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1  receptors by candesartan on the exaggerated tubuloglomerular feedback (TGF) activity in 7-wk-old, eu
2  total autoregulatory efficiency, reflecting tubuloglomerular feedback (TGF) and possibly one or two
3                                Initiation of tubuloglomerular feedback (TGF) depends on Na-K-2Cl co-t
4                                              Tubuloglomerular feedback (TGF) describes the negative r
5 densa nitric oxide generation and actions on tubuloglomerular feedback (TGF) during salt restriction.
6 he pathogenesis of diabetic nephropathy, and tubuloglomerular feedback (TGF) has been suggested to pl
7 ngement suggested that a marked reduction in tubuloglomerular feedback (TGF) in Cx40-ko mice was resp
8 studies demonstrated that stimulation of the tubuloglomerular feedback (TGF) mechanism by increasing
9 ion, and failure to regulate GFR through the tubuloglomerular feedback (TGF) mechanism.
10               Direct measurements of maximal tubuloglomerular feedback (TGF) responses were made from
11                                              Tubuloglomerular feedback (TGF) stabilizes nephron funct
12                                          The tubuloglomerular feedback (TGF) system was used as a too
13 after an overshoot at 40 s (second response, tubuloglomerular feedback (TGF)).
14 -transporter may be a site for regulation of tubuloglomerular feedback (TGF), and recently angiotensi
15 terioles has been suggested to contribute to tubuloglomerular feedback (TGF), the vasoconstriction el
16 stments in GFR through the normal actions of tubuloglomerular feedback (TGF).
17 al reabsorption which reduces the signal for tubuloglomerular feedback (TGF).
18            Nephron function is stabilized by tubuloglomerular feedback (TGF).
19 n tubules and afferent arterioles (so-called tubuloglomerular feedback [TGF]).
20                           On the other hand, tubuloglomerular feedback activity is often directly pro
21                                              Tubuloglomerular feedback function curve as determined b
22 omerular feedback responses were normal, but tubuloglomerular feedback function curves were right-shi
23 rular apparatus was still able to respond to tubuloglomerular feedback in isolated perfused juxtaglom
24                                     Although tubuloglomerular feedback is normal in these animals, th
25                                         This tubuloglomerular feedback mechanism plays an important r
26  consisting of the myogenic response and the tubuloglomerular feedback mechanism, the myogenic respon
27  NKCC2 may permit transport and Cl-dependent tubuloglomerular feedback regulation to occur over a wid
28 tubule, consistent with a role of MD nNOS in tubuloglomerular feedback resetting.
29 rms (MD-NOS1KO) had a significantly enhanced tubuloglomerular feedback response and after acute volum
30 lt sensitivity of BP and the significance of tubuloglomerular feedback response in long-term control
31                                          The tubuloglomerular feedback response, the change in affere
32 ressed in the macula densa and regulates the tubuloglomerular feedback response, the natriuretic resp
33 nsin-aldosterone system (RAAS) and the renal tubuloglomerular feedback response.
34              Angiotensin II (AngII) enhances tubuloglomerular feedback responses and is considered to
35                         Furthermore, whereas tubuloglomerular feedback responses did not change signi
36 AT1 receptor blockade by candesartan reduced tubuloglomerular feedback responses to a flow rate step
37 sence of NKCC2A in the macula densa, maximum tubuloglomerular feedback responses were normal, but tub
38 nd salt-sensitive hypertension by decreasing tubuloglomerular feedback responsiveness.
39 e (NO) is an important negative modulator of tubuloglomerular feedback responsiveness.
40 e via AT1 receptors and therefore may affect tubuloglomerular feedback signal transmission, at least
41 vide compelling new evidence indicating that tubuloglomerular feedback signals are coupled to autoreg
42 proximal tubular natriuresis activates renal tubuloglomerular feedback through increased macula densa
43 the TALH was reduced but not eliminated, and tubuloglomerular feedback was severely impaired.
44 s, we studied NaCl-dependent GFR regulation (tubuloglomerular feedback) in mice with targeted deletio
45                   Furthermore, we found that tubuloglomerular feedback, a mechanism that links proxim
46 tion via its effects on renal arterioles and tubuloglomerular feedback, but effects of adenosine bloc
47 tribute to the enhanced basal vascular tone, tubuloglomerular feedback, monocyte/macrophage infiltrat
48                                Activation of tubuloglomerular feedback, previously thought to contrib
49                                              Tubuloglomerular feedback, which is an angiotensin II-de
50  flow past the macula densa, thus minimizing tubuloglomerular feedback-dependent influences on affere
51 he GFR supranormal through the physiology of tubuloglomerular feedback.
52 whereas glomeruli respond to tubules through tubuloglomerular feedback.
53 absorption of NaCl in the TALH, and impaired tubuloglomerular feedback.
54 macula densa, providing the error signal for tubuloglomerular feedback.
55 omerular hemodynamics, including the role of tubuloglomerular feedback.

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