ライフサイエンスコーパス: reabsorption

1 tubule in mice resulted in impaired renal Pi reabsorption.

2 %) for pseudouridine, indicating partial net reabsorption.

3 n exchange rather than the effect on glucose reabsorption.

4 was related to the changes in tubular Na(+) reabsorption.

5 ular filtration rate (GFR) and tubular Na(+) reabsorption.

6 novel method of regulation for distal sodium reabsorption.

7 V5 endocytosis and increases urinary calcium reabsorption.

8 l tubule, which is the site of renal glucose reabsorption.

9 dney, claudin-2 mediates paracellular sodium reabsorption.

10 epithelia, thus contributing to renal Ca(2+) reabsorption.

11 ubule is the major pathway for renal glucose reabsorption.

12 bone resorption and increasing renal calcium reabsorption.

13 regulating calcium and phosphate absorption/reabsorption.

14 rapid renal clearance followed by high renal reabsorption.

15 tion via increased proximal tubule phosphate reabsorption.

16 glucose stimulates NHE3-mediated bicarbonate reabsorption.

17 (DCT) plays a critical role in renal sodium reabsorption.

18 etion and increases fractional renal calcium reabsorption.

19 mechanisms that ensure proper salt and water reabsorption.

20 subunits expression and ENaC-mediated sodium reabsorption.

21 buminuria, and the oxygen demand for tubular reabsorption.

22 fundamental for renal and intestinal sodium reabsorption.

23 NaPi-IIa is responsible for most P(i) renal reabsorption.

24 absorption of vitamin B12 and renal protein reabsorption.

25 lation of renal HCO(3(-)) secretion and salt reabsorption.

26 C-terminal half of cubilin in renal albumin reabsorption.

27 protecting Na(+) balance to promoting water reabsorption.

28 pathway permeability but did not change NaCl reabsorption.

29 provides the driving force for renal sodium reabsorption.

30 ted that SGLT2 mediates 90% of renal glucose reabsorption.

31 ier and increases the oxygen demand to drive reabsorption.

32 protein uptake via endocytosis and PT water reabsorption.

33 decreased paracellular calcium and magnesium reabsorption.

34 d-loop perfusion system to investigate renal reabsorption.

35 enable fundamental studies of filtration and reabsorption.

36 hose renal excretion is coupled to uric acid reabsorption.

37 fluconazole increased transepithelial water reabsorption.

38 d eclosion, and promoting an increase in egg reabsorption.

39 metabolism, including hepatic synthesis and reabsorption.

40 nduced sodium release did not undergo distal reabsorption.

41 order membrane of RPTCs, and reduced glucose reabsorption.

42 AT in the regulation of intestinal bile acid reabsorption..

43 es in glomerular permselectivity and tubular reabsorption account, at least in part, for the proteins

44 in the proximal tubule and Henle's loop from reabsorption (acid load) to secretion (base load).

45 mediates the effect of vasopressin on sodium reabsorption along the distal nephron.

46 delivery are the main determinants of Na(+) reabsorption along the kidney tubule.

47 Upon reduced Na(+) intake, reabsorption along the nephron is adjusted with activati

48 Lymphatic reabsorption also may contribute to UFF, but little is k

49 MAGE-D2 is essential for fetal renal salt reabsorption, amniotic fluid homeostasis, and the mainte

50 Given the critical role of TRPM6 in Mg(2+) reabsorption, an inducible kidney-specific Adcy3 deletio

51 The alveolar ridge undergoes reabsorption and atrophy subsequent to tooth removal and

52 ns (CV) are required for cerebrospinal fluid reabsorption and brain homeostasis, but mechanisms that

53 The tubular nephron is responsible for reabsorption and catabolism of filtered low molecular we

54 e inner ear, where they are involved in NaCl reabsorption and endolymph production, respectively.

55 bute to calcium homeostasis by adjusting the reabsorption and excretion of filtered calcium through p

56 trators free of toxic elements, with reduced reabsorption and extended coverage of the solar spectrum

57 Thanks to the suppressed reabsorption and high emission efficiencies of the quant

58 ese changes associated with less bicarbonate reabsorption and higher lithium clearance in females.

59 lemia resulting from constitutive renal salt reabsorption and impaired K(+) secretion.

60 and cubilin, mediates renal proximal-tubular reabsorption and is decreased in Dent disease because of

61 orchestrating the balance between renal salt reabsorption and K(+) and H(+) excretion.

62 sporter-2 (SGLT2) inhibitors prevent glucose reabsorption and lower serum uric acid levels.

63 -glucose cotransport enhance proximal tubule reabsorption and make the GFR supranormal through the ph

64 The FcRn pathway facilitates reabsorption and mediates transcytosis by its pH-depende

65 tical TAL, CaSR inhibitors increased calcium reabsorption and paracellular pathway permeability but d

66 m, coordination between transcellular sodium reabsorption and paracellular permeability may prevent t

67 nsing receptor (CaR) modulates renal calcium reabsorption and parathyroid hormone (PTH) secretion and

68 ride pores to facilitate electrogenic sodium reabsorption and potassium and acid secretion.

69 eceptor, that differentially controls sodium reabsorption and potassium secretion in the late distal

70 vide insights into the mechanisms of protein reabsorption and potential targets for treating diabetic

71 This dye has significant probability of reabsorption and re-emission in concentrated solutions w

72 ivation, which is relevant for kidney sodium reabsorption and salt-sensitive hypertension.

73 cellular pH (pHo), and contributes to solute reabsorption and secretion in many epithelia.

74 tes to the regulation of AQP2-mediated water reabsorption and suggest new potential therapeutic strat

75 s regulating hypoxia signalling, lung liquid reabsorption and surfactant maturation, which may be an

76 Thus, the mechanisms of albumin reabsorption and transcytosis are undergoing intense stu

77 This pathway fine-tunes renal water reabsorption and urinary concentration, and its perturba

78 ated water channel that controls renal water reabsorption and urine concentration.

79 ortant physiological function in renal water reabsorption, and AQP3-mediated hydrogen peroxide (H(2)O

80 en KLHL3 and CUL3 mutations, increased Na-Cl reabsorption, and disease pathogenesis.

81 photoluminescence quantum yield (PLQY), low reabsorption, and high stability.

82 rmation of angiotensinogen, increased sodium reabsorption, and increased renal fibrosis.

83 that vascular flow, tubular dilation, water reabsorption, and intratubular flow all play important r

84 vated serum FGF23, decreased renal phosphate reabsorption, and low serum concentrations of phosphate

85 ts high photoluminescence quantum yield, low reabsorption, and relatively low refractive indices for

86 ncreased urine cAMP levels, water and sodium reabsorption, and urine osmolality and decreased urine o

87 ecreased urine cAMP levels, water and sodium reabsorption, and urine osmolality and increased urine o

88 Ab), decreased urine cAMP levels, free water reabsorption, and urine osmolality and increased urine o

89 renal hemodynamics, inhibits salt and fluid reabsorption, antagonizes the renin-angiotensin system,

90 a regulated paracellular pathway for calcium reabsorption, approaches to regulate this transport path

91 O2 consumption and the efficiency of sodium reabsorption are dependent on sodium diet.

92 egment, luminal delivery and transepithelial reabsorption are directly coupled, a phenomenon called g

93 this model, both albumin uptake and glucose reabsorption are quantified as a function of time.

94 f transporters mediating renal tubular Na(+) reabsorption are well established causes of hypertension

95 ely filtered at the renal glomerulus without reabsorption at the tubule.

96 on of the pH-sensitive fluorophore, provides reabsorption based excitation of the dye, the spectrally

97 lly attributed to primary impairments in CSF reabsorption, but little experimental evidence supports

98 DR due to compensatory distal tubular sodium reabsorption, but whether this translates to human DR is

99 in, the two major hormones regulating sodium reabsorption by CD, generate a coordinated stimulation o

100 l Na/K/2Cl cotransporter NKCC2 regulate NaCl reabsorption by epithelial cells of the renal thick asce

101 phrocytes and studied the effects on protein reabsorption by lacuna channels and filtration by the sl

102 l anion exchanger AE2; and (3) inhibits NaCl reabsorption by mediating (with AE2) net NaCl backflux i

103 Impaired albumin reabsorption by proximal tubular epithelial cells (PTECs

104 receptor (CSR), in the regulation of Ca(2+) reabsorption by salivary gland ducts.

105 Inhibiting glucose reabsorption by sodium glucose co-transporter proteins (

106 Klotho, a protein that supports renal Ca(2+) reabsorption by stabilizing the transient receptor poten

107 glomerular filtration barrier and subsequent reabsorption by the downstream proximal tubule, causing

108 The results indicate that the reabsorption corrections, applied on molecular emission

109 etion of d-lactate in exchange for uric acid reabsorption culminated in hyperuricemia and gout.

110 tical modelling predicted that tubular Na(+) reabsorption decreased in the proximal tubule but increa

111 ion results predicted that the segment's Na+ reabsorption decreased significantly, resulting in natri

112 invaginations offered a strong indication of reabsorption defects.

113 ll facilitate studies of mechanisms in renal reabsorption, demonstrate that Dent disease-causing CLC-

114 an oxidative stress and AQP2-dependent water reabsorption disturbs.

115 sed 2.8-fold, suggesting enhanced intestinal reabsorption due to induction of ileal transporters (Slc

116 ) uptake during MAc; (2) inhibits HCO(3) (-) reabsorption during MAlk by opposing HCO(3) (-) efflux v

117 nce of this pathway in the control of sodium reabsorption during the initiation of chronic kidney dis

118 during exercise, resulting in a decrease in reabsorption efficiency at higher sweat rates.

119 lar mechanisms underlying AVP-mediated water reabsorption, evidenced by our identification of 4-acety

120 FABP in the liver, and renal elimination and reabsorption facilitated by OAT proteins.

121 lucocorticoid by 11betaHSD1 stimulates Na(+) reabsorption; failure to downregulate the enzyme during

122 contributes to the increase in renal sodium reabsorption following a meal.

123 tive distal nephron where it performs sodium reabsorption from the lumen.

124 consuming cellular processes such as glucose reabsorption, gluconeogenesis and cytoskeletal remodelli

125 or which targets the kidney to block glucose reabsorption, has the potential to improve kidney diseas

126 porin-2 trafficking and the consequent water reabsorption, however, are not completely understood.

127 Increased renal tubular sodium reabsorption impairs pressure natriuresis and plays an i

128 ivation of beta1-AR stimulates active Ca(2+) reabsorption in DCT2/CNT; an increase in TRPV5 activity

129 y, proteins involved in transcellular Ca(2+) reabsorption in DCTs were not decreased.

130 r excretion is achieved by continuous sodium reabsorption in distal nephron segments with low water p

131 and suggest that reduced PT sodium and water reabsorption in Fanconi syndrome may contribute to prote

132 the nephron and suggest that lower proximal reabsorption in female rats expedites excretion of a sal

133 hy are they unable to inhibit 90% of glucose reabsorption in humans?

134 -)-cotransporter (NKCC2) is crucial for NaCl reabsorption in kidney thick ascending limb (TAL) and dr

135 tion and electroneutral transepithelial NaCl reabsorption in microperfused CCDs of wild-type mice but

136 Factors that contribute to increased sodium reabsorption in obesity include kidney compression by vi

137 asolateral step of transepithelial HCO(3)(-) reabsorption in proximal tubule epithelia, contributing

138 e regulation of HCO(3)(-) secretion and NaCl reabsorption in the CNT/CCD under acid-base stress and e

139 ensitive rats, promoting ENaC-mediated Na(+) reabsorption in the collecting duct and the development

140 Vasopressin modulates sodium reabsorption in the collecting duct through adenylyl cyc

141 activity of which is instrumental in Mg(2+) reabsorption in the DCT.

142 This channel is crucial for calcium reabsorption in the distal convoluted tubule (DCT).

143 porter (NCC) is the primary mediator of salt reabsorption in the distal convoluted tubule and is a ke

144 Ca(2+) excretion by mediating active Ca(2+) reabsorption in the distal convoluted tubule of the kidn

145 Transcellular magnesium (Mg(2+)) reabsorption in the distal convoluted tubule represents

146 (ENaC) is the limiting entry point for Na(+) reabsorption in the distal kidney nephron and is regulat

147 daptive upregulation of ENaC-mediated sodium reabsorption in the distal nephron in the conditions of

148 orters NKCC2 and NCC (key components of salt reabsorption in the distal renal tubule), possibly throu

149 a(+)/Cl(-) cotransporter (NCC) mediated salt reabsorption in the distal tubules of the kidney.

150 we developed a mathematical model of protein reabsorption in the human proximal tubule (PT) using Mic

151 (OH)2D3; calcitriol) formation and phosphate reabsorption in the kidney and counteracts vascular calc

152 iltrate in wild-type mice and the absence of reabsorption in the kidney in Glut2(-/-) mice confirm th

153 d are vital for cell volume regulation, salt reabsorption in the kidney, and gamma-aminobutyric acid

154 as an endocrine cell that controls phosphate reabsorption in the kidney, insulin secretion in the pan

155 ich mediates a large proportion of phosphate reabsorption in the kidney, might be a good therapeutic

156 as been attributed to enhanced distal sodium reabsorption in the kidney, the structural defects have

157 hormonal cAMP-dependent regulation of Mg(2+) reabsorption in the kidney.

158 (NKCC2) co-transporters, which regulate salt reabsorption in the kidney.

159 o may play important roles regarding calcium reabsorption in the kidney.

160 lay a key role in mediating paracellular ion reabsorption in the kidney.

161 muscle cells, neuronal signalling and Ca(2+) reabsorption in the kidney.

162 g limb (TAL) of Henle is critical for Ca(++) reabsorption in the kidney.

163 te the physiological role of CNNM2 in Mg(2+) reabsorption in the kidney.

164 at acts as the rate-limiting step of calcium reabsorption in the kidney.

165 ats due to loss of AVP facilitation of water reabsorption in the kidney.

166 Active Ca(2+) reabsorption in the late distal convoluted and connectin

167 nsporter (NCC) is the major pathway for salt reabsorption in the mammalian distal convoluted tubule.

168 (+) shunting but oppose HCO(3) (-) and NaCl reabsorption in the mTAL, and thus are at the nexus of t

169 Low dietary Na(+) intake increased Na(+) reabsorption in the proximal tubule and decreased it in

170 High dietary Na(+) intake decreased Na(+) reabsorption in the proximal tubule and increased it in

171 By inhibiting glucose reabsorption in the proximal tubule, these agents promot

172 fusion pressure can directly regulate sodium reabsorption in the proximal tubule.

173 nless (AMN), two major receptors for protein reabsorption in the proximal tubule.

174 r blood glucose levels by inhibiting glucose reabsorption in the proximal tubule.

175 ldren) and is the result of impaired cystine reabsorption in the renal proximal tubule.

176 lucose uptake regulates NHE3-mediated NaHCO3 reabsorption in the renal proximal tubule.

177 ignaling through Na/K-ATPase regulate sodium reabsorption in the renal proximal tubule.

178 the ClC-Kb chloride channel involved in NaCl reabsorption in the renal tubule.

179 dins Cldn10b, -16, and -19 facilitate cation reabsorption in the TAL, and their absence leads to a se

180 e of claudin-16 and -19, critical for Ca(++) reabsorption in the TAL.

181 d transporters involved in mediating NH4 (+) reabsorption in the thick ascending limb of the loop of

182 ta suggest that renal Casr regulates calcium reabsorption in the thick ascending limb, independent of

183 Blocking ileal CBA reabsorption in transferred Rag1(-/-) mice restored Mdr1

184 This is physiologically relevant to Ca(2+) reabsorption in vivo, as short hairpin RNA knockdown of

185 tical modelling predicted that tubular Na(+) reabsorption increased in the proximal tubule but decrea

186 n and associated increases in tubular sodium reabsorption initiate hypertension, which is often mild

187 cate that distal tubular compensatory sodium reabsorption is a primary driver of DR.

188 P(i) reabsorption is a transcellular process that occurs alon

189 The 3-->1 transformation through acetone reabsorption is also demonstrated.

190 The overall capacity for proximal reabsorption is augmented by growth of the proximal tubu

191 Renal water reabsorption is controlled by arginine vasopressin (AVP)

192 Our data show that fractional Na(+) reabsorption is distributed differently according to die

193 Renal Ca(2+) reabsorption is essential for maintaining systemic Ca(2+

194 Reabsorption is primarily handled by SGLT2, and SGLT2-sp

195 Water reabsorption is regulated by AQP2 trafficking between in

196 a novel mechanism by which TRPV5 and Ca(2+) reabsorption is regulated by the kidney and support the

197 , we found that Cubilin/AMN-mediated protein reabsorption is required for the maintenance of nephrocy

198 ry transporter responsible for renal glucose reabsorption is sodium-glucose cotransporter-2 (SGLT2).

199 ion (nearly the same as the rate of HCO3 (-) reabsorption, JHCO3 ) in response to changes in blood [C

200 isease (CLCN5 mutation) abolishes PT protein reabsorption leaving glomerular function intact.

201 s natriuresis with correspondent renal water reabsorption, limits natriuretic osmotic diuresis, and r

202 large Stokes shift necessary for suppressing reabsorption losses in large-area devices.

203 These alterations, known to increase water reabsorption, may be responsible, at least in part, for

204 ot downregulated, and proximal tubule sodium reabsorption, measured by lithium clearance, was unaffec

205 fication of the integrated compensatory NaCl reabsorption mechanisms provides insight into thiazide d

206 Moreover, we associated the egg reabsorption observed in infected females, with a decrea

207 embrane of salivary gland ducts and regulate reabsorption of [Ca(2+)] from the saliva via TRPC3, thus

208 an be reversed to the original material upon reabsorption of acetone.

209 However, high renal reabsorption of Affibody molecules prevents the use of r

210 essed by proximal tubular cells mediates the reabsorption of ALA, and variants of PEPT2 have differen

211 ASBT, SLC10A2) is responsible for intestinal reabsorption of bile acids and plays a key role in chole

212 Bile acid sequestrants interrupt intestinal reabsorption of bile acids, decreasing their circulating

213 rolaemia, because inhibition of ASBT reduces reabsorption of bile acids, thus increasing bile acid sy

214 esterol and triglycerides as a result of the reabsorption of biliary lipids from the intestine.

215 which is primarily mediated by altering the reabsorption of Ca(2+) filtered by the glomerulus.

216 the ductal tree into the oral cavity, ductal reabsorption of Ca(2+) remains enigmatic.

217 cending limb, claudins are important for the reabsorption of calcium and magnesium and are tightly re

218 crease in intestinal absorption and/or renal reabsorption of calcium.

219 or approximately 25% of Abeta clearance, and reabsorption of cerebrospinal fluid Abeta accounts for a

220 Passive reabsorption of chloride and water also increases.

221 Future reabsorption of CO(2) will be significant (~30% of cumul

222 h as Na(+) and a spatially distinct site for reabsorption of divalent cations such as Ca(2+) and Mg(2

223 permits proximal tubule luminal exposure and reabsorption of fatty acid/albumin complexes, we hypothe

224 relatively narrow range by control of renal reabsorption of filtered inorganic phosphate (P(i)).

225 cotransporter NPT2a plays a key role in the reabsorption of filtered phosphate in proximal renal tub

226 Reabsorption of filtered sodium by CD cells occurs via a

227 Tubular reabsorption of filtered sodium is tightly controlled to

228 olume decline is consistent with atrophy and reabsorption of globally sclerotic glomeruli and hypertr

229 e in the glomerular filtrate drive increased reabsorption of glucose and sodium by the sodium-glucose

230 ine to absorb glucose and contributes to the reabsorption of glucose filtered by the kidney.

231 is important in glucose liver transport and reabsorption of glucose in the kidney along with SGLT2 a

232 ted physiologic functions, including tubular reabsorption of macromolecules, that gained access to th

233 Complete reabsorption of Me-4FDG from the glomerular filtrate in

234 SGLT2 is responsible for reabsorption of most of the glucose filtered by the kidn

235 ay be different dynamics in the assembly and reabsorption of pericellular and septal elastic fibres,

236 I], 0.59 to 0.96; P=0.02), decreased tubular reabsorption of phosphate (OR, 0.41; 95% CI, 0.23 to 0.7

237 vitamin D (VITD) supplementation on tubular reabsorption of phosphate (TRP), parathyroid hormone (PT

238 (FGF23) axis, creatinine, and renal tubular reabsorption of phosphate (TRP).

239 al metabolism by directly modulating tubular reabsorption of phosphate and calcium and by acting as a

240 osis had significantly lower percent tubular reabsorption of phosphate and fibroblast growth factor-2

241 Intestinal absorption and renal reabsorption of phosphate are mediated by members of the

242 plasma phosphate concentration, and tubular reabsorption of phosphate increased during the proteinur

243 s, suggesting a role of Oatp1a1 in the renal reabsorption of rosuvastatin.

244 mal tubule, claudins have a role in the bulk reabsorption of salt and water.

245 SGLT2 inhibitors attenuate the proximal reabsorption of sodium and glucose, normalize tubuloglom

246 Half-dose PDT induced a more rapid reabsorption of the fluid, a more lasting effect, and eq

247 n induces premature senescence by preventing reabsorption of the primary cilium, which inhibits centr

248 as probably due to glomerular filtration and reabsorption of the protein tracer in proximal tubular c

249 ed that SGLT2 is responsible for >80% of the reabsorption of the renal filtered glucose load.

250 ptor-mediated endocytosis is responsible for reabsorption of transferrin (Tf) in renal proximal tubul

251 Reabsorption of water from the luminal fluid of the neph

252 is ensured by the selective transepithelial reabsorption of water into the hypertonic medullary inte

253 channels creates the major driving force for reabsorption of water through the alveolar epithelium in

254 proximal tubules are very important for the reabsorption of water, ions and organic solutes from the

255 tatic organ required for waste excretion and reabsorption of water, salts and other macromolecules.

256 ribe and reproduce the distortions caused by reabsorption on emission spectra and quantum yields.

257 tribute to pH(i) regulation, and promote ion reabsorption or secretion by many epithelia.

258 ermined by production and the net balance of reabsorption or secretion by the kidney and intestine.

259 filtration or impaired proximal tubule (PT) reabsorption, or both.

260 maintain stable fractional solute and fluid reabsorption over a wide range of glomerular filtration

261 Salt reabsorption pathways were created by the coordinate ind

262 DCT2/CNT region, their role in active Ca(2+) reabsorption remains elusive.

263 The physiological relevance of PiT-2 to P(i) reabsorption remains to be elucidated.

264 ge can lead to increased or decreased sodium reabsorption, respectively, through the Na(+)/Cl(-) cotr

265 inhibits K(+) secretion and stimulates Na(+) reabsorption, respectively.

266 eptually, modest inhibition of renal tubular reabsorption should provide effective relief for the mil

267 ificant loci possibly related to its tubular reabsorption, SLC6A19, and its production, ERO1A, which

268 explored how altered endocytic uptake, water reabsorption, SNGFR and glomerular protein filtration af

269 directly or indirectly reduces renal calcium reabsorption, suggesting the presence of a novel calcium

270 d by a greater TRAP-positive cell number and reabsorption surface on both the pressure and tension si

271 d flow and decreases in distal tubule sodium reabsorption that offset acute rises in BP are impaired

272 r characterized by defective urinary cystine reabsorption that results in the formation of cystine-ba

273 ting the expression of genes associated with reabsorption, the major function of PT cells.

274 potassium by increasing electroneutral NaCl reabsorption, therefore reducing Na(+)/K(+) exchange.

275 Aldosterone promotes electrogenic sodium reabsorption through the amiloride-sensitive epithelial

276 he kidney that underlies paracellular Ca(++) reabsorption through the tight junction.

277 ass vasopressin signaling and increase water reabsorption through two different intracellular signali

278 aximum renal tubular threshold for phosphate reabsorption (TmP/GFR), serum Pi, and 1,25(OH)2D compare

279 In contrast, the bile salt reabsorption transporters Ostalpha and Ostbeta were up-r

280 urine output (P </= 0.04, except for sodium reabsorption under constant pressure [P = 0.17]).

281 cular volume expansion, increased free water reabsorption, urinary prostaglandin E2 excretion, and re

282 nephrocyte combines filtration with protein reabsorption, using evolutionarily conserved genes and s

283 ole of SOCE in the regulation of renal water reabsorption, using the inbred rat strain SHR-A3 as an a

284 ular balance, such that proximal tubular Na+ reabsorption varies proportionally to the single-nephron

285 asopressin stimulates renal water and sodium reabsorption via increased tubular cell cAMP levels, we

286 Aldosterone increases NaCl reabsorption via NCC over the long-term by altering gene

287 Altered glucose reabsorption via the facilitative glucose transporter 2

288 ineralocorticoid release promoted free water reabsorption via the renal concentration mechanism.

289 rives paracellular Na(+), Ca(2+), and Mg(2+) reabsorption via the tight junction (TJ).

290 y develop from impaired transcellular Ca(2+) reabsorption via TRPV5 in the distal convoluted tubule (

291 nd vascular endothelium that exhibits active reabsorption via tubular-vascular exchange of solutes ak

292 Salt reabsorption was also activated by induction of an alpha

293 In this case, PT albumin reabsorption was markedly increased.

294 Renal glucose reabsorption was measured with the stepped hyperglycemic

295 learance suggested that distal tubule sodium reabsorption was not downregulated with increased BP in

296 e renal medullary blood flow, tubular sodium reabsorption was not downregulated, and proximal tubule

297 n of efferent ductal genes involved in fluid reabsorption was significantly lower in AF2ERKI males.

298 alocorticoid-coupled increases in free water reabsorption were counterbalanced by rhythmical glucocor

299 ring normal downregulation of tubular sodium reabsorption when BP was increased.

300 vascular volume depletion (promotion of salt reabsorption without K(+) secretion), a condition that i