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1 so expressed in thick ascending limb and the macula densa.
2 marily adjusting transport downstream of the macula densa.
3 ortant in its highly specialized role in the macula densa.
4 helial cells of the thick ascending limb and macula densa.
5 ck ascending limb of Henle's loop and of the macula densa.
6 , with the most pronounced expression in the macula densa.
7 old in the cortical thick ascending limb and macula densa.
8 in vitro and stimulates NO generation at the macula densa.
9  immunoreactive COX-2 expression inthe cTALH/macula densa.
10 nificantly fell 2-fold in arterioles and the macula densa.
11 is had low AT1R expression in arterioles and macula densa.
12 r upregulation of NOS1beta expression in the macula densa affects sodium excretion and salt-sensitive
13 onship between (a) NaCl concentration at the macula densa and (b) glomerular filtration rate or glome
14 at tubular epithelial cells located near the macula densa and associated with the renal arterioles ex
15  1 (NOS1)-dependent nitric oxide (NO) in the macula densa and blunting the tubuloglomerular feedback
16 rtical pp38 expression, predominantly in the macula densa and cTALH.
17 a is a primary NOS1 isoform expressed in the macula densa and regulates the tubuloglomerular feedback
18 nal cortex, COX-2 expression is localized to macula densa and surrounding cortical thick ascending li
19 ocalized to cTALH cells in the region of the macula densa, and that dietary salt restriction increase
20               Evidence for the regulation of macula densa apical Na/H exchange by AngII was recently
21 lar elements involves ATP release across the macula densa basolateral membrane through a maxi-anion c
22 These results indicate that AngII stimulates macula densa basolateral Na/H exchange via AT1 receptors
23 p38 stimulates COX-2 expression in cTALH and macula densa by transcriptional regulation predominantly
24 erences in glomerular tuft contractility and macula densa cell calcium handling were observed.
25 activity or expression we clonally derived a macula densa cell line (MMDD1 cells) from SV-40 transgen
26 nd AT(2) receptor expression in the cultured macula densa cell line MMDD1.
27                                      Because macula densa cells also express a basolateral Na/H excha
28                                              Macula densa cells are renal sensor elements that detect
29                                              Macula densa cells detect changes in luminal sodium chlo
30                                              Macula densa cells in the distal nephron, according to t
31                           Communication from macula densa cells to the glomerular vascular elements i
32 tion, sodium-glucose cotransport by SGLT1 on macula densa cells triggers the production of nitric oxi
33 rabbit kidney, the intracellular pH (pHi) of macula densa cells was measured with fluorescence micros
34 neuronal isoform of nitric oxide synthase in macula densa cells, reduces the constrictor effect of ad
35     The Ca2+ oscillations were absent in the macula densa cells.
36 e expressed Nos1 and Avpr1a, consistent with macula densa cells.
37 trated marked accumulation of elastin in the macula densa, collecting ducts, and pelvicalyceal epithe
38 r and outer medullary collecting ducts), and macula densa-containing segments.
39   In summary, these results demonstrate that macula densa COX-2 expression is oppositely regulated by
40                                              Macula densa cyclooxygenase 2 (COX-2)-derived prostaglan
41 ice had decreased hyperfiltration, decreased macula densa cyclooxygenase-2 expression, decreased albu
42 al delivery of fluid yet does not activate a macula densa-dependent fall in SNGFR because it blunts t
43 ) senses increases in luminal glucose at the macula densa, enhancing generation of neuronal nitric ox
44                                              Macula densa epithelial cells displayed bright AE2 immun
45 lar epithelial cells at the perimeter of the macula densa exhibit spontaneous oscillations in intrace
46                       We recently found that macula densa expresses alpha-, beta-, and gamma-splice v
47 ty NKCC2B contributes to salt absorption and macula densa function in the low NaCl concentration rang
48 on microscopy is providing new insights into macula densa-glomerular signaling.
49 e also showed that SGLT1 is expressed at the macula densa; in the presence of tubular glucose, SGLT1
50 ase 1 (NOS1), and NOS1beta expression in the macula densa increases on a high-salt diet.
51 luminal chloride [Cl(-)] at the level of the macula densa increases renin production and secretion, w
52 nt of nitric oxide synthase 1 (NOS1B) in the macula densa is a primary modulator of TGF, we evaluated
53 sed by a change in NaCl concentration at the macula densa, is likely initiated by the generation of a
54 that ATP consumed in active transport by the macula densa leads to formation of adenosine, which caus
55     Because of the presence of NKCC2A in the macula densa, maximum tubuloglomerular feedback response
56                                              Macula densa (MD) cells detect changes in distal tubular
57                                              Macula densa (MD) cells express COX-2 and COX-2-derived
58                                              Macula densa (MD) cells of the juxtaglomerular apparatus
59 nd G(olf) colocalize in renal tubules and in macula densa (MD) cells which modulate glomerular filtra
60  of neuronal nitric oxide synthase (nNOS) in macula densa (MD) cells, experiments were performed in a
61                                          The macula densa (MD) is a distinct cluster of approximately
62 d NKCC2A were shown to be coexpressed in the macula densa (MD) segment of the mouse TAL.
63 TGF) depends on Na-K-2Cl co-transport in the macula densa (MD), but it is less clear whether Na,K-ATP
64 che of a minority renal cell type called the macula densa (MD).
65 merular cell granules and exhibit an altered macula densa morphology.
66          Here, we tested the hypothesis that macula densa neuronal nitric oxide synthase (NOS1) is up
67  and/or cellular uptake of L-arginine limits macula densa nitric oxide generation and actions on tubu
68 tion, which was prevented with inhibitors of macula densa nitric oxide synthase (NOS).
69                                 Furthermore, macula densa NO production was similar in the isolated p
70 S (NOS-I) blockers correlated with increased macula densa NOS-I immunoreactivity.
71 flow and SNGFR through a mechanism involving macula densa NOS.
72 etion of SGLT1 prevented the upregulation of macula densa NOS1 and attenuated inhibition of TGF in di
73                Diabetic mice had upregulated macula densa NOS1, inhibited TGF and elevated GFR.
74                                              Macula densa NOS1B plays a critical role in the control
75                                              Macula densa NOS1B was upregulated during pregnancy, res
76 dition, RUPP resulted in a downregulation in macula densa NOS1B, enhanced TGF, decreased GFR, and hyp
77 reduced uterine perfusion pressure (RUPP) on macula densa NOS1B/NO levels, TGF responsiveness, GFR, a
78 sting that it had blunted the effects of the macula densa on SNGFR.
79 ine and autocrine factors of endothelial and macula densa origins.
80            It also suggests that the altered macula densa phenotype is related to the activity of the
81 lar cells that were within 100 microm of the macula densa plaque using four-dimensional multiphoton m
82 the thick ascending loop of Henle (TALH) and macula densa, providing the error signal for tubuloglome
83   Reducing luminal NaCl concentration in the macula densa region of the nephron stimulates renin secr
84 ited by changes in NaCl concentration in the macula densa region of the nephron, thereby serving as a
85 tion elicited by elevations in [NaCl] in the macula densa region of the nephron.
86                                              Macula densa-selective NOS1 knockout attenuated the diab
87  we discuss recent advances in understanding macula densa sensing and suggest these cells, in additio
88      Thus, our findings demonstrate that the macula densa SGLT1-NOS1-TGF pathway plays a crucial role
89  tubuloglomerular feedback through increased macula densa sodium and chloride delivery, leading to af
90        Compared with control mice, mice with macula densa-specific knockout of all nitric oxide synth
91 responsiveness, GFR, and BP in wild-type and macula densa-specific NOS1 knockout (MD-NOS1KO) mice.
92                                           In macula densa-specific NOS1 knockout mice, glucose had no
93  macula densa, TGF, and GFR in wild-type and macula densa-specific NOS1 knockout mice.
94 -deficient (Akita) diabetes in wild-type and macula densa-specific NOS1 knockout mice.
95 was unable to rescue the abnormality seen in macula densa structure.
96 sphorylation, nitric oxide production in the macula densa, TGF response, and GFR during the early sta
97 s of tubular glucose on NO generation at the macula densa, TGF, and GFR in wild-type and macula densa
98 tracellular calcium dynamics in cells of the macula densa, the observation was made that tubular epit
99 ized that pregnancy upregulates NOS1B in the macula densa, thus blunting TGF, allowing the GFR to inc
100 interrupt distal tubular fluid flow past the macula densa, thus minimizing tubuloglomerular feedback-
101 e induces tubuloglomerular feedback from the macula densa to increase GFR.
102  the context of signal transduction from the macula densa to the mesangial cells and afferent arterio
103  at least in part, through direct effects on macula densa transport processes.
104  wherein increases in luminal glucose at the macula densa upregulate the expression and activity of N

 
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