scholarly journals The inhibition of parathyroid-hormone actions on gluconeogenesis and phosphate transport by 3-mercaptopicolinate in rabbit renal proximal tubules

1986 ◽  
Vol 233 (1) ◽  
pp. 271-273
Author(s):  
N Yanagawa ◽  
O D Jo
Keyword(s):  
Parathyroid Hormone ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Renal Tubule ◽  
Phosphate Transport ◽  
Proximal Tubules ◽  
Transport Rate ◽  
Renal Proximal Tubules ◽  
Straight Tubules ◽  
Isolated Renal Tubule

By using a glucose microassay and the technique for isolated renal-tubule perfusion in vitro, the addition of 3-mercaptopicolinate, a gluconeogenesis inhibitor which inhibits phosphoenolpyruvate carboxykinase specifically, was found to abolish the effects of parathyroid hormone on gluconeogenesis and phosphate-transport rate in isolated rabbit renal proximal straight tubules, suggesting that these parathyroid-hormone actions may share some unknown, yet 3-mercaptopicolinate-inhibitable, intracellular processes.

Possible role of calcium in parathyroid hormone actions in rabbit renal proximal tubules

1986 ◽  
Vol 250 (5) ◽  
pp. F942-F948
Author(s):  
N. Yanagawa ◽  
O. D. Jo
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubules ◽  
Inhibitory Effects ◽  
Renal Proximal Tubules ◽  
Intracellular Ca ◽  
Altered Response ◽  
Isolated Renal Tubule ◽  
Convoluted Tubules

Using a glucose microassay and in vitro isolated renal tubule perfusion technique, we have studied the actions of parathyroid hormone (PTH) on gluconeogenesis (GNG) and fluid (Jv) and phosphate (Jp) transport rates in isolated rabbit renal proximal tubules. In proximal straight tubules (PST), PTH stimulated GNG and inhibited Jv and Jp. In proximal convoluted tubules (PCT), PTH inhibited Jv but failed to affect GNG and Jp. An increase in Ca concentration, however, stimulated GNG and allowed PTH to inhibit Jp in PCT. Addition of the intracellular Ca antagonists trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) abolished the inhibitory effects of PTH on Jv and Jp in both PCT and PST. In conclusion, these studies suggest that Ca-dependent intracellular pathways may be involved in the actions of PTH in rabbit renal proximal tubules. The altered response to PTH in rabbit PCT may be due to alterations in the response of intracellular Ca to the hormone.

Effect of parathyroid hormone on bicarbonate absorption by proximal tubules in vitro

1979 ◽  
Vol 236 (4) ◽  
pp. F387-F391 ◽  
Author(s):  
Y. Iino ◽  
M. B. Burg
Keyword(s):  
Steady State ◽  
Parathyroid Hormone ◽  
Proximal Tubules ◽  
Renal Tubules ◽  
Bicarbonate Concentration ◽  
Flow Rates ◽  
Straight Tubules ◽  
Convoluted Tubules ◽  
Tubule Fluid

The effect of parathyroid hormone on bicarbonate absorption was tested in rabbit proximal renal tubules perfused in vitro. In proximal straight tubules 0.05 U/ml of parathyroid hormone caused a large and reversible increase in the steady-state bicarbonate concentration in tubule fluid. Further, the rates of bicarbonate and fluid absorption (measured at faster flow rates) were inhibited approximately 50% by the hormone. We conclude that parathyroid hormone directly inhibits fluid and bicarbonate absorption by proximal straight tubules, causing an increase in the bicarbonate concentration in the tubule fluid, and we suggest that this action of the hormone contributes to the increase in renal bicarbonate excretion that is generally caused by the hormone. In proximal convoluted tubules, parathyroid hormone was previously demonstrated by other investigators to inhibit fluid and bicarbonate absorption approximately proportionally, so that there was little or no change in the bicarbonate concentration in tubule fluid. In agreement we found in the present studies that 0.05 U/ml of the hormone did not affect the steady-state bicarbonate concentration in proximal convoluted tubule fluid and that 5 U/ml caused only an equivocal increase in tubule fluid bicarbonate concentration.

scholarly journals SUN-140 EFFECTS OF PARATHYROID HORMONE ON GLUCOSE METABOLISM IN RENAL PROXIMAL TUBULES

2019 ◽  
Vol 4 (7) ◽  
pp. S216
Author(s):  
H. Tsukada ◽  
M. Nakamura ◽  
N. Satoh ◽  
T. Mizuno ◽  
Y. Sato ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Glucose Metabolism ◽  
Proximal Tubules ◽  
Renal Proximal Tubules

Establishment of a Parathyroid Hormone-Responsive Phosphate Transport System in Vitro Using Cultured Renal Cells*

Endocrinology ◽  
1986 ◽  
Vol 119 (5) ◽  
pp. 1954-1963 ◽  
Author(s):  
YOSHIKAZU KINOSHITA ◽  
MASAAKI FUKASE ◽  
AKIMITSU MIYAUCHI ◽  
MUTSUMI TAKENAKA ◽  
MASAKI NAKADA ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Transport System ◽  
Phosphate Transport ◽  
Renal Cells

cAMP-stimulated rise of [Ca2+]i in rabbit connecting tubules: role of peritubular Ca

1990 ◽  
Vol 258 (3) ◽  
pp. F751-F755 ◽  
Author(s):  
J. E. Bourdeau ◽  
B. K. Eby
Keyword(s):  
Parathyroid Hormone ◽  
Ethylene Glycol ◽  
Cell Activation ◽  
Proximal Tubules ◽  
Tetraacetic Acid ◽  
Luminal Membrane ◽  
Dose Dependent Fashion ◽  
Dose Dependent

Parathyroid hormone (PTH) increases cytosolic free Ca concentration ([ Ca2+]i) by mechanisms that depend on extracellular Ca in both cultured renal proximal tubules and isolated rabbit connecting tubules (CNTs). In CNTs 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) mimics this action, implicating cAMP as a second messenger, and part of the rise, due to increased luminal membrane Ca entry, is likely related to Ca absorption. In cultured proximal tubules the rise in [Ca2+]i, presumably mediated by increased Ca entry across the basolateral plasmalemma, activates gluconeogenesis and shortens microvilli. In the present study we examined cAMP-mediated Ca entry across the basolateral membranes of CNT cells, an effect potentially related to cell activation. Single CNTs were dissected from rabbit kidneys and loaded with fura-2. [Ca2+]i was measured by dual-wavelength excitation during perfusion of isolated segments in vitro. With 1.8 or 2.0 mM Ca in the lumen and the bath, suffusate 8-BrcAMP increased [Ca2+]i within minutes in a dose-dependent fashion. The increase persisted as long as 8-BrcAMP was present and reversed on its withdrawal. With 0.1 microM Ca in the lumen and the bath, 8-BrcAMP, but not ionomycin, failed to increase [Ca2+]i, implying that extracellular Ca is the major source. In tubules perfused with 2 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid to eliminate luminal Ca, but suffused with 1.8 or 2.0 mM Ca, 8-BrcAMP increased [Ca2+]i (though less so than with Ca in the lumen), implying Ca entry across basolateral cell membranes. This rise in [Ca2+]i was attenuated markedly by the presence of 50 microM LaCl3 in the bath.(ABSTRACT TRUNCATED AT 250 WORDS)

Cimetidine and procainamide secretion by proximal tubules in vitro

1982 ◽  
Vol 242 (6) ◽  
pp. F672-F680 ◽  
Author(s):  
T. D. McKinney ◽  
K. V. Speeg
Keyword(s):  
Competitive Inhibition ◽  
Proximal Tubules ◽  
Renal Tubules ◽  
Co2 Absorption ◽  
Organic Base ◽  
Organic Bases ◽  
Straight Tubules ◽  
Tubule Lumen ◽  
High Concentrations

Previous studies have shown that organic bases, including some drugs, are secreted by renal proximal tubules. The present studies examined the transport of the organic bases cimetidine and procainamide by rabbit proximal straight tubules perfused in vitro. Both drugs were secreted into the tubule lumen. [3H]cimetidine secretion was reduced by quinidine, procainamide, and N-acetylprocainamide. Previous studies showed that cimetidine secretion was reduced by other organic bases. Hypothermia and ouabain inhibited [3H]procainamide secretion as was shown previously for cimetidine secretion. [3H]procainamide secretion was also reduced by quinidine, cimetidine, procainamide, and N-acetylprocainamide but not by probenecid. High concentrations of cimetidine (10(-3) M) had no effect on the rates of fluid or total CO2 absorption. When analyzed in terms of Michaelis-Menten kinetics, the effect of cimetidine on procainamide secretion and procainamide on cimetidine secretion was consistent with competitive inhibition. The results suggest that both cimetidine and procainamide are secreted into the lumen of proximal straight tubules predominately by an organic base transport mechanism. These studies raise the possibility that some of these drugs might compete for a common secretory mechanism in renal tubules and reduce the elimination of each other.

scholarly journals Fibroblast growth factor-23 increases mouse PGE2 production in vivo and in vitro

2006 ◽  
Vol 290 (2) ◽  
pp. F450-F455 ◽  
Author(s):  
Ashu Syal ◽  
Susan Schiavi ◽  
Sumana Chakravarty ◽  
Vangipuram Dwarakanath ◽  
Raymond Quigley ◽  
...  
Keyword(s):  
Fibroblast Growth Factor 23 ◽  
Phosphate Transport ◽  
Proximal Tubules ◽  
Fibroblast Growth ◽  
Transport Defect ◽  
Map Kinase Pathway ◽  
Fgf 23 ◽  
Kinase Pathway

Fibroblast growth factor-23 (FGF-23) has been implicated in the renal phosphate wasting in X-linked hypophosphatemia, tumor-induced osteomalacia, and autosomal dominant hypophosphatemic rickets. Recently, we demonstrated that Hyp mice have greater urinary PGE2 levels compared with C57/B6 mice and that indomethacin administration in vivo and in vitro ameliorates the phosphate transport defect in Hyp mice. To determine further whether altered prostaglandin metabolism plays a role in the renal phosphate transport defect in Hyp mice, we incubated renal proximal tubules with arachidonic acid. We find that PGE2 production was higher in Hyp mice than in C57/B6 mice. Incubation of C57/B6 mouse renal proximal tubules with FGF-23R176Q, an active mutant form of FGR23, increased tubular PGE2 production, an effect that was inhibited by 50 μM PD-98059 and 10 μM SB-203580, inhibitors of the MAP kinase pathway. C57/B6 mice injected with FGF-23R176Q had a ∼10-fold increase in PGE2 excretion 24 h after intraperitoneal injection of FGF-23R176Q compared with vehicle-treated controls. Finally, we show that PGE2 inhibited both phosphate and volume absorption in mouse proximal convoluted tubules perfused in vitro and reduced brush-border membrane vesicle NaPi-2a protein abundance from renal cortex incubated in vitro with PGE2. In conclusion, FGF-23 increases urinary and renal tubular PGE2 production via the MAP kinase pathway and PGE2 inhibits proximal tubule phosphate transport.

Origins of Isolated Tubule Microperfusion Methodology

Physiology ◽  
1988 ◽  
Vol 3 (4) ◽  
pp. 176-180
Author(s):  
Maurice B. Burg
Keyword(s):  
Renal Function ◽  
Analytical Methods ◽  
Renal Tubule ◽  
National Institutes Of Health ◽  
Electrolyte Metabolism ◽  
Basic Technology ◽  
Isolated Renal Tubule ◽  
Single Tubules

Understanding of renal function has been facilitated by the technique of perfusion of isolated renal tubule segments in vitro. The basic technology originated in the Laboratory of Kidney and Electrolyte Metabolism of the National Institutes of Health in the early 1960s and then was expanded to apply a variety of analytical methods to single tubules.

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