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.

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.

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.

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.

Control of steady-state pH in rabbit proximal straight tubules

1987 ◽  
Vol 253 (2) ◽  
pp. F282-F289
Author(s):  
J. L. Atkins ◽  
M. B. Burg
Keyword(s):  
Steady State ◽  
Proximal Tubule ◽  
The Other ◽  
Slow Flow ◽  
Bicarbonate Concentration ◽  
Flow Rates ◽  
Other Hand ◽  
Straight Tubules

Steady-state pH (defined as the limiting pH reached at slow flow rates) was measured in isolated perfused rabbit proximal straight tubules (S2). With normal bath conditions (pH 7.4, bicarbonate 25 mM) the luminal steady-state pH was 6.85. Steady-state pH was directly related to bath pH and bicarbonate, but not to bath PCO2. Lowering of bath pH or bicarbonate consistently decreased luminal steady-state pH, and raising either caused steady-state pH to increase. When bath PCO2 was increased, on the other hand, steady-state pH either increased or decreased, depending on the concomitant changes in bicarbonate and pH. The changes in steady-state pH observed in the present studies following alterations in bath pH and bicarbonate concentration should, when extrapolated to the in vivo kidney, result in decreased delivery of bicarbonate from the proximal tubule in acidosis and increased delivery in alkalosis. The effects of potassium and chloride were also determined. Removal of potassium from the bath increased the steady-state pH, but removal of chloride from both the perfusate and bath had no significant effect.

Experimental Cystinuria: the Cycloleucine Model. I. Amino Acid Interactions in Renal and Intestinal Epithelia

1975 ◽  
Vol 53 (6) ◽  
pp. 1027-1036 ◽  
Author(s):  
André G. Craan ◽  
Michel Bergeron
Keyword(s):  
Amino Acids ◽  
Renal Tubules ◽  
Intestinal Epithelia ◽  
Luminal Membrane ◽  
Luminal Side ◽  
Convoluted Tubules ◽  
Dibasic Amino Acids ◽  
Everted Sacs

The injection of cycloleucine (1-aminocyclopentanecarboxylic acid (ACPC)) into rats produces a hyperexcretion of dibasic amino acids and cystine, an aberration resembling cystinuria. This may constitute a model of experimental cystinuria, and the transport of amino acids involved in this disease was studied with the techniques of everted intestinal sacs (in vitro) and microinjections into renal tubules (in vivo). In everted sacs from normal rats, there was a decrease in transfer and in accumulation of L-cystine (0.03 mM), L-lysine (0.065 mM) and L-valine (0.065 mM) when ACPC was on the mucosal (luminal) side. Dibasic amino acids such as L-ariginine and L-lysine caused a similar inhibition of the transport of L-cystine. However, when ACPC was on the serosal (antiluminal) side, a lesser effect was noted while arginine and lysine had no effect. Intestinal sacs from treated rats (ACPC, 300 mg/kg × 3 days) transferred and accumulated as much L-cystine as those from control rats. The interaction between cycloleucine and L-cystine was competitive at the luminal and non-competitive at the antiluminal side of the intestine. Cycloleucine inhibited L-lysine transport in a non-competitive fashion at either side of the intestine. L-Lysine also interacted in a non-competitive fashion with L-cystine transport at the luminal membrane. In proximal convoluted tubules, the presence of L-arginine or ACPC caused a decrease in the transport of L-cystine and L-lysine. L-Valine exerted no effect. Furthermore, L-lysine and ACPC did not impair the reabsorption of L-valine significantly.These results suggest a functional heterogeneity between luminal and antiluminal membranes of renal and intestinal epithelia and the existence, at both membranes, of different transport sites for cystine and dibasic amino acids.

Effects of calcium on synthesis and secretion of parathyroid hormone and secretory protein I

1988 ◽  
Vol 255 (3) ◽  
pp. E299-E305
Author(s):  
R. R. MacGregor ◽  
D. A. Hinton ◽  
R. D. Ridgeway
Keyword(s):  
Protein Synthesis ◽  
Steady State ◽  
Parathyroid Hormone ◽  
Total Protein ◽  
Secretory Protein ◽  
Hormone Synthesis ◽  
Synthesis And Degradation

Bovine parathyroid organoids were cultured for up to 3 wk in medium containing 1.4 or 1.8 mM calcium. Steady-state secretion of parathyroid hormone and secretory protein I was two- to fourfold greater at 1.4 mM. At the end of culture, organoids were incubated 3.5 h in 1 or 2 mM calcium to examine maximum and minimum acute secretory rates. Relative to organoids cultured at 1.8 mM calcium, culture at 1.4 mM induced a hypersecretory state, i.e., both the maximum and minimum acute secretory rates of organoids previously cultured at 1.4 mM calcium were up to threefold greater than those of organoids previously at 1.8 mM calcium. Proparathyroid hormone synthesis was up to 50% greater in organoids cultured at 1.4 mM calcium, whereas secretory protein I and total protein synthesis were unaltered. The results showed that parathyroid hypersecretion can be induced by chronic hypocalcemic conditions in vitro. We conclude that the secretory adaptation to chronic hypocalcemia in vitro involves alterations in both synthesis and degradation of parathyroid hormone.

Calcium transport across the pars recta of cortical segment 2 proximal tubules

1986 ◽  
Vol 251 (4) ◽  
pp. F718-F724
Author(s):  
J. E. Bourdeau
Keyword(s):  
Proximal Tubule ◽  
Driving Forces ◽  
Proximal Tubules ◽  
Ion Diffusion ◽  
Low Concentrations ◽  
Pars Recta ◽  
Transepithelial Voltage ◽  
Lower Temperature ◽  
Tubule Fluid

Partes rectae of cortical segment 2 proximal tubules were dissected from rabbit kidneys and perfused in vitro. Ca concentrations of perfused and collected fluids were measured by continuous-flow microcolorimetry. Epithelial Ca permeability (P) was estimated from the bath-to-lumen movement of 45Ca. The transepithelial voltage (psi) and [Ca2+] difference were varied simultaneously by changing perfusate composition. Tubules that were perfused and bathed with an identical artificial ultrafiltrate of plasma displayed a lumen-negative psi, a collectate [Ca] greater than perfusate, and net Ca secretion. Tubules perfused with "late" proximal tubule fluid (high [Cl], low [HCO3], low concentrations of Na+-cotransported solutes) demonstrated a lumen-positive psi, a perfusate [Ca2+] greater than the bath, a collectate [Ca] less than perfusate, and net Ca absorption. Under each of these conditions, net Ca flux was in the direction predicted by the experimentally measured driving forces for diffusional Ca transport. Tubules that were cooled while being perfused with late proximal tubule fluid showed an increased lumen-positive psi but reduced net Ca absorption. The latter finding was consistent with reduced Ca ion diffusion related to a smaller P at the lower temperature. I conclude that Ca2+ diffusion is an important component of net Ca absorption in this segment of the nephron.

CFD Challenge: Solutions Using the In-House Finite-Element-Based Solver NEWTETR

2012 ◽  
Author(s):  
Yiemeng Hoi ◽  
David A. Steinman
Keyword(s):  
Steady State ◽  
Pressure Measurements ◽  
Surface Geometry ◽  
Flow Rates ◽  
Pressure Drops ◽  
Or Groups ◽  
Giant Cerebral Aneurysm ◽  
Pulsatile Pressure ◽  
Nominal Surface

Briefly, this Challenge aims to test the sensitivity of steady and pulsatile pressure drops as predicted by different CFD solvers or groups, and ultimately against in vitro pressure measurements. The current study focuses on the Phase I of the Challenge. We simulated steady state and pulsatile pressure drops based on the nominal surface geometry and specific inlet flow rates on a giant cerebral aneurysm with proximal stenosis.

Secretory NaCl and volume flow in renal tubules

1986 ◽  
Vol 250 (5) ◽  
pp. R753-R763 ◽  
Author(s):  
K. W. Beyenbach
Keyword(s):  
Fluid Secretion ◽  
Renal Tissue ◽  
Tubular Secretion ◽  
Proximal Tubules ◽  
Epithelial Cell Line ◽  
Renal Tubules ◽  
Genetic Potential ◽  
Dog Kidney ◽  
Nacl Secretion

This review attempts to give a retrospective survey of the available evidence concerning the secretion of NaCl and fluid in renal tubules of the vertebrate kidney. In the absence of glomerular filtration, epithelial secretory mechanisms, which to this date have not been elucidated, are responsible for the renal excretion of NaCl and water in aglomerular fish. However, proximal tubules isolated from glomerular fish kidneys of the flounder, killifish, and the shark also have the capacity to secrete NaCl and fluid. In shark proximal tubules, fluid secretion appears to be driven via secondary active transport of Cl. In another marine vertebrate, the sea snake, secretion of Na (presumably NaCl) and fluid is observed in freshwater-adapted and water-loaded animals. Proximal tubules of mammals can be made to secrete NaCl in vitro together with secretion of aryl acids. An epithelial cell line derived from dog kidney exhibits secondary active secretion of Cl when stimulated with catecholamines. Tubular secretion of NaCl and fluid may serve a variety of renal functions, all of which are considered here. The occurrence of NaCl and fluid secretion in glomerular proximal tubules of teleosts, elasmobranchs, and reptiles and in mammalian renal tissue cultures suggests that the genetic potential for NaCl secretion is present in every vertebrate kidney.

Contribution of leaked load to solute transport by renal tubules

1978 ◽  
Vol 234 (6) ◽  
pp. F480-F484 ◽  
Author(s):  
D. G. Warnock ◽  
C. S. Patlak ◽  
M. B. Burg
Keyword(s):  
Substantial Part ◽  
Renal Tubules ◽  
In Vitro Perfusion ◽  
Tubule Lumen ◽  
Tubular Transport ◽  
Glomerular Filtrate ◽  
The Relationship ◽  
Convoluted Tubules ◽  
Filtered Load

Renal tubules reabsorb solutes from the glomerular filtrate. The relationship between "filtered load" and reabsorption has been previously discussed and analyzed in detail. One aspect which has not been emphasized, however, is that, when reabsorption of a solute causes its concentration (or activity) in the tubule lumen to decrease below the level in the blood, solute may enter the tubule down this concentration gradient adding a "leaked load" to the filtered load. The leaked load should be taken into account when quantifying tubular transport. In the present study we derived equations for estimating the leaked load and its contribution to transport. The importance of the leaked load of glucose in the rabbit proximal convoluted tubules is evaluated with parameters derived from in vitro perfusion and by solving the equations numerically. It is shown that, depending on the conditions, the leaked load of glucose may account for a substantial part of the glucose present in the tubule lumen and reabsorbed from the tubule. Also, the leaked load could conceivably be an important factor in the transport of other solutes such as lactase and bicarbonate in proximal tubules.

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