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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
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
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
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
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
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
32 ressed in the macula densa and regulates the tubuloglomerular feedback response, the natriuretic resp
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
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
44 s, we studied NaCl-dependent GFR regulation (tubuloglomerular feedback) in mice with targeted deletio
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
50 flow past the macula densa, thus minimizing tubuloglomerular feedback-dependent influences on affere
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