scholarly journals Consequences of potassium recycling in the renal medulla. Effects of ion transport by the medullary thick ascending limb of Henle's loop.

1982 ◽  
Vol 70 (2) ◽  
pp. 219-229 ◽  
Author(s):  
J B Stokes
Keyword(s):  
Ion Transport ◽  
Renal Medulla ◽  
Thick Ascending Limb ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop ◽  
Potassium Recycling

Effects of adenosine on ion transport in rat medullary thick ascending limb

1992 ◽  
Vol 263 (3) ◽  
pp. F482-F487 ◽  
Author(s):  
R. E. Beach ◽  
D. W. Good
Keyword(s):  
Oxygen Consumption ◽  
Ion Transport ◽  
Receptor Antagonist ◽  
Arginine Vasopressin ◽  
Renal Medulla ◽  
Thick Ascending Limb ◽  
Cyclic Monophosphate ◽  
Nacl Absorption ◽  
Medullary Thick Ascending Limb ◽  
A1 Receptor

Previously, we demonstrated that adenosine (Ado) was released by the medullary thick ascending limb (MTAL) during hypoxia. The present experiments were designed to examine the effects of Ado and adenosine analogues on net chloride (JCl) and bicarbonate (JHCO3) absorption by the isolated, perfused MTAL of the rat. Ado, 10 nM, in the presence or absence of arginine vasopressin (AVP, 10(-10) M) reduced JCl by 50%. The inhibition of Ado was reproduced with the selective A1 agonist, N-6-phenylisopropyladenine (2 nM), and was reversed by 8-cyclopentyl-1,3-dipropylxanthine, an A1-receptor antagonist. Thus the inhibition of JCl is likely mediated through A1 receptors. In contrast, Ado had no effect on (JHCO3) either in the presence or absence of AVP. Ado also had no influence on the effect of AVP to inhibit JHCO3. The lack of effect on JHCO3 suggests that the inhibition of JCl by Ado is unlikely to be mediated through changes in cellular adenosine 3',5'-cyclic monophosphate. These results support the hypothesis that Ado released into the renal medulla during hypoxia may protect the MTAL from ischemic injury by directly inhibiting NaCl absorption and reducing transport-related oxygen consumption.

Cytokines affect ion transport in primary cultured thick ascending limb of Henle's loop cells

1994 ◽  
Vol 266 (6) ◽  
pp. C1568-C1576 ◽  
Author(s):  
B. A. Escalante ◽  
N. R. Ferreri ◽  
C. E. Dunn ◽  
J. C. McGiff
Keyword(s):  
Ion Transport ◽  
Prostaglandin E2 ◽  
Interleukin 1 ◽  
Inhibitory Effect ◽  
Biologically Active ◽  
Thick Ascending Limb ◽  
Necrosis Factor Alpha ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop ◽  
Factor Alpha

Tumor necrosis factor-alpha (TNF) and interleukin-1 (IL-1) affect epithelial cell ion transport. However, the site of action along the nephron has not been elucidated fully for these cytokines. Thus, the effect of TNF and IL-1 on the ion transport function of primary cultured medullary thick ascending limb of Henle's loop (mTALH) cells was determined by measuring rubidium (86Rb) uptake. TNF, IL-1, and lipopolysaccharide (LPS), a known activator of cytokine production, inhibited 86Rb uptake by cultured mTALH cells after a 24-h incubation period but had no effect when incubated with the cells for 1 or 4 h. Furthermore, mTALH cells produced biologically active TNF after stimulation with LPS for 24 h, and the LPS-induced inhibition of 86Rb uptake was abolished in the presence of an anti-TNF antibody, suggesting that TNF produced by the mTALH cells acted in an autocrine manner to inhibit 86Rb uptake. The effects of LPS on 86Rb uptake also were inhibited by the cyclooxygenase inhibitor, indomethacin. As TNF increased prostaglandin E2 synthesis by cultured mTALH cells and as prostaglandin E2 also inhibited 86Rb uptake, LPS presumably inhibited 86Rb uptake by inducing a TNF-mediated increase in prostaglandin synthesis. These data demonstrate that a prostanoid produced by mTALH cells mediates the inhibitory effect of LPS and TNF on 86Rb uptake and imply that endogenous TNF inhibits ion fluxes in the mTALH via a prostaglandin-dependent mechanism.

Urea inhibits Na-K-2Cl cotransport in medullary thick ascending limb cells

1997 ◽  
Vol 272 (2) ◽  
pp. C615-C621 ◽  
Author(s):  
D. M. Kaji ◽  
J. Diaz ◽  
J. C. Parker
Keyword(s):  
Ion Transport ◽  
Cell Volume ◽  
Okadaic Acid ◽  
Binding Sites ◽  
Cultured Cells ◽  
Renal Medulla ◽  
Significant Inhibition ◽  
Prior Treatment ◽  
Thick Ascending Limb ◽  
Medullary Thick Ascending Limb

We examined the effect of physiological concentrations of urea (100-500 mM) on Na-K-2Cl cotransport in cultured cells from mouse medullary thick ascending limb (mTAL). Urea acutely inhibited bumetanide-sensitive K influx in mTAL cells in a concentration-dependent fashion, with a statistically significant inhibition (19%) at 100 mM and 86% inhibition at 500 mM. The effect of urea was entirely reversible and was blocked by prior treatment with okadaic acid, a phosphatase inhibitor, suggesting that urea exerts its action upstream of the phosphorylation-dephosphorylation step. Cell volume was unchanged in the presence of 500 mM urea. The number of [3H]bumetanide binding sites, a measure of the number of functioning cotransporter sites, was decreased in the presence of urea, and the decrease in bumetanide binding was proportional to the decrease in bumetanide-sensitive K influx. Urea also stimulated the Ba-sensitive swelling-activated K efflux from mTAL cells. Thus urea, in concentrations that prevail in the renal medulla, alters ion transport in mTAL cells.

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 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.

Effect of acute potassium load on reabsorption in Henle's loop in the rat

1983 ◽  
Vol 245 (5) ◽  
pp. F569-F576 ◽  
Author(s):  
C. R. Sufit ◽  
R. L. Jamison
Keyword(s):  
Renal Medulla ◽  
Distal Tubule ◽  
Potassium Excretion ◽  
Water Delivery ◽  
Henle's Loop ◽  
Low Potassium ◽  
Collecting Tubule ◽  
Before And After ◽  
Potassium Recycling ◽  
Tubule Fluid

Rats fed a low potassium diet were studied before and after KCl infusion to determine whether potassium recycling in the renal medulla accelerates potassium excretion by increasing delivery of sodium, water, and potassium to the distal tubule. Fluid samples were obtained from the end-proximal and beginning-distal tubule before and at the same sites after KCl loading by re-collection micropuncture and were compared with samples obtained from similarly fed control animals not infused with KCl. Potassium excretion increased in the KCl group from 3 to 48% but remained low in the controls. Fractional sodium and water delivery to end-proximal and beginning-distal tubule increased with time equally in both groups. Potassium reabsorption in Henle's loop fell from 75 to 58% (P less than 0.005) after KCl infusion but not significantly in the controls (from 77 to 75%). Fractional potassium delivery to the distal tubule increased from 12 to 26% (P less than 0.005) in the KCl group, which could account for over half the potassium excreted. The increase in controls from 12 to 17% was significantly less (P less than 0.02). These findings suggest that potassium recycling reduces potassium reabsorption in Henle's loop, enabling the loop to participate with the distal and collecting tubule in accelerating urinary excretion of an acute potassium load.

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