AVP dynamically increases paracellular Na+ permeability and transcellular NaCl transport in the medullary thick ascending limb of Henle’s loop

2016 ◽  
Vol 469 (1) ◽  
pp. 149-158 ◽  
Author(s):  
Nina Himmerkus ◽  
Allein Plain ◽  
Rita D. Marques ◽  
Svenja R. Sonntag ◽  
Alexander Paliege ◽  
...  
Keyword(s):  
Thick Ascending Limb ◽  
Nacl Transport ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop ◽  
Na Permeability

scholarly journals Modulation of outer medullary NaCl transport and oxygenation by nitric oxide and superoxide

2011 ◽  
Vol 301 (5) ◽  
pp. F979-F996 ◽  
Author(s):  
Aurélie Edwards ◽  
Anita T. Layton
Keyword(s):  
Nitric Oxide ◽  
Active Transport ◽  
Collecting Duct ◽  
Thick Ascending Limb ◽  
Outer Medulla ◽  
Nacl Transport ◽  
Complex Interactions ◽  
Medullary Thick Ascending Limb ◽  
The Impact ◽  
Stimulation Of

We expanded our region-based model of water and solute exchanges in the rat outer medulla to incorporate the transport of nitric oxide (NO) and superoxide (O2−) and to examine the impact of NO-O2− interactions on medullary thick ascending limb (mTAL) NaCl reabsorption and oxygen (O2) consumption, under both physiological and pathological conditions. Our results suggest that NaCl transport and the concentrating capacity of the outer medulla are substantially modulated by basal levels of NO and O2−. Moreover, the effect of each solute on NaCl reabsorption cannot be considered in isolation, given the feedback loops resulting from three-way interactions between O2, NO, and O2−. Notwithstanding vasoactive effects, our model predicts that in the absence of O2−-mediated stimulation of NaCl active transport, the outer medullary concentrating capacity (evaluated as the collecting duct fluid osmolality at the outer-inner medullary junction) would be ∼40% lower. Conversely, without NO-induced inhibition of NaCl active transport, the outer medullary concentrating capacity would increase by ∼70%, but only if that anaerobic metabolism can provide up to half the maximal energy requirements of the outer medulla. The model suggests that in addition to scavenging NO, O2− modulates NO levels indirectly via its stimulation of mTAL metabolism, leading to reduction of O2 as a substrate for NO. When O2− levels are raised 10-fold, as in hypertensive animals, mTAL NaCl reabsorption is significantly enhanced, even as the inefficient use of O2 exacerbates hypoxia in the outer medulla. Conversely, an increase in tubular and vascular flows is predicted to substantially reduce mTAL NaCl reabsorption. In conclusion, our model suggests that the complex interactions between NO, O2−, and O2 significantly impact the O2 balance and NaCl reabsorption in the outer medulla.

scholarly journals TNF production by the medullary thick ascending limb of Henle's loop

1994 ◽  
Vol 46 (1) ◽  
pp. 113-121 ◽  
Author(s):  
Carolyn M. Macica ◽  
Bruno A. Escalante ◽  
Michael S. Conners ◽  
Nicholas R. Ferreri
Keyword(s):  
Thick Ascending Limb ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop

ANG II is a mitogen for a murine cell line isolated from medullary thick ascending limb of Henle's loop

1995 ◽  
Vol 268 (5) ◽  
pp. F940-F947 ◽  
Author(s):  
G. Wolf ◽  
F. N. Ziyadeh ◽  
U. Helmchen ◽  
G. Zahner ◽  
R. Schroeder ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Cell Line ◽  
Thick Ascending Limb ◽  
Dependent Manner ◽  
Ang Ii ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop ◽  
Proximal Tubular

A murine SV40-transformed renal epithelial cell line derived from medullary thick ascending limb of Henle's loop (MTAL) was established and characterized by morphology, antigen expression, and biochemical criteria. These MTAL cells express a single class of high-affinity receptors for angiotensin II (ANG II) and transcripts for the AT1 subtype of ANG II receptors. ANG II, in a dose-dependent manner, induced proliferation of MTAL cells. This observation is in striking contrast to syngeneic proximal tubular cells in which it was previously shown that the peptide induced cellular hypertrophy and slightly inhibited proliferation [G. Wolf and E. G. Neilson. Am. J. Physiol. 259 (Renal Fluid Electrolyte Physiol. 28: F768-F777, 1990]. The AT1-receptor antagonist losartan (10(-6) M), but not an AT2-receptor antagonist, blocked the mitogenic effects of ANG II in MTAL cells. Coincubation of quiescent MTAL cells with ANG II and 5% fetal calf serum further increased proliferation compared with cells grown only in serum. In contrast to proximal tubular cells, ANG II failed to induce transforming growth factor-beta 1 mRNA and protein synthesis in MTAL cells. Our data collectively suggest that ANG II is a mitogen for MTAL cells in vitro. Therefore, epithelial cells derived from different parts of the nephron, even when transformed with SV40 virus and while under cell culture conditions, exhibit a distinct pattern of growth behavior after stimulation with ANG II.

Cyclooxygenase inhibitors increase Na-K-2Cl cotransporter abundance in thick ascending limb of Henle’s loop

1999 ◽  
Vol 277 (2) ◽  
pp. F219-F226 ◽  
Author(s):  
Patricia Fernández-Llama ◽  
Carolyn A. Ecelbarger ◽  
Joseph A. Ware ◽  
Peter Andrews ◽  
Alanna J. Lee ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Cyclooxygenase Inhibitors ◽  
Thick Ascending Limb ◽  
Outer Medulla ◽  
Nacl Transport ◽  
Expression Levels ◽  
Henle's Loop ◽  
Urinary Concentrating Ability ◽  
Ep3 Receptor ◽  
Type 3

Cyclooxygenase inhibitors, such as indomethacin and diclofenac, have well-described effects to enhance renal water reabsorption and urinary concentrating ability. Concentrating ability is regulated in part at the level of the thick ascending limb of Henle’s loop, where active NaCl absorption drives the countercurrent multiplication mechanism. We used semiquantitative immunoblotting to test the effects of indomethacin and diclofenac, given over a 48-h period, on the expression levels of the ion transporters responsible for active NaCl transport in the thick ascending limb. Both agents strongly increased the expression level of the apical Na-K-2Cl cotransporter in both outer medulla and cortex. Neither agent significantly altered outer medullary expression levels of other thick ascending limb proteins, namely, the type 3 Na/H exchanger (NHE-3), Tamm-Horsfall protein, or α1- or β1-subunits of the Na-K-ATPase. Administration of the EP3-selective PGE2analog, misoprostol, to indomethacin-treated rats reversed the stimulatory effect of indomethacin on Na-K-2Cl cotransporter expression. We conclude that cyclooxygenase inhibitors enhance urinary concentrating ability in part through effects to increase Na-K-2Cl cotransporter expression in the thick ascending limb of Henle’s loop. This action is most likely due to elimination of an EP3-receptor-mediated tonic inhibitory effect of PGE2 on cAMP production.

Stimulation of Na+/K+-ATPase activity by polyamines in the rat renal medullary cells of the thick ascending limb of Henle's loop

1990 ◽  
Vol 127 (3) ◽  
pp. 377-382 ◽  
Author(s):  
J. A. Charlton ◽  
P. H. Baylis
Keyword(s):  
Atpase Activity ◽  
Arginine Vasopressin ◽  
Thick Ascending Limb ◽  
Stimulus Response ◽  
Spermine Synthase ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop ◽  
Specific Inhibitors ◽  
Stimulation Of

ABSTRACT Previous studies have indicated that ornithine decarboxylase (ODC) may be involved in the stimulation of Na+/K+-ATPase activity by arginine vasopressin (AVP) in the rat renal medullary thick ascending limb of Henle's loop. The present study was aimed at establishing the role of the polyamines, the conversion products of ODC activity, in the stimulation of Na+/K+-ATPase by AVP. Using cytochemical methods, we have demonstrated an increase in Na+/K+-ATPase activity after stimulation with putrescine, spermidine and spermine (each 1 mmol/l) for 2·5,2 and 1·5 min respectively. The specific inhibitors of spermidine and spermine synthase, bis-cyclohexylammonium sulphate and N-alkylated-1,3-diaminopropane respectively, inhibited the stimulation of Na+/K+-ATPase by AVP, this inhibition being reversed by spermine. These findings suggest that polyamines are involved in the stimulus-response coupling of the hormone-mediated response. Journal of Endocrinology (1990) 127, 377–382

Enhanced glomerular filtration and Na+-K+-ATPase with furosemide administration

1987 ◽  
Vol 252 (5) ◽  
pp. F910-F915 ◽  
Author(s):  
P. Scherzer ◽  
H. Wald ◽  
M. M. Popovtzer
Keyword(s):  
Glomerular Filtration ◽  
Collecting Duct ◽  
Thick Ascending Limb ◽  
Cortical Collecting Duct ◽  
Nephron Segments ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop ◽  
Proximal Straight Tubule ◽  
X 24 ◽  
Furosemide Administration

To evaluate the effect of furosemide on kidney function, glomerular filtration rate (GFR), urinary Na excretion (UNaV), Na reabsorption (NAR), and Na+-K+-ATPase in isolated nephron segments were measured in 1) rats treated with furosemide 10 mg X 100 g-1 X 24 h-1 ip for 7 days, and 2) rats receiving an oral Na load for 12 days. In furosemide-treated rats, GFR rose from 0.61 +/- 0.03 (mean +/- SD) to 0.83 +/- 0.06 ml/min (P less than 0.01), UNaV rose from 904 +/- 71 to 1,402 +/- 85 mueq/day (P less than 0.001), and net NAR rose from 87.5 +/- 3.7 to 116.7 +/- 9.0 mueq/min (P less than 0.01). Na+-K+-ATPase remained unchanged in the proximal convoluted tubule (PCT), proximal straight tubule (PST), cortical thick ascending limb of Henle's loop (cTALH), and medullary thick ascending limb of Henle's loop (mTALH), but was increased in the distal convoluted tubule (DCT) and in cortical collecting duct (CCD) from 48.5 +/- 1.2 to 75.3 +/- 0.7 (P less than 0.001) and from 18.6 +/- 0.7 to 27.1 +/- 2.7 (P less than 0.02) X 10(-11) mol X mm-1 X min-1, respectively. In Na-loaded rats GFR rose from 0.61 +/- 0.04 to 0.86 +/- 0.03 ml/min (P less than 0.001), UNaV rose from 1,064 +/- 118 to 18,532 +/- 2,045 mueq/day (P less than 0.001), net NAR from 88.1 +/- 3.0 to 107.8 +/- 3.9 mueq/min and Na-K-ATPase in the mTALH rose from 40.3 +/- 1.4 to 56.2 +/- 2.11 (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulation of rat renal medullary Na+/K+-ATPase by arginine vasopressin is mediated by the V2 receptor

1990 ◽  
Vol 127 (2) ◽  
pp. 213-216 ◽  
Author(s):  
J. A. Charlton ◽  
P. H. Baylis
Keyword(s):  
Atpase Activity ◽  
Arginine Vasopressin ◽  
Thick Ascending Limb ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop ◽  
Cytochemical Bioassay ◽  
V2 Receptor ◽  
Stimulation Of

ABSTRACT In previous studies, we have demonstrated that 1–10 fmol arginine vasopressin (AVP)/l maximally stimulates the activity of the enzyme Na+/K+-ATPase in the rat renal medullary thick ascending limb (MTAL) of Henle's loop after 4 or 10 min of stimulation when measured using a cytochemical bioassay. We have tested the hypothesis that this stimulation is mediated by the V2 receptor in the MTAL. A cytochemical bioassay was used to investigate the effect of specific V1 and V2/V1 antagonists and a synthetic V2 agonist [1-deamino,8-d-arginine]-vasopressin (dDAVP), on the activity of Na+/K+-ATPase. There was no effect of the V1 antagonist (1 fmol-1 μmol/l) in inhibiting the activity of Na+/K+-ATPase stimulated by 1 fmol AVP/l. In contrast, 100 pmol of the V2/V1 antagonist/l significantly (P < 0·001) inhibited the stimulation of Na+/K+-ATPase activity by 1 fmol AVP/l from 55·5±4·3 (s.e.m.) to 31·9±1·6 mean integrated extinction (MIE) after 4 min of stimulation and from 67·0±3·2 to 36·9±0·7 MIE after 10 min of stimulation. Similarly, the stimulation of Na+/K+-ATPase by 10 fmol dDAVP/l was inhibited by the V2/V1 antagonist from 55·1±1·0 to 26·1±0·5 MIE after 4 min of stimulation. We conclude that the stimulation of Na+/K+-ATPase by AVP is mediated by the V2 receptor in the rat renal MTAL. Journal of Endocrinology (1990) 127, 213–216

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