scholarly journals Reabsorption of betaine in Henle's loops of rat kidney in vivo

2000 ◽  
Vol 278 (3) ◽  
pp. F434-F439 ◽  
Author(s):  
Stefan Pummer ◽  
William H. Dantzler ◽  
Yeong-Hau H. Lien ◽  
Gilbert W. Moeckel ◽  
Katharina Völker ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Proximal Convoluted Tubule ◽  
Vasa Recta ◽  
Tubular Lumen ◽  
Menten Constant

This study was designed 1) to localize and 2) to characterize betaine reabsorption from the tubular lumen in rat kidney in vivo, and 3) to test whether reabsorption is modulated by the diuretic state. [14C]betaine (+ [3H]inulin) was microperfused through the proximal convoluted tubule (PCT) and microinfused into late proximal (LP) and early distal (ED) tubules, long loops of Henle (LLH), and vasa recta of the rat in vivo et situ, and the fractional recovery of the14C label was determined endproximally (PCT) and in the final urine, respectively. [14C]betaine was not reabsorbed during ED microinfusion, whereas fractional reabsorption during LP microinfusion was 82% at 0.06 mM betaine and decreased gradually to 4.8% at 60 mM. l-Proline had lower Michaelis-Menten constant ( K m) and sarcosine a higher K m than betaine. Chronic, but not acute, diuresis inhibited betaine reabsorption in Henle's loops. Fractional [14C]betaine reabsorption in PCT was much smaller than that during LP microinfusion. [14C]betaine (7.28 mM) microinfused 1) into LLH was reabsorbed to 30% and 2) into vasa recta appeared in the ipsilateral urine to a much higher extent than contralaterally. In both cases, no saturation was detected at 70 mM. We conclude that betaine is reabsorbed by mediated transport from descending limbs of short Henle's loops by a proline-preferring carrier in a diuresis-modulated manner. In the deep medulla, bidirectional blood/urine betaine transport exists.

D-Glucose enhancement of water reabsorption in proximal tubule of the rat kidney

1976 ◽  
Vol 231 (3) ◽  
pp. 777-780 ◽  
Author(s):  
EJ Weinman ◽  
WN Suki ◽  
G Eknoyan
Keyword(s):  
Proximal Tubule ◽  
Rat Kidney ◽  
Specific Effect ◽  
Proximal Convoluted Tubule ◽  
Water Reabsorption ◽  
Perfusion Solution ◽  
Tubular Lumen ◽  
Artificial Solution

Water reabsorption in the proximal convoluted tubule of the rat kidney was examined by in vivo microperfusion techniques in order to examine the effect of D-glucose within the tubular lumen. When tubules were perfused with a balanced artificial solution containing Na, K, Cl, HCO3, urea, and D-glucose, absolute reabsorption averaged 4.01 +/- 0.24 nl/min per mm. Addition of D-glucose to the NaCl perfusate enhanced water reabsorption to values similar to those obtained with the balanced artificial perfusate. The enhanced water reabsorption consequent to the addition of D-glucose to the NaCl perfusion solution was completely inhibited by addition of phloridzin to the perfusate. The addition of an unabsorbed hexose, 2-deoxy-D-glucose, to the NaCl perfusate failed to enhance water reabsorption, whereas the addition of an incompletely reabsorbed sugar that is not metabolized, 3-O-methyl-D-glucose, resulted in partial enhancement of theabsolute rate of water reabsorption. These studies demonstrate that D-glucose has the specific effect of augmenting water reabsorption in the proximal tubule of the rat kidney.

Effects of intraluminal D-glucose and probenecid on urate absorption in the rat proximal tubule

1979 ◽  
Vol 236 (6) ◽  
pp. F526-F529 ◽  
Author(s):  
T. F. Knight ◽  
H. O. Senekjian ◽  
S. Sansom ◽  
E. J. Weinman
Keyword(s):  
Proximal Tubule ◽  
Water Absorption ◽  
Rat Kidney ◽  
Proximal Convoluted Tubule ◽  
Perfusion Solution ◽  
Hexose Sugars ◽  
Tubular Absorption ◽  
Rat Proximal Tubule ◽  
Fractional Absorption

The in vivo microperfusion technique was employed to examine urate absorption in the proximal convoluted tubule of the rat kidney using [2–14C]urate as the marker for fractional urate absorption. With NaCl as the perfusion solution, water absorption averaged 2.53 +/- 0.16 nl.min-1.mm tubule-1, and the fractional absorption of [2–14C]urate averages 11.6 +/- 1.0%/mm tubule. The addition of D-glucose (50 mg/100 ml) enhanced water absorption to 3.62 +/- 0.19 nl.min-1.mm tubule-1, but inhibited fractional urate absorption to 6.6 +/- 1.2%/mm tubule. Phloridzin (4.4 mg/100 ml), 2-deoxy-D-glucose (45.6 mg/100 ml), and 3-O-methyl-D-glucose (53.9 mg/100 ml) also inhibited the absorption of [2–14C]urate to the same degree as did D-glucose despite differing effects on water absorption. The addition of probenecid (2.8 mg/100 ml) to the NaCl perfusion solution had no effect on water absorption but inhibited [2–14C]urate absorption to 6.4 +/- 0.6%/mm tubule. The addition of both probenecid and phloridzin further reduced [2–14C-A1urate absorption to 3.8 +/- 0.7%/mm tubule. Probenecid alone had no effect on glucose transport. These studies suggest that the presence of either certain hexose sugars, phloridzin, or probenecid in the lumen of the proximal convoluted tubule inhibits the tubular absorption of urate.

scholarly journals FILTRATION AND REABSORPTION OF PROTEIN BY THE KIDNEY

1954 ◽  
Vol 100 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Alvin L. Sellers ◽  
Neilyn Griggs ◽  
Jessie Marmorston ◽  
Howard C. Goodman
Keyword(s):  
Plasma Protein ◽  
Plasma Proteins ◽  
Renal Tubule ◽  
Rat Kidney ◽  
Proximal Convoluted Tubule ◽  
Protein Reabsorption ◽  
Perfused Kidney

Plasma proteins of the rat have been labelled by the in vivo injection of the dye T-1824. From a study of the rate of disappearance of T-1824 from the circulating blood, and the total T-1824 content of the perfused kidney the rate of protein reabsorption from the glomerular fluid by the cells of the renal tubule has been calculated. It is concluded that protein reabsorption by the cells lining the proximal convoluted tubule of the rat kidney proceeds at a rate of at least 5 mg. per hour, equivalent to a daily filtration and reabsorption of 33 per cent of the circulating plasma protein.

Autoradiographic localization of atrial natriuretic peptide receptor subtypes in rat kidney

1990 ◽  
Vol 259 (1) ◽  
pp. F26-F39 ◽  
Author(s):  
J. Brown ◽  
S. P. Salas ◽  
A. Singleton ◽  
J. M. Polak ◽  
C. T. Dollery
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Dissociation Constants ◽  
Rat Kidney ◽  
Arterial System ◽  
Receptor Subtypes ◽  
Vasa Recta ◽  
Atrial Natriuretic

The distribution of atrial natriuretic peptide (ANP) clearance receptors in rat kidney was investigated by in vitro autoradiography using des[Gln18,Ser19,Gly20,Leu21,Gly22]-ANP-(4- 23) (C-ANP) and 125I-Tyr0-ANP-(5-25) as relatively specific ligands of this receptor. Alpha-125I-ANP (100 pM) bound reversibly but with high affinity to glomeruli, outer medullary vasa recta bundles, and inner medulla. C-ANP (10 microM) inhibited greater than 60% of this glomerular binding but did not inhibit the binding of alpha-125I-ANP to medullary tissues. Alpha-125I-ANP also bound reversibly to the renal arteries up to the glomerulus. This arterial binding was only partly inhibited by 10 microM C-ANP. In the presence of 10 microM C-ANP, increasing concentrations of alpha-125I-ANP bound to a residue of glomerular sites with apparent dissociation constants of 0.82 +/- 0.16 to 2.73 +/- 1.20 nM at different cortical levels. 125I-Tyr0-ANP-(5-25) bound significantly to glomeruli and intrarenal arteries but not to vasa recta bundles or inner medulla. This glomerular binding also occurred with nanomolar dissociation constants. It was completely inhibited by 1 microM alpha-ANP and 10 microM C-ANP, but not by unrelated peptides such as gastrin. These results suggest that renal ANP clearance receptors are restricted in vivo to the glomeruli and renal arterial system of the rat.

Tubular reabsorption of myo-inositol vs. that ofd-glucose in rat kidney in vivo et situ

2003 ◽  
Vol 284 (6) ◽  
pp. F1181-F1189 ◽  
Author(s):  
Stefan Silbernagl ◽  
Katharina Völker ◽  
William H. Dantzler
Keyword(s):  
Rat Kidney ◽  
Distal Tubule ◽  
Tubular Structures ◽  
Nephron Segments ◽  
Short Loop ◽  
Organic Osmolyte ◽  
Vasa Recta ◽  
Collecting Ducts ◽  
High Concentrations

Filtered myo-inositol, an important renal intracellular organic osmolyte, is almost completely reabsorbed. To examine tubule sites and specificity and, thus possible mechanism of this reabsorption, we microinfused myo-[3H]inositol ord-[3H]glucose into early proximal (EP), late proximal (LP), or early distal tubule sections of superficial nephrons and into long loops of Henle (LLH) of juxtamedullary nephrons and papillary vasa recta in rats in vivo et situ and determined urinary fractional recovery of the 3H label compared with comicroinfused [14C]inulin. To determine the extent to which the proximal convoluted tubule (PCT) alone contributes to myo-inositol reabsorption, we also microperfused this tubule segment between EP and LP puncture sites. We examined specificity of reabsorptive carrier(s) by adding high concentrations of other polyols and monosaccharides to the infusate. The results show that >60% of the physiological glomerular load of myo-inositol can be reabsorbed in the PCT and >90% in the short loop of Henle (SLH) by a saturable, phloridzin-sensitive process. myo-Inositol can also be reabsorbed in the ascending limb of LLH and can move from papillary vasa recta blood into ipsilateral tubular structures. Essentially no reabsorption occurred in nephron segments beyond the SLH or in collecting ducts. Specificity studies indicate that reabsorption probably occurs via a luminal Na+- myo-inositol cotransporter.

The Fine Structure of Rat Renal Microbodies and Cytoplasmic Bodies Following Perfusion Fixation

1973 ◽  
Vol 31 ◽  
pp. 620-621
Author(s):  
J. M. Barrett ◽  
P. M. Heidger
Keyword(s):  
Fine Structure ◽  
Proximal Tubule ◽  
Rat Kidney ◽  
Renal Proximal Tubule ◽  
Convincing Evidence ◽  
Cytoplasmic Bodies ◽  
Rat Renal Proximal Tubule ◽  
Renal Proximal Tubule Cells ◽  
Perfusion Fixation

Microbodies have received extensive morphological and cytochemical investigation since they were first described by Rhodin in 1954. To our knowledge, however, all investigations of microbodies and cytoplasmic bodies of rat renal proximal tubule cells have employed immersion fixation. Tisher, et al. have shown convincing evidence of fine structural alteration of microbodies in rhesus monkey kidney following immersion fixation; these alterations were not encountered when in vivo intravascular perfusion was employed. In view of these studies, and the fact that techniques for perfusion fixation have been established specifically for the rat kidney by Maunsbach, it seemed desirable to employ perfusion fixation to study the fine structure and distribution of microbodies and cytoplasmic bodies within the rat renal proximal tubule.

Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat kidney

1987 ◽  
Vol 252 (2) ◽  
pp. F331-F337 ◽  
Author(s):  
W. Lieberthal ◽  
M. L. Vasilevsky ◽  
C. R. Valeri ◽  
N. G. Levinsky
Keyword(s):  
Sodium Excretion ◽  
Rat Kidney ◽  
Urine Osmolality ◽  
Sodium Reabsorption ◽  
Urinary Osmolality ◽  
Hemodynamic Characteristics ◽  
Urinary Concentrating Ability ◽  
Tubular Morphology ◽  
Isolated Kidneys

Interactions between antidiuretic hormone (ADH) and renal prostaglandins in the regulation of sodium reabsorption and urinary concentrating ability were studied in isolated erythrocyte-perfused rat kidneys (IEPK). In this model, hemodynamic characteristics are comparable to those found in vivo, and tubular morphology is preserved throughout the period of perfusion. [Deamino]-D-arginine vasopressin (dDAVP) markedly reduced fractional sodium excretion (FE Na) in the IEPK from 3.5 +/- 0.6 to 0.45 +/- 0.14%. After indomethacin, FE Na fell still further to 0.08 +/- 0.02%. In the absence of dDAVP indomethacin had no effect on sodium excretion; FE Na was 2.4 +/- 0.6% in control and 2.0 +/- 0.4% in indomethacin-treated groups. dDAVP increased urine osmolality in the IEPK to 741 +/- 26 mosmol/kg. When prostaglandin synthesis was blocked with indomethacin, urinary osmolality increased further to 1,180 +/- 94 mosmol/kg. In isolated kidneys perfused without erythrocytes (IPK), dDAVP decreased FENa from 14.5 +/- 1.8% to 9.6 +/- 1.2%; addition of indomethacin had no further effect. dDAVP increased urine osmolality only modestly to 350 +/- 12 mosmol/kg in the IPK and indomethacin did not increase concentrating ability further (342 +/- 7 mosmol/kg). Thus the IEPK (unlike the IPK) can excrete a markedly hypertonic urine in response to ADH. ADH also enhances tubular reabsorption of sodium in the IEPK. Prostaglandins inhibit both these actions of ADH but do not directly affect sodium excretion in the absence of the hormone.

11 beta-hydroxysteroid dehydrogenase and corticosteroid hormone receptors in the rat colon

1993 ◽  
Vol 264 (6) ◽  
pp. E951-E957 ◽  
Author(s):  
C. B. Whorwood ◽  
P. C. Barber ◽  
J. Gregory ◽  
M. C. Sheppard ◽  
P. M. Stewart
Keyword(s):  
Epithelial Cells ◽  
Lamina Propria ◽  
Hormone Receptors ◽  
Rat Kidney ◽  
Distal Colon ◽  
Hydroxysteroid Dehydrogenase ◽  
Neuroendocrine Cells ◽  
Rat Colon ◽  
Mrna Levels

In the rat kidney 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) maintains normal in vivo specificity for mineralocorticoid receptor (MR) by converting the active steroid corticosterone to inactive 11-dehydrocorticosterone, leaving aldosterone to occupy the MR. Clinical observations support the hypothesis that 11 beta-HSD also protects the distal colonic MR from glucocorticoid excess. We have measured 11 beta-HSD mRNA and activity along the rat colon and have analyzed the distribution of 11 beta-HSD, MR, and glucocorticoid receptor (GR) mRNA within rat distal colon using in situ hybridization. Levels of 11 beta-HSD mRNA (1.7 and 3.4 kb) and activity were higher in distal vs. proximal colon, paralleling reported MR mRNA levels. Within the distal colon mucosa both 11 beta-HSD immunoreactivity and mRNA was observed in cells in the lamina propria but not in epithelial cells. MR mRNA was present in surface epithelial cells, but was also colocalized with the same 11 beta-HSD-expressing cells in the lamina propria. In contrast GR mRNA was more uniformly distributed. The localization of MR mRNA to nonepithelial cells in the lamina propria, possibly neuroendocrine cells, suggests that mineralocorticoid-regulated sodium transport across colonic epithelial cells may also involve a paracrine mechanism. As with the kidney, exposure of active mineralocorticoid to the MR in these cells in the lamina propria is dictated by 11 beta-HSD in an autocrine fashion.

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