates the expression or function of renal outer medullary potassium (ROMK) channels, ENaCs, and Cl
45 epithelial sodium channel (ENaC), the renal outer medullary potassium channel (ROMK), and other tran
47 ne abundance of the renal K(+) channel renal outer medullary potassium channel 1 (ROMK1) by removing
48 n-tyrosine phosphatase (PTP) decreased renal outer medullary potassium channel 1 (ROMK1) channel acti
49 observe a decreased expression of the renal outer medullary potassium channel in the late distal con
50 +) (epithelial sodium channel), Cl(-), renal outer medullary potassium channel(+), and H(2)O channels
52 ty of epithelial sodium channel-alpha, renal outer medullary potassium channel, and Na(+), K(+)-ATPas
54 as localized predominantly to the recovering outer medullary proximal tubular cells and was highly co
55 ta) (flox) kidneys showed more cell death in outer medullary S3 segments at 2 hours but less tubular
56 cted, being detected only in differentiating outer medullary tubules and the vasa recta bundle area.
57 was markedly increased and extended into the outer medullary tubules in db/db mice, a model of type 2
59 chemia-related activation of JNK and p38 and outer medullary vascular congestion were markedly mitiga
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