Stimulation by antidiuretic hormone of electrolyte tubular reabsorption in rat kidney

1983 ◽  
Vol 244 (2) ◽  
pp. F156-F164 ◽  
Author(s):  
C. de Rouffignac ◽  
B. Corman ◽  
N. Roinel
Keyword(s):  
Rat Kidney ◽  
Phosphate Transport ◽  
Urinary Flow ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Excretion Rates ◽  
In Vivo Administration

The effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on renal excretion and tubular transport of water and electrolytes were investigated in homozygous DI Brattleboro rats. To ascertain these effects on the loop of Henle, circulating glucagon, parathyroid hormone, and thyrocalcitonin were reduced before the experiments, as these hormones are believed to stimulate the same cells of the thick ascending limb as ADH. dDAVP did not alter either glomerular or proximal tubular functions. In the loop, it consistently raised reabsorption of Mg, Ca, K, and, to a lesser extent, Na and Cl, but phosphate transport was not affected. dDAVP lowered the urinary excretion rates for Mg, Ca, K, Cl, and total solutes. For Mg, this reduction was independent of the drop in the urinary flow rate following dDAVP administration but was significantly correlated to this drop in the case of Ca, K, Cl, and total solutes. Na and P excretions were not altered by dDAVP. It is concluded that, in vivo, administration of ADH 1) stimulates reabsorption of Na, Cl, Mg, Ca, and K by the thick ascending limb, 2) consistently enhances Mg reabsorption by the whole kidney by enhancing reabsorption in the loop of Henle, and 3) at maximal antidiuresis, raises Ca, K, Cl, and total solute reabsorption, probably because of the drop in tubular flow rates in the distal parts of the nephron consequent to the hormone administration.

ADH-like effects of calcitonin on electrolyte transport by Henle's loop of rat kidney

1984 ◽  
Vol 246 (2) ◽  
pp. F213-F220 ◽  
Author(s):  
J. M. Elalouf ◽  
N. Roinel ◽  
C. de Rouffignac
Keyword(s):  
Rat Kidney ◽  
Phosphate Transport ◽  
Hormonal Control ◽  
Electrolyte Transport ◽  
Human Calcitonin ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
The One ◽  
In Vivo Administration

The effects of physiological doses of human calcitonin (HCT) on renal excretion and tubular transport of water and electrolytes were investigated in hormone-deprived rats, i.e., homozygous DI Brattleboro rats with reduced levels of circulating glucagon, parathyroid hormone, and thyrocalcitonin, as these hormones are believed, together with ADH, to stimulate the same cells of the thick ascending limb. The experimental design was similar to the one used in a preceding study aimed at determining the effects of ADH in hormone-deprived rats [C. de Rouffignac et al. Am. J. Physiol. 244 (Renal Fluid Electrolyte Physiol. 13): F156-F164, 1983]. In the present experiments, HCT consistently increased the reabsorption of Mg, Ca, and K and, to a lesser extent, Na and Cl in the loop of Henle, but phosphate transport did not rise. The urinary excretion rate of Mg and Ca fell significantly. These data are very similar to the findings obtained with ADH on hormone-deprived rats. It is concluded that, in vivo, administration of HCT 1) stimulates reabsorption of Na, Cl, Mg, Ca, and K by the thick ascending limb, and 2) consistently enhances Mg and Ca reabsorption by the whole kidney by enhancing reabsorption in the loop of Henle. The similarity of the physiological responses elicited by ADH and calcitonin on the thick ascending limb supports the hypothesis of multiple hormonal control of electrolyte transport by the thick ascending limb.

Inhibition of heme oxygenase decreases sodium and fluid absorption in the loop of Henle

2003 ◽  
Vol 285 (3) ◽  
pp. F484-F490 ◽  
Author(s):  
Tong Wang ◽  
Hyacinth Sterling ◽  
Wei A. Shao ◽  
QingShang Yan ◽  
Matthew A. Bailey ◽  
...  
Keyword(s):  
Renal Clearance ◽  
Heme Oxygenase ◽  
Rat Kidney ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Fluid Absorption ◽  
High K ◽  
Normal Chow ◽  
Normal Rat

We previously demonstrated that carbon monoxide (CO) stimulates the apical 70-pS K+ channel in the thick ascending limb (TAL) of the rat kidney (Liu HJ, Mount DB, Nasjletti A, and Wang WH. J Clin Invest 103: 963-970, 1999). Because the apical K+ channel plays a key role in K+ recycling, we tested the hypothesis that heme oxygenase (HO)-dependent metabolites of heme may affect Na+ transport in the TAL. We used in vivo microperfusion to study the effect of chromium mesoporphyrin (CrMP), an inhibitor of HO, on fluid absorption ( Jv) and Na+ absorption ( JNa) in the loop of Henle and renal clearance methods to examine the effect of CrMP on renal sodium excretion. Microperfusion experiments demonstrated that addition of CrMP to the loop of Henle decreased Jv by 13% and JNa by 20% in animals on normal rat chow and caused a decrease in Jv (39%) and JNa (40%) in rats on a high-K+ (HK) diet. The effect of CrMP is the result of inhibition of HO because addition of MgPP, an analog of CrMP that does not inhibit HO, had no effect on Jv. Western blot analysis showed that HO-2 is expressed in the kidney and that the level of HO-2 was significantly elevated in animals on a HK diet. Renal clearance studies demonstrated that the infusion of CrMP increased the excretion of urinary Na+ (ENa) and volume (UV) without changes in glomerular filtration rate. The effect of CrMP on ENa and UV was larger in HK rats than those kept on normal chow. We conclude that HK intake increases HO-2 expression in the kidney and that HO-dependent metabolites of heme, presumably CO, play a significant role in the regulation of Na+ transport in the loop of Henle.

Localization and regulation of the rat renal Na(+)-K(+)-2Cl- cotransporter, BSC-1

1996 ◽  
Vol 271 (3) ◽  
pp. F619-F628 ◽  
Author(s):  
C. A. Ecelbarger ◽  
J. Terris ◽  
J. R. Hoyer ◽  
S. Nielsen ◽  
J. B. Wade ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Rat Colon ◽  
Thick Ascending Limb ◽  
Outer Medulla ◽  
Water Excretion ◽  
Saline Loading ◽  
Cloned Cdna ◽  
Urinary Concentrating Ability

To investigate the role of the thick ascending limb (TAL) Na(+)-K(+)-2Cl- cotransporter in regulation of water excretion, we have prepared a peptide-derived polyclonal antibody based on the cloned cDNA sequence of the rat type 1 bumetanide-sensitive cotransporter, BSC-1 (also termed "NKCC-2"). Immunoblots revealed a single broad 161-kDa band in membrane fractions of rat renal outer medulla and cortex but not from rat colon or parotid gland. A similar protein was labeled in mouse kidney. Immunoperoxidase immunohistochemistry in rat kidney revealed labeling restricted to the medullary and cortical TAL segments. Because long-term regulation of urinary concentrating ability may depend on regulation of Na(+)-K(+)-2Cl- cotransporter abundance, we used immunoblotting to evaluate the effects of several in vivo factors on expression levels of BSC-1 protein in rat kidney outer medulla. Chronic oral saline loading with 0.16 M NaCl markedly increased BSC-1 abundance. However, long-term vasopressin infusion or thirsting of rats did not affect BSC-1 abundance. Chronic furosemide infusion caused a 9-kDa upward shift in apparent molecular mass and an apparent increase in expression level. These results support the previous identification of BSC-1 as the TAL Na(+)-K(+)-2Cl- transporter and demonstrate that the expression of this transporter is regulated.

Effects of dopamine blockade on renal sodium excretion

1983 ◽  
Vol 245 (2) ◽  
pp. F247-F253 ◽  
Author(s):  
J. C. Pelayo ◽  
R. D. Fildes ◽  
G. M. Eisner ◽  
P. A. Jose
Keyword(s):  
Sodium Excretion ◽  
Dopamine Antagonist ◽  
Single Nephron ◽  
Proximal Tubular ◽  
In Trans ◽  
Series Of Experiments ◽  
Tubular Flow ◽  
Excretion Rates ◽  
A Site ◽  
Renal Responses

The renal responses to a specific dopamine antagonist (cis-flupentixol) and its stereoisomer (trans-flupentixol), a weak dopamine antagonist, were examined during hydropenia and Ringer loading in anesthetized rats. During hydropenia glomerular filtration (GFR), absolute (UNaV), and fractional (FENa) sodium excretion rates were similar as were single-nephron filtration (SNGFR) and proximal tubular flow rate (VTF). After Ringer loading GFR, UNaV, and FENa increased in all groups, but the increments were less in the cis-flupentixol than in the control or trans-flupentixol group. SNGFR and VTF increased similarly in all groups. In another series of experiments Ringer loading was performed prior to drug administration. Perfusion pressure (PP) was decreased in trans-flupentixol rats by aortic constriction to control for cis-flupentixol-induced reduction in PP. UNAV and FENa were lower in the cis-flupentixol- than trans-flupentixol-treated rats at comparable PP and GFR. In conclusion, dopamine blockade attenuated the natriuresis of Ringer loading; the mechanism is uncertain but may be related to a tubular effect at a site beyond the proximal convoluted tubule and/or in deeper nephrons.

Ontogeny of triamcinolone-acetonide binding sites in outer cortical tissue from rat kidneys

1985 ◽  
Vol 249 (6) ◽  
pp. F891-F897
Author(s):  
A. Aperia ◽  
L. A. Haldosen ◽  
L. Larsson ◽  
J. A. Gustafsson
Keyword(s):  
Triamcinolone Acetonide ◽  
Binding Sites ◽  
Cortical Tissue ◽  
Tubular Cells ◽  
Proximal Tubular ◽  
Old Rats ◽  
In Vivo Administration ◽  
Adrenalectomized Rats ◽  
Intact Rats

The ontogeny of glucocorticoid binding sites and the glucocorticoid hormone (GC) feedback control of available glucocorticoid binding sites was studied using the cytosolic fraction of outer cortical tissue obtained from kidneys in 20- and 40-day-old intact and adrenalectomized rats. Morphometric analysis showed that this tissue contained 85.7% (20 days) and 88.7% (40 days) of proximal tubular cells. Glucocorticoid binding sites were determined by [3H]triamcinolone-acetonide (TA) binding and isoelectric focusing analysis. In intact rats, TA binding sites (fmol/mg DNA) were significantly higher at 20 (3,624) than at 40 (1,640) days. Adrenalectomy significantly increased TA binding sites (fmol/mg DNA) at 40 (to 8,445) but not at 20 days. TA binding sites related to DNA were significantly higher in 20- than in 40-day-old intact rats and significantly higher in 40- than in 20-day-old adrenalectomized rats. Serum corticosterone (nM) was not significantly different in 20- (230) and 40- (189) day-old rats. After in vivo administration of a synthetic GC, TA binding sites were replenished to the cytosol after 20-24 h. Prolonged GC treatment (1-60 micrograms X 100 g body wt-1 X day-1) depressed the replenishment of TA binding sites significantly more in 40- than in 20-day-old adrenalectomized rats. Kd was determined in both intact and adrenalectomized 20- and 40-day-old rats and ranged between 1.30 and 4.33 nM. The steroidal specificity for the TA binding sites was the same in 20- and 40-day-old rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Intraluminal sulfate on electrolyte transfers along the perfused rat nephron

1981 ◽  
Vol 59 (2) ◽  
pp. 122-130 ◽  
Author(s):  
Gary A. Quamme
Keyword(s):  
Proximal Tubule ◽  
Chloride Transport ◽  
Distal Tubule ◽  
Phosphate Transport ◽  
Loop Of Henle ◽  
Magnesium Transport ◽  
Calcium And Magnesium ◽  
A Site ◽  
Distal Delivery

Superficial nephrons were perfused in vivo to determine the effect of intraluminal sulfate (1–20 mM) on electrolyte reabsorption in the rat with special reference to calcium and magnesium transport. This technique allowed us the opportunity of investigating separate electrolyte transfers without alteration of extrarenal influences. The major amount of perfused sulfate was absorbed in the proximal tubule with little absorption distal to the late proximal collection site. Phosphate transport was not affected by high luminal sulfate concentrations indicating distinct reabsorptive mechanisms for these two anions. Intraluminal sulfate significantly inhibited calcium and magnesium reabsorption in the proximal tubule, loop of Henle, and superficial distal tubule, in distinction to modest effects on sodium transport in these nephron segments. Chloride transport was not altered. The inhibition of divalent cation transfer was not quantitively similar in the different tubule segments. Small amounts of sulfate completely inhibited proximal calcium and magnesium reabsorption with little effect on transport within the loop of Henle. Enhanced distal delivery of sulfate significantly inhibited calcium and magnesium reabsorption in the distal tubule, a site where the sulfate anion is not reabsorbed. These results demonstrate the importance of distal delivery of anionic ligands capable of forming nonreabsorbable complexes. Thus distal calcium and magnesium transport may be greatly modified by proximal control of anion reabsorption.

scholarly journals In vivo nuclear translocation of mineralocorticoid and glucocorticoid receptors in rat kidney: differential effect of corticosteroids along the distal tubule

2010 ◽  
Vol 299 (6) ◽  
pp. F1473-F1485 ◽  
Author(s):  
Daniel Ackermann ◽  
Nikolay Gresko ◽  
Monique Carrel ◽  
Dominique Loffing-Cueni ◽  
Daniel Habermehl ◽  
...  
Keyword(s):  
Nuclear Localization ◽  
Glucocorticoid Receptors ◽  
Nuclear Translocation ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Distal Tubule ◽  
Plasma Aldosterone ◽  
Thick Ascending Limb ◽  
Cell Nuclei

Aldosterone and corticosterone bind to mineralocorticoid (MR) and glucocorticoid receptors (GR), which, upon ligand binding, are thought to translocate to the cell nucleus to act as transcription factors. Mineralocorticoid selectivity is achieved by the 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) that inactivates 11β-hydroxy glucocorticoids. High expression levels of 11β-HSD2 characterize the aldosterone-sensitive distal nephron (ASDN), which comprises the segment-specific cells of late distal convoluted tubule (DCT2), connecting tubule (CNT), and collecting duct (CD). We used MR- and GR-specific antibodies to study localization and regulation of MR and GR in kidneys of rats with altered plasma aldosterone and corticosterone levels. In control rats, MR and GR were found in cell nuclei of thick ascending limb (TAL), DCT, CNT, CD cells, and intercalated cells (IC). GR was also abundant in cell nuclei and the subapical compartment of proximal tubule (PT) cells. Dietary NaCl loading, which lowers plasma aldosterone, caused a selective removal of GR from cell nuclei of 11β-HSD2-positive ASDN. The nuclear localization of MR was unaffected. Adrenalectomy (ADX) resulted in removal of MR and GR from the cell nuclei of all epithelial cells. Aldosterone replacement rapidly relocated the receptors in the cell nuclei. In ASDN cells, low-dose corticosterone replacement caused nuclear localization of MR, but not of GR. The GR was redistributed to the nucleus only in PT, TAL, early DCT, and IC that express no or very little 11β-HSD2. In ASDN cells, nuclear GR localization was only achieved when corticosterone was replaced at high doses. Thus ligand-induced nuclear translocation of MR and GR are part of MR and GR regulation in the kidney and show remarkable segment- and cell type-specific characteristics. Differential regulation of MR and GR may alter the level of heterodimerization of the receptors and hence may contribute to the complexity of corticosteroid effects on ASDN function.

Localization of kallikrein in the rat kidney and its anatomical relationship to renin.

1982 ◽  
Vol 30 (4) ◽  
pp. 385-390 ◽  
Author(s):  
T B Orstavvik ◽  
T Inagami
Keyword(s):  
Collecting Duct ◽  
Rat Kidney ◽  
Distal Tubule ◽  
Juxtaglomerular Apparatus ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Afferent Arteriole ◽  
Epitheloid Cells ◽  
Anatomical Relationship

The anatomical relationship between kallikrein and renin in the rat kidney was investigated immunohistochemically by the peroxidase-antiperoxidase method. Kallikrein was localized to the convoluted distal tubule, starting at a point, distal to the juxtaglomerular apparatus, where the thick ascending limb of loop of Henle transformed into the convoluted distal tubule. The thick ascending limb was identified by its content of uromucoid (Tamm-Horsfall glycoprotein). Kallikrein was never observed within the juxtaglomerular apparatus itself. The kallikrein-containing tubule ended where the distal tubule submerged into the collecting duct. Renin was found in epitheloid cells of the afferent arteriole. When neighboring sections were stained for kallikrein and renin, respectively, no close anatomical relationship was observed between the kallikrein-containing and the renin-containing structures.

Proximal tubular Na, Cl, and HCO3 reabsorption and renal oxygen consumption

1984 ◽  
Vol 247 (1) ◽  
pp. F151-F157 ◽  
Author(s):  
S. W. Weinstein ◽  
R. Klose ◽  
J. Szyjewicz
Keyword(s):  
Oxygen Consumption ◽  
Ion Transport ◽  
Rat Kidney ◽  
Fluid Reabsorption ◽  
Bicarbonate Reabsorption ◽  
Renal Oxygen Consumption ◽  
Proximal Tubular ◽  
Tubular Fluid Reabsorption ◽  
Renal Oxygen

The majority of the oxygen consumed by the rat kidney appears to occur in the proximal tubule. Therefore changes in metabolically linked ion transport in this segment of the nephron should result in changes in renal oxygen consumption. To study the role of bicarbonate reabsorption in metabolically linked proximal tubular ion transport a series of micropuncture-clearance-extraction experiments were performed comparing the effects of the carbonic anhydrase inhibitor benzolamide and of hypertonic sodium bicarbonate infusion with control conditions in the rat. End-proximal tubular fluid and chloride reabsorption were measured. From these, the rates of sodium and bicarbonate reabsorption were estimated. Simultaneously with the tubular fluids, extraction collections were obtained for determination of renal oxygen consumption. Both benzolamide and hypertonic bicarbonate reduced proximal tubular fluid reabsorption while concomitantly reducing the transepithelial gradient for chloride. The mean rate of renal oxygen consumption did not differ from the control rate in either experimental group and could be dissociated from the calculated net rates of proximal tubular sodium, chloride, and bicarbonate reabsorption. We interpret these data as evidence that proximal tubular hydrogen ion secretion supporting bicarbonate reabsorption requires at most small amounts of oxidative energy, less than detectable by these techniques. The data, in contrast, support the conclusion that the chloride-bicarbonate transepithelial gradient appears to be an important passive driving force in vivo for proximal tubular fluid reabsorption.

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