ライフサイエンスコーパス: tubuloglomerular feedback

1 he GFR supranormal through the physiology of tubuloglomerular feedback.

2 whereas glomeruli respond to tubules through tubuloglomerular feedback.

3 absorption of NaCl in the TALH, and impaired tubuloglomerular feedback.

4 macula densa, providing the error signal for tubuloglomerular feedback.

5 eabsorption in the proximal tubule, altering tubuloglomerular feedback.

6 omerular hemodynamics, including the role of tubuloglomerular feedback.

7 Furthermore, we found that tubuloglomerular feedback, a mechanism that links proxim

8 On the other hand, tubuloglomerular feedback activity is often directly pro

9 e GFR by a mechanism that partially involves tubuloglomerular feedback, and suppressing gut microbes

10 tion via its effects on renal arterioles and tubuloglomerular feedback, but effects of adenosine bloc

11 anism, we tested the hypothesis that altered tubuloglomerular feedback contributes to elevated GFR us

12 ek 3 but not week 5, suggesting that altered tubuloglomerular feedback contributes to the initial inc

13 flow past the macula densa, thus minimizing tubuloglomerular feedback-dependent influences on affere

14 rreabsorption of sodium and chloride induces tubuloglomerular feedback from the macula densa to incre

15 Tubuloglomerular feedback function curve as determined b

16 omerular feedback responses were normal, but tubuloglomerular feedback function curves were right-shi

17 odium to the distal nephron and may activate tubuloglomerular feedback in a similar way to SGLT2is wi

18 rular apparatus was still able to respond to tubuloglomerular feedback in isolated perfused juxtaglom

19 s, we studied NaCl-dependent GFR regulation (tubuloglomerular feedback) in mice with targeted deletio

20 Tubuloglomerular feedback initially contributes to the m

21 Although tubuloglomerular feedback is normal in these animals, th

22 This tubuloglomerular feedback mechanism plays an important r

23 consisting of the myogenic response and the tubuloglomerular feedback mechanism, the myogenic respon

24 tribute to the enhanced basal vascular tone, tubuloglomerular feedback, monocyte/macrophage infiltrat

25 Activation of tubuloglomerular feedback, previously thought to contrib

26 NKCC2 may permit transport and Cl-dependent tubuloglomerular feedback regulation to occur over a wid

27 isturbances, including hypertension, altered tubuloglomerular feedback, renal hypoxia, lipotoxicity,

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 e (NO) is an important negative modulator of tubuloglomerular feedback responsiveness.

39 nd salt-sensitive hypertension by decreasing tubuloglomerular feedback responsiveness.

40 e via AT1 receptors and therefore may affect tubuloglomerular feedback signal transmission, at least

41 eabsorption of sodium and glucose, normalize tubuloglomerular feedback signals and mitigate hyperfilt

42 vide compelling new evidence indicating that tubuloglomerular feedback signals are coupled to autoreg

43 receptors by candesartan on the exaggerated tubuloglomerular feedback (TGF) activity in 7-wk-old, eu

44 total autoregulatory efficiency, reflecting tubuloglomerular feedback (TGF) and possibly one or two

45 Initiation of tubuloglomerular feedback (TGF) depends on Na-K-2Cl co-t

46 Tubuloglomerular feedback (TGF) describes the negative r

47 densa nitric oxide generation and actions on tubuloglomerular feedback (TGF) during salt restriction.

48 he pathogenesis of diabetic nephropathy, and tubuloglomerular feedback (TGF) has been suggested to pl

49 ngement suggested that a marked reduction in tubuloglomerular feedback (TGF) in Cx40-ko mice was resp

50 Regulation of renal hemodynamics and BP via tubuloglomerular feedback (TGF) may be an important adap

51 studies demonstrated that stimulation of the tubuloglomerular feedback (TGF) mechanism by increasing

52 ion, and failure to regulate GFR through the tubuloglomerular feedback (TGF) mechanism.

53 ic myogenic response and the kidney-specific tubuloglomerular feedback (TGF) mechanism.

54 e 1 (SGLT1) in diabetes, which then inhibits tubuloglomerular feedback (TGF) promoting glomerular hyp

55 de (NO) in the macula densa and blunting the tubuloglomerular feedback (TGF) response, thereby promot

56 Direct measurements of maximal tubuloglomerular feedback (TGF) responses were made from

57 Tubuloglomerular feedback (TGF) stabilizes nephron funct

58 The tubuloglomerular feedback (TGF) system was used as a too

59 after an overshoot at 40 s (second response, tubuloglomerular feedback (TGF)).

60 -transporter may be a site for regulation of tubuloglomerular feedback (TGF), and recently angiotensi

61 terioles has been suggested to contribute to tubuloglomerular feedback (TGF), the vasoconstriction el

62 stments in GFR through the normal actions of tubuloglomerular feedback (TGF).

63 al reabsorption which reduces the signal for tubuloglomerular feedback (TGF).

64 Nephron function is stabilized by tubuloglomerular feedback (TGF).

65 n tubules and afferent arterioles (so-called tubuloglomerular feedback [TGF]).

66 proximal tubular natriuresis activates renal tubuloglomerular feedback through increased macula densa

67 the TALH was reduced but not eliminated, and tubuloglomerular feedback was severely impaired.

68 Tubuloglomerular feedback, which is an angiotensin II-de

69 odium to the distal tubule and activation of tubuloglomerular feedback, which lowers GFR and intraglo