Development and application of a dual-excitation, digital imaging, fluorescence microscope to investigate parathyroid hormone-stimulated calcium transport in kidney distal tubule cells.

1989 ◽  
Author(s):  
Brian J. Bacskai
Keyword(s):  
Parathyroid Hormone ◽  
Digital Imaging ◽  
Calcium Transport ◽  
Distal Tubule ◽  
Fluorescence Microscope ◽  
Tubule Cells

Effects of Parathyroid Hormone on Sodium and Calcium Transport in the Dog Nephron

1976 ◽  
Vol 51 (4) ◽  
pp. 345-351 ◽  
Author(s):  
R. A. L. Sutton ◽  
N. L. M. Wong ◽  
J. H. Dirks
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Transport ◽  
Distal Tubule ◽  
Tubular Reabsorption ◽  
Puncture Site ◽  
Calcium Reabsorption ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Selective Enhancement ◽  
Bovine Parathyroid Hormone

1. The effect of purified bovine parathyroid hormone on renal tubular reabsorption of sodium and calcium has been studied by micropuncture in intact and recently thyroparathyroidectomized dogs. 2. Parathyroid hormone increased the rejection of sodium and calcium proportionately at the late proximal tubule in both intact and operated dogs. 3. In both groups of dogs, there was increased delivery of sodium and calcium to the distal tubule after the hormone. However, the Ca/Na ratio decreased, suggesting some selective enhancement of calcium reabsorption before the superficial distal puncture site. 4. In the final urine, the Ca/Na ratio decreased highly significantly in both groups of dogs, indicating a further selective effect of parathyroid hormone on calcium reabsorption in or beyond the distal convoluted tubule.

Ca2+-Mg2+-ATPase Calcium Pumps in the Kidney

Physiology ◽  
1988 ◽  
Vol 3 (5) ◽  
pp. 219-222
Author(s):  
R Kumar ◽  
JT Penniston ◽  
JL Borke
Keyword(s):  
Calcium Transport ◽  
Rat Kidney ◽  
Distal Tubule ◽  
Calcium Pump ◽  
Red Cell ◽  
Calcium Pumps ◽  
Nephron Segment ◽  
Hormone Sensitive ◽  
Tubule Cells ◽  
A Site

Epitopes of the calmodulin-sensitive erythrocyte Ca2+-Mg2+-ATPase enzyme were found exclusively in basolateral membranes of distal tubule cells of the human and rat kidney;other kidney segments did not contain this enzyme in detectable amounts. The calmodulin-sensitive Ca2+-Mg2+-ATPase acts as a calcium pump in the red cell and other tissues. Its presence in the kidney distal tubule, a site where hormone-sensitive calcium transport is known to occur, raises the possibility that this enzyme may act as a hormone-regulated pump in this nephron segment.

Aminoglycosides inhibit hormone-stimulated Mg2+ uptake in mouse distal convoluted tubule cells

2000 ◽  
Vol 78 (8) ◽  
pp. 595-602 ◽  
Author(s):  
Hyung Sub Kang ◽  
Dirk Kerstan ◽  
Long-jun Dai ◽  
Gordon Ritchie ◽  
Gary A Quamme
Keyword(s):  
Parathyroid Hormone ◽  
Distal Tubule ◽  
Distal Convoluted Tubule ◽  
Thick Ascending Limb ◽  
Clinical Use ◽  
Cellular Mechanisms ◽  
Nephron Segment ◽  
Tubule Cells ◽  
Renal Magnesium Wasting ◽  
Camp Formation

The clinical use of aminoglycosides often leads to renal magnesium wasting and hypomagnesemia. Of the nephron segments, both the thick ascending limb of Henle's loop and the distal tubule play significant roles in renal magnesium conservation but the distal convoluted tubule exerts the final control of urinary excretion. An immortalized mouse distal convoluted tubule (MDCT) cell line has been extensively used to study the cellular mechanisms of magnesium transport in this nephron segment. Peptide hormones, such as parathyroid hormone (PTH), glucagon, calcitonin, and arginine vasopressin (AVP) stimulate Mg2+ uptake in MDCT cells that is modulated by extracellular polyvalent cations, Ca2+ and Mg2+. The present studies determined the effect of aminoglycosides on parathyroid hormone (PTH)-mediated cAMP formation and Mg2+ uptake in MDCT cells. Gentamicin, a prototypic aminoglycoside, illicited transient increases in intracellular Ca2+ from basal levels of 102 ± 13 nM to 713 ± 125 nM, suggesting a receptor-mediated response. In order to determine Mg2+ transport, MDCT cells were Mg2+-depleted by culturing in Mg2+-free media for 16 h and Mg2+ uptake was measured by microfluorescence after placing the depleted cells in 1.0 mM MgCl2. The mean rate of Mg2+ uptake, d([Mg2+]i)/dt, was 138 ± 24 nM/s in control MDCT cells. Gentamicin (50 µM) did not affect basal Mg2+ uptake (105 ± 29 nM/s), but inhibited PTH stimulated Mg2+ entry, decreasing it from 257 ± 36 nM/s to 108 ± 42 nM/s. This was associated with diminished PTH-stimulated cAMP formation, from 80 ± 2.5 to 23 ± 1 pmol/mg protein·5 min. Other aminoglycosides such as tobramycin, streptomycin, and neomycin also inhibited PTH-stimulated Mg2+ entry and cAMP formation. As these antibiotics are positively charged, the data suggest that aminoglycosides act through an extracellular polyvalent cation-sensing receptor present in distal convoluted tubule cells. We infer from these studies that aminoglycosides inhibit hormone-stimulated Mg2+ absorption in the distal convoluted tubule that may contribute to the renal magnesium wasting frequently observed with the clinical use of these antibiotics.Key words: intracellular Mg2+, Mg2+ uptake, aminoglycosides, gentamicin, tobramycin, streptomycin, neomycin, parathyroid hormone, microfluorescence, cAMP measurements.

scholarly journals Insulin-like growth factor binding protein 7 and tissue inhibitor of metalloproteinases-2: differential expression and secretion in human kidney tubule cells

2017 ◽  
Vol 312 (2) ◽  
pp. F284-F296 ◽  
Author(s):  
David R. Emlet ◽  
Nuria Pastor-Soler ◽  
Allison Marciszyn ◽  
Xiaoyan Wen ◽  
Hernando Gomez ◽  
...  
Keyword(s):  
Cell Culture ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Human Kidney ◽  
Distal Tubule ◽  
Cell Types ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tubule Cell ◽  
Tubule Cells

We have characterized the expression and secretion of the acute kidney injury (AKI) biomarkers insulin-like growth factor binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2) in human kidney epithelial cells in primary cell culture and tissue. We established cell culture model systems of primary kidney cells of proximal and distal tubule origin and observed that both proteins are indeed expressed and secreted in both tubule cell types in vitro. However, TIMP-2 is both expressed and secreted preferentially by cells of distal tubule origin, while IGFBP7 is equally expressed across tubule cell types yet preferentially secreted by cells of proximal tubule origin. In human kidney tissue, strong staining of IGFBP7 was seen in the luminal brush-border region of a subset of proximal tubule cells, and TIMP-2 stained intracellularly in distal tubules. Additionally, while some tubular colocalization of both biomarkers was identified with the injury markers kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin, both biomarkers could also be seen alone, suggesting the possibility for differential mechanistic and/or temporal profiles of regulation of these early AKI biomarkers from known markers of injury. Last, an in vitro model of ischemia-reperfusion demonstrated enhancement of secretion of both markers early after reperfusion. This work provides a rationale for further investigation of these markers for their potential role in the pathogenesis of acute kidney injury.

Effects of dDAVP on rat juxtamedullary nephrons: stimulation of medullary K recycling

1985 ◽  
Vol 249 (2) ◽  
pp. F291-F298 ◽  
Author(s):  
J. M. Elalouf ◽  
N. Roinel ◽  
C. de Rouffignac
Keyword(s):  
Parathyroid Hormone ◽  
Adenylate Cyclase ◽  
Excretion Rate ◽  
Distal Tubule ◽  
Fractional Excretion ◽  
The Other ◽  
Thick Ascending Limb ◽  
Adenylate Cyclase System ◽  
Circulating Levels ◽  
Stimulation Of

The effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on the handling of water and electrolytes by the juxtamedullary nephrons were studied on rats with reduced circulating levels of antidiuretic hormone (ADH), parathyroid hormone, calcitonin, and glucagon, all of which stimulate the adenylate cyclase system of the thick ascending limb and the distal tubule. In such hormone-deprived rats and in hormone-deprived + dDAVP rats, the concentration of Na, Cl, and total solutes was lower in the ascending than in the descending limbs, whereas the inulin concentration was similar at both sites. dDAVP did not alter the fraction of NaCl remaining in the thin limbs, but tended to reduce that of Mg and Ca. On the other hand, dDAVP significantly increased the fraction of filtered K remaining from 65.8 +/- 5.2 to 107.3 +/- 15.8%. A direct correlation was observed between the fraction of filtered K remaining at the tip of the juxtamedullary loops and the fractional excretion rate of K in urine. Since dDAVP enhances distal K net secretion, as previously shown in our laboratory, these results indicate that the medullary recycling of K from nephron terminal segments to Henle's loop of juxtamedullary nephrons is stimulated by this peptide.

NaCl and Ca delivery at the bend of rat deep nephrons decreases during antidiuresis

1987 ◽  
Vol 252 (6) ◽  
pp. F1055-F1064 ◽  
Author(s):  
J. M. Elalouf ◽  
D. Chabane Sari ◽  
N. Roinel ◽  
C. de Rouffignac
Keyword(s):  
Parathyroid Hormone ◽  
Diabetes Insipidus ◽  
Arginine Vasopressin ◽  
Distal Tubule ◽  
Water Removal ◽  
Loop Of Henle ◽  
Brattleboro Rats ◽  
Previous Hypothesis

The effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on superficial and juxtamedullary nephrons were investigated by micropuncture in diabetes insipidus (DI) Brattleboro rats chronically treated with the peptide. The rats, acutely deprived of endogenous calcitonin, parathyroid hormone (PTH), and glucagon [hormone-deprived (HD) rats], were examined either 4 days after cessation of dDAVP treatment (HDT, control diuretic rats) or when the treatment was continued until the micropuncture experiment, during which dDAVP was also given intravenously (HDT + dDAVP, experimental nondiuretic rats). In the presence of dDAVP, the reabsorption of Cl, Na, Mg, and Ca by the superficial loop of Henle was significantly increased, as previously observed in HD-untreated rats during acute infusion of dDAVP. The effects on the superficial distal tubule were also similar. The effects on K, however, were different both in the loop and in the distal tubule. At the bend of the juxtamedullary nephrons, the treatment alone (HDT rats) increased fractional delivery (FD%) of Na and Cl, whereas FD% of Mg, Ca, K, and P was unaltered. In HDT + dDAVP rats, FD% of H2O, Cl, Na, and Ca was significantly lower than in HDT rats, and FD% of K, Mg, and P did not differ significantly. In conclusion, in the presence of dDAVP, the FD% of H2O, Na, and Cl at the bend of the long-loop nephrons decreases, in accordance with our previous hypothesis that water removal along the rat descending limb increases outward NaCl diffusion along this segment.

Hormonal regulation of calcium transport in thick ascending limb renal tubules

1981 ◽  
Vol 241 (2) ◽  
pp. F171-F174 ◽  
Author(s):  
W. N. Suki ◽  
D. Rouse
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Hormonal Regulation ◽  
Calcium Transport ◽  
Rabbit Kidney ◽  
Renal Tubules ◽  
Similar Response ◽  
Thick Ascending Limb ◽  
Calcium Efflux ◽  
Bathing Medium

Net calcium efflux (JCanet) was compared in isolated perfused cortical and medullary segments of the thick ascending limb of Henle of the rabbit kidney. In response to the addition of calcitonin to the bathing medium, cortical segments showed no change in JCanet, whereas in medullary segments JCanet increased significantly. Similar studies substituting 8-bromo-cyclic AMP (8-BrcAMP) in concentrations of 10(-4) M or lower in the bath showed no effect on JCanet in either segment. When the concentration of 8-BrcAMP in the bath was increased to 10(-3) M, JCanet rose significantly in both segments. These results indicate heterogeneity of response to calcitonin in the cortical and medullary segments of the thick ascending limb of Henle, but a similar response of calcium transport to cAMP. Because we have previously shown that parathyroid hormone stimulates net calcium efflux in the cortical but not in the medullary segments of the thick ascending limb of Henle, the present observations suggest that cAMP may be the mediator of the actions of both calcitonin and parathyroid hormone.

Glucagon and arginine vasopressin stimulate Mg2+ uptake in mouse distal convoluted tubule cells

1998 ◽  
Vol 274 (2) ◽  
pp. F328-F335 ◽  
Author(s):  
Long-Jun Dai ◽  
Brian Bapty ◽  
Gordon Ritchie ◽  
Gary A. Quamme
Keyword(s):  
Arginine Vasopressin ◽  
Channel Blocker ◽  
Phorbol Esters ◽  
Distal Tubule ◽  
Distal Convoluted Tubule ◽  
Hormone Action ◽  
Camp Pathway ◽  
Tubule Cells ◽  
Free Media ◽  
Stimulation Of

Glucagon and arginine vasopressin (AVP) enhance renal magnesium conservation through actions within the loop of Henle and the distal tubule. Studies were performed on an immortalized mouse distal convoluted tubule (MDCT) cell line to characterize the cellular actions of these hormones on Mg2+transport in this segment of the distal tubule. Glucagon and AVP increased cellular cAMP concentrations by about fivefold above basal levels in normal and Mg2+-depleted cells. Intracellular free Mg2+concentration ([Mg2+]i) was determined on single MDCT cells using microfluorescence with mag-fura 2. To assess Mg2+ uptake, MDCT cells were first Mg2+depleted (0.22 ± 0.01 mM) by culturing in Mg2+-free media for 16 h and then placed in 1.5 mM MgCl2, and the [Mg2+]iwas determined. [Mg2+]ireturned to basal levels, 0.53 ± 0.02 mM, with a mean refill rate, d([Mg2+]i)/d t, of 164 ± 5 nM/s. Both glucagon and AVP stimulated Mg2+ uptake into MDCT cells, 196 ± 11 and 189 ± 6 nM/s, respectively, at concentrations of 3 × 10−7 M and 10−7 M, respectively. Enhanced Mg2+ uptake for each of the hormones was concentration dependent and inhibited by the channel blocker, nifedipine. Hormone stimulation of Mg2+ entry was not dependent on protein synthesis. 8-Bromo-cAMP, 10−4 M, enhanced Mg2+ uptake (225 ± 13 nM/s), whereas phorbol esters were without effect. Finally, protein kinase A inhibition prevented glucagon and AVP stimulation of Mg2+ uptake, supporting the notion that the cAMP pathway is important as expected in the hormone action. These studies demonstrate that glucagon and AVP stimulate Mg2+ uptake in MDCT cells and suggest that these hormones act to control magnesium conservation in the convoluted segment of the distal tubule.

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