Glucocorticoid-induced Inhibition of the Reabsorption of Inorganic Phosphate in the Proximal Tubule in the Absence of Parathyroid Hormone

1984 ◽  
Vol 7 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Ivan Durasin ◽  
Anselm Frick ◽  
Mechtild Neuweg
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Inorganic Phosphate

Secretion of Inorganic Phosphate in the Rat Nephron

1975 ◽  
Vol 48 (6) ◽  
pp. 475-489 ◽  
Author(s):  
J.-F. Boudry ◽  
U. Troehler ◽  
M. Touabi ◽  
H. Fleisch ◽  
J.-P. Bonjour
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Inorganic Phosphate ◽  
Specific Radioactivity ◽  
Distal Tubule ◽  
High Plasma ◽  
Tubular Secretion ◽  
Tubular Reabsorption ◽  
Anaesthetized Rats ◽  
Terminal Nephron

1. The existence of tubular secretion of inorganic phosphate (Pi) in the mammalian kidney has been investigated by studying the renal response of rats infused with sodium phosphate by three different techniques. 2. Clearance studies indicate that, in anaesthetized rats, the net tubular reabsorption decreases markedly in response to Pi infusion. In conscious rats, the clearance of Pi slightly exceeded that of inulin at high plasma Pi concentration. 3. Free-flow micropuncture in control rats showed a net tubular reabsorption of Pi along the proximal tubule, and probably between the end of the distal tubule and the ureteral urine. In phosphate-loaded rats, whether receiving parathyroid hormone or not, an apparent net secretion of Pi was observed between the end of the distal tubule and the ureteral urine. In the phosphate-loaded group receiving parathyroid hormone, net secretion was also observed very early in the proximal tubule followed by a predominant reabsorption along this segment. Thus the early proximal tubule and probably also the terminal nephron can be the site of either net reabsorption or net secretion. 4. Microperfusions of proximal tubules show a fall in the specific radioactivity of the perfused radioactive Pi solution, indicating entry of Pi into the lumen.

Response to parathyroid hormone in defined segments of proximal tubule

1976 ◽  
Vol 230 (2) ◽  
pp. 286-290 ◽  
Author(s):  
RJ Hamburger ◽  
NL Lawson ◽  
JH Schwartz
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Proximal Convoluted Tubule ◽  
Base Line ◽  
Fluid Absorption ◽  
Functional Heterogeneity ◽  
Intrinsic Absorption ◽  
Pars Recta ◽  
Intrinsic Capacity ◽  
Control Fluid

Previous investigations have suggested that there is a functional heterogeneity along the length of the proximal convoluted tubule. This study was designed to confirm and extend these suggestions by examining the intrinsic absorption of fluid and the effect of parathyroid hormone (PTH) on net fluid absorption in isolated, anatomically defined segments of rabbit superficial proximal tubules. The EPCT (early proximal convoluted tubule), LPCT (late proximal convoluted tubule), and PR (pars recta) segments were studied under controlled conditions by the isolated perfused tubule technique. In 23 EPCT, base-line fluid absorption was 1.38 +/- 0.04 (SE), a rate significantly higher than those of 11 LPCT (0.62 +/- 0.02; P less than 0.001) and 12 PR (0.52 +/- 0.03 nl mm-1 min-1, P less than 0.001) segments. In 10 EPCT, mean control fluid absorption was 1.31 +/- 0.04 nl mm-1 min-1; addition of PTH resulted in a decrease to 0.95 +/- 0.05 nl mm-1 min-1 (P less than 0.001); and, after removal of PTH, fluid absorption increased (P less than 0.001). Parathyroid hormone had no effect on either seven LPCT segments or six PR segments. These results demonstrate differences in intrinsic capacity to absorb fluid by anatomically defined segments of the rabbit proximal tubule. This functional heterogeneity is further supported by the observed differential response to PTH by the various anatomic segments of the proximal tubule.

Stimulation of avian renal phosphate secretion by parathyroid hormone

1981 ◽  
Vol 241 (3) ◽  
pp. F263-F272 ◽  
Author(s):  
R. F. Wideman ◽  
E. J. Braun
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Phosphate ◽  
Domestic Fowl ◽  
Inorganic Phosphate ◽  
Minor Component ◽  
Sodium Potassium ◽  
Tubule Lumen ◽  
Tubular Transport ◽  
A Minor ◽  
Stimulation Of

Phosphate buffers (ammonium, sodium, potassium, and calcium phosphate, pH 5.5, 7.2, 8.5) and 32P were infused unilaterally into the renal portal systems of intact, parathyroidectomized (PTX), and parathyroid hormone-infused (PTH) domestic fowl to study the secretory flux for inorganic phosphate (Pi). Urine samples were collected simultaneously from both kidneys, with the uninfused kidney serving as a control for the portal-perfused kidney (modified Sperber technique). No consistent unilateral excess of Pi or 32P excretion occurred for any of the experimental groups. For intact birds, fractional 32P excretion by both kidneys (FE32p) was identical to fractional Pi excretion (FEpi) (determined by chemical analysis) and reflected net reabsorption (0.64). However, during PTH infusion, FE32p was 0.82 (net reabsorption) while FEPi was 1.21 (net secretion). These results indicate that a) the peritubular-to-lumen flux for Pi and 32P is a minor component of net tubular transport, regardless of the parathyroid status, counterion availability, or peritubular Pi concentration; b) plasma Pi and 32P enter the tubule lumen predominantly by filtration; c) PTH stimulates tubular Pi secretion; and d) the secreted Pi is derived from an organic or inorganic pool that does not readily equilibrate with infused 32P (or presumably peritubular Pi).

Effect of acute hypercapnia on PTH-stimulated phosphaturia in dietary Pi-deprived rat

1987 ◽  
Vol 253 (1) ◽  
pp. F34-F40 ◽  
Author(s):  
J. Guntupalli ◽  
B. Matthews ◽  
B. Carlin ◽  
E. Bourke
Keyword(s):  
Glomerular Filtration Rate ◽  
Parathyroid Hormone ◽  
Glomerular Filtration ◽  
Inorganic Phosphate ◽  
Filtration Rate ◽  
Direct Evidence ◽  
Respiratory Acidosis ◽  
Urinary Ph ◽  
Renal Handling ◽  
Per Se

The effects of respiratory acidosis on renal inorganic phosphate (Pi) handling are controversial. Clearance experiments, therefore, were performed in fasted, chronically parathyroidectomized (PTX), dietary Pi-deprived rats. The objectives were twofold: to study the effects of compensated and uncompensated hypercapnia per se on renal Pi excretion and to examine the interaction between acute hypercapnia, dietary Pi, and parathyroid hormone (PTH) on the renal handling of Pi. Acute hypercapnia increased the plasma Pi (delta 2.82 +/- 0.65 mg/dl, P less than 0.05) without altering the glomerular filtration rate (GFR). The FEPi increased (delta 7.26 +/- 0.48%, P less than 0.001) but the TRPi/GFR also increased. PTH (3 U X kg-1 X h-1) superimposed on hypercapnia resulted in a plasma Pi comparable to hypercapnia alone. The FEPi (7.56 +/- 0.78 vs. 24.43 +/- 2.20%; P less than 0.001) was higher and the TRPi/GFR (117 +/- 4 vs. 80 +/- 2 micrograms/min, P less than 0.01) lower, in the former group. PTH infusion during normocapnia resulted in a lower FEPi (0.20 +/- 0.10 vs. 24.43 +/- 2.20%, P less than 0.001) and a higher TRPi/GFR (106 +/- 2 vs. 80 +/- 2 micrograms/min, P less than 0.01) compared with PTH infusion during hypercapnia. Urinary adenosine 3',5'-cyclic monophosphate (cAMP) excretion was similar between the groups. During hypercapnia, when the extracellular acidemia was neutralized, the phosphaturic action of PTH persisted. These studies offer direct evidence that in chronically PTX, dietary Pi-deprived rats, the phosphaturic action of PTH is restored by hypercapnia per se. This effect appears to be independent of extracellular acidemia, changes in the plasma Pi and calcium, urinary pH and Na and cAMP excretion.

Fluoride mobilizes intracellular calcium and promotes Ca2+ influx in rat proximal tubules

1991 ◽  
Vol 261 (2) ◽  
pp. F318-F327 ◽  
Author(s):  
J. H. Dominguez ◽  
J. G. Garcia ◽  
J. K. Rothrock ◽  
D. English ◽  
C. Mann
Keyword(s):  
Signal Transduction ◽  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
G Protein ◽  
Pertussis Toxin ◽  
Time Course ◽  
Proximal Tubules ◽  
Signal Transduction Pathways ◽  
Pi Hydrolysis

In the renal proximal tubule, external Ca2+ ([Ca2+]o) is required for parathyroid hormone to elevate cytosolic Ca2+ ([Ca2+]i). However, other hormones increase [Ca2+]i in the absence of [Ca2+]o. These differences may arise from a diversity of signal transduction pathways acting on external and internal Ca2+ pools. However, Ca2+ influx may be necessary to expedite and maintain the rise of [Ca2+]i for a period after the initial surge. In this study, F- was used to probe the roles of intracellular Ca2+ mobilization, Ca2+ influx, and phosphoinositide (PI) hydrolysis on the surge of [Ca2+]i in rat proximal tubules. In the presence of external Ca2+; 1-20 mM F- evoked incremental rises of [Ca2+]i in tubules loaded with aequorin. Whereas 10 mM F- increased [Ca2+]i in the absence of [Ca2+]o, the time constant for the [Ca2+]i surge was increased. These findings are consistent with a role of Ca2+ influx on the effect of F- on [Ca2+]i. Indeed, 10 mM F- also enhanced the uptake of 45Ca2+, and promoted Ca2+ influx in aequorin- and fura-2-loaded, Ca(2+)-deprived tubules. In tubules, F- also activated PI hydrolysis with a time course that paralleled Ca2+ mobilization. The effect of F- on [Ca2+]i was not altered when the 39-kDa pertussis toxin substrate was inactivated with the toxin. This G protein was most likely Gi, because prostaglandin E2, an activator of Gi in tubules, dissociated the pertussis toxin-sensitive protein. The results support the notion that activation of a signal-transduction complex, the F- substrate, causes Ca2+ influx, mobilizes internal Ca2+, and activates PI hydrolysis in rat proximal tubules.(ABSTRACT TRUNCATED AT 250 WORDS)

Posttranscriptional regulation of the proximal tubule NaPi-II transporter in response to PTH and dietary Pi

1999 ◽  
Vol 277 (5) ◽  
pp. F676-F684 ◽  
Author(s):  
Heini Murer ◽  
Ian Forster ◽  
Nati Hernando ◽  
Georg Lambert ◽  
Martin Traebert ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Posttranscriptional Regulation ◽  
Apical Membrane ◽  
Tubular Reabsorption ◽  
Transport Capacity ◽  
Phosphate Intake ◽  
Proximal Tubular ◽  
Dietary Phosphate ◽  
Proximal Tubular Reabsorption

The rate of proximal tubular reabsorption of phosphate (Pi) is a major determinant of Pi homeostasis. Deviations of the extracellular concentration of Piare corrected by many factors that control the activity of Na-Pi cotransport across the apical membrane. In this review, we describe the regulation of proximal tubule Pi reabsorption via one particular Na-Pi cotransporter (the type IIa cotransporter) by parathyroid hormone (PTH) and dietary phosphate intake. Available data indicate that both factors determine the net amount of type IIa protein residing in the apical membrane. The resulting change in transport capacity is a function of both the rate of cotransporter insertion and internalization. The latter process is most likely regulated by PTH and dietary Pi and is considered irreversible since internalized type IIa Na-Picotransporters are subsequently routed to the lysosomes for degradation.

Hormonal regulation of rat renal proximal tubule brush-border membrane ionic permeability

1992 ◽  
Vol 263 (1) ◽  
pp. F144-F151 ◽  
Author(s):  
M. S. Lipkowitz ◽  
R. D. London ◽  
J. C. Beck ◽  
R. G. Abramson
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Brush Border ◽  
Renal Proximal Tubule ◽  
Ionic Permeability ◽  
Brush Border Membranes ◽  
Rat Renal Proximal Tubule ◽  
Selective Increase ◽  
Gi Proteins ◽  
Cl Permeability

The effects on ionic permeability of toxins and hormones that activate or deactivate the guanine nucleotide regulatory (G) proteins that govern adenylate cyclase activity were examined in rat renal proximal tubule cell brush-border membranes. These studies demonstrate that activation of stimulatory G (Gs) proteins by cholera toxin or parathyroid hormone and deactivation of inhibitory (G (Gi) proteins by pertussis toxin result in a selective increase in Cl- permeability relative to that of K+ as determined with the potential-sensitive fluorescent probe 3,3'-dipropylthiadicarbocyanine iodide [diS-C3-(5)]. In contrast, activation of Gi by angiotensin II significantly decreases relative Cl- permeability. The selective increase in relative Cl- permeability induced by parathyroid hormone results in an inside-negative potential in membrane vesicles exposed to an inward NaCl gradient that is of sufficient magnitude to stimulate electrogenic, Na(+)-dependent glucose transport. These data suggest that the relative ionic permeabilities of brush-border membranes are tonically regulated by the opposing effects of hormones that act via Gs or Gi proteins. Changes in membrane potential resulting from this regulation may play an important role in modifying transport in the proximal tubule.

Nephron heterogeneity of phosphate reabsorption: effect of parathyroid hormone

1984 ◽  
Vol 246 (2) ◽  
pp. F155-F158
Author(s):  
A. Haramati ◽  
J. A. Haas ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Proximal Tubules ◽  
Loop Of Henle ◽  
Phosphate Reabsorption ◽  
Phosphate Excretion ◽  
Before And After ◽  
Superficial And Deep Nephrons ◽  
Nephron Heterogeneity

We evaluated the response of superficial and deep nephron proximal tubules to PTH in thyroparathyroidectomized (TPTX) rats fed a normal phosphate diet (0.7%). As phosphate reabsorption is not detectable in the ascending limb of the loop of Henle, fractional phosphate delivery (FDPi%) to the superficial early distal tubule and papillary loop of Henle reflects delivery from superficial and deep nephron proximal tubules, respectively. Re-collection micropuncture experiments were performed in nine acutely TPTX rats before and after the infusion of PTH (33 U/kg bolus; 1 U X kg-1 X min-1). In response to PTH, fractional phosphate excretion increased from 3.3 to 26.2% (P less than 0.05). FDPi% was less from the deep than from the superficial proximal tubule (5.7 vs. 15.7%, P less than 0.05) prior to PTH, indicating enhanced phosphate reabsorption by deep compared with superficial proximal tubules. During PTH infusion, FDPi% was increased in both nephron groups compared with control (P less than 0.05), but there were no differences in phosphate delivery between deep (28.0%) and superficial (29.7%) proximal tubules. We conclude that in acutely volume-expanded TPTX rats, infusion of a pharmacologic dose of PTH decreases phosphate reabsorption in both superficial and deep nephrons. Furthermore, the heterogeneity of FDPi% from deep compared with superficial proximal tubules seen in TPTX rats is absent during PTH infusion.

scholarly journals Defective Parathyroid Hormone Regulation of NHE3 Activity and Phosphate Adaptation in Cultured NHERF-1-/-Renal Proximal Tubule Cells

2004 ◽  
Vol 279 (36) ◽  
pp. 37815-37821 ◽  
Author(s):  
Rochelle Cunningham ◽  
Deborah Steplock ◽  
Fengying Wang ◽  
Huijun Huang ◽  
Xiaofei E ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Renal Proximal Tubule ◽  
Hormone Regulation ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Renal Proximal Tubule Cells
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