Localization of urine acidification in the mammalian kidney

1960 ◽  
Vol 198 (3) ◽  
pp. 581-585 ◽  
Author(s):  
Carl W. Gottschalk ◽  
William E. Lassiter ◽  
Margaret Mylle
Keyword(s):  
Ammonium Chloride ◽  
Renal Tubules ◽  
Loop Of Henle ◽  
Mammalian Kidney ◽  
Urine Acidification ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Collecting Ducts ◽  
Distal Convolution ◽  
Quantitative Importance

Fluid was collected by micropuncture from individual renal tubules of anesthetized rats and its pH determined with the quinhydrone microelectrode. The single glomerular sample and early proximal fluid were isohydric with arterial blood, but later proximal fluid usually showed progressive acidification. The maximum proximal fall in pH was 0.43 u in nondiuretic rats, 0.56 u during profuse glucose or mannitol diuresis, and 0.78 u in rats previously loaded with ammonium chloride and undergoing glucose diuresis. Fluid from the early distal convolution was usually acidified relative to arterial blood but was not significantly different from late proximal fluid. Progressive acidification probably also occurred in the distal convolution. The pH decreased further in the collecting ducts, much more so in the nondiuretic state than during diuresis. The quantitative importance of proximal reabsorption of HCO3– and, by inference, H+ secretion is emphasized. It is suggested that the pH of tubular fluid may increase in the thin descending limb of the loop of Henle, especially in a kidney elaborating a concentrated urine, because of increased concentration of HCO3–.

Micropuncture study of renal tubular reabsorption of calcium in normal rodents

1963 ◽  
Vol 204 (5) ◽  
pp. 771-775 ◽  
Author(s):  
William E. Lassiter ◽  
Carl W. Gottschalk ◽  
Margaret Mylle
Keyword(s):  
Proximal Tubule ◽  
Active Transport ◽  
Tubular Reabsorption ◽  
Loop Of Henle ◽  
Anesthetized Rats ◽  
Micropuncture Study ◽  
Calcium Reabsorption ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Distal Convolution

Anesthetized rats and hamsters were given Ca45 intravenously, and fluid was subsequently collected by micropuncture from glomeruli and surface tubules in the rats, and from loops of Henle in the hamsters. In nondiuretic animals, fluid:plasma calcium ratios averaged 0.71 in the glomerulus; 0.76 in the proximal tubule; 2.0 in the loop of Henle; 0.47 in the distal convolution; and 0.9 in ureteral urine. In mannitol diuresis, the calcium ratio of glomerular fluid was unchanged, but ratios as low as 0.21 were noted in the proximal tubule. In this circumstance, the average proximal ratio was 0.61, and the distal ratio 0.07. These results indicate active transport of calcium out of all major parts of the nephron, with the bulk of calcium reabsorption occurring in the convoluted portion of the proximal tubule. Furthermore, the pattern of tubular reabsorption of calcium is similar to that of sodium, suggesting that the two are related.

Micropuncture study of net transtubular movement of water and urea in nondiuretic mammalian kidney

1961 ◽  
Vol 200 (6) ◽  
pp. 1139-1147 ◽  
Author(s):  
William E. Lassiter ◽  
Carl W. Gottschalk ◽  
Margaret Mylle
Keyword(s):  
Carboxylic Acid ◽  
Active Transport ◽  
Water Loss ◽  
Urine Concentration ◽  
Passive Movement ◽  
Osmotic Gradient ◽  
Loop Of Henle ◽  
Mammalian Kidney ◽  
Collecting Ducts ◽  
Micropuncture Study

Anesthetized, nondiuretic rats and hamsters were infused with C14-labeled inulin-carboxylic acid or urea, and fluid was subsequently collected by micropuncture from surface tubules in the rats and from loops of Henle and collecting ducts in the hamsters. Osmolality and radioactivity of tubular fluid, ureteral urine, and plasma were determined. There was net loss of both water and solute from all segments of the nephron. In the loop of Henle, water loss occurred primarily from the descending limb and solute loss from the ascending limb. Urea was reabsorbed from the proximal and distal convolutions and collecting ducts but was added to the tubular fluid in the descending limb of the loop of Henle. These results lend support to the countercurrent theory of urine concentration and indicate that the osmotic gradient in the medulla is established by active transport of solute out of the ascending limb of the loop of Henle. The results are compatible with passive movement of water and urea, but the possibility of active transport of urea is not excluded.

Evidence of calcium phosphate supersaturation in the loop of Henle

1996 ◽  
Vol 270 (4) ◽  
pp. F604-F613 ◽  
Author(s):  
J. R. Asplin ◽  
N. S. Mandel ◽  
F. L. Coe
Keyword(s):  
Calcium Phosphate ◽  
Calcium Concentration ◽  
Loop Of Henle ◽  
X Ray ◽  
Ion Interactions ◽  
Collecting Ducts ◽  
Phosphate Phase ◽  
Dietary Phosphate ◽  
Calcium Phosphate Phase

We have used published rat micropuncture data to construct a matrix of ion concentrations along the rat nephron. With an iterative computer model of known ion interactions, we calculated relative supersaturation ratios in all nephron segments. The collecting ducts and urine showed expected supersaturation with stone-forming salts. Fluid in the thin segment of the loop of Henle may be supersaturated with calcium carbonate and calcium phosphate under certain conditions. Because calculations cannot predict the actual course of crystallization, we made solutions to mimic, in vitro, presumed conditions in the loop of Henle. The solid phases that formed were analyzed by X-ray powder diffraction, electron microprobe, and infrared spectroscopy. All samples were identified as poorly crystallized or immature apatite. The descending limb of Henle's loop creates a unique condition as it extracts water but not sodium, bicarbonate, calcium, or phosphate, giving a calcium concentration at the bend of 3 mM, pH 7.4, and a phosphate concentration that varies from 0.8 to 48 mM, depending on parathyroid hormone and dietary phosphate. We conclude that conditions in the thin segment potentially could create a solid calcium phosphate phase, which may initiate nucleation of calcium oxalate salts in the collecting ducts, potentiating nephrolithiasis and nephrocalcinosis.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

scholarly journals Urine Acidification After Ammonium Chloride

2018 ◽  
Vol 72 (6) ◽  
pp. 909-911
Author(s):  
Anneke P. Bech ◽  
Tom Nijenhuis ◽  
Jack F.M. Wetzels
Keyword(s):  
Ammonium Chloride ◽  
Urine Acidification

Effects of vasoactive intestinal peptide on vascular conductance are unaffected by anesthesia

1988 ◽  
Vol 255 (6) ◽  
pp. R968-R973 ◽  
Author(s):  
T. G. Bouder ◽  
L. J. Huffman ◽  
G. A. Hedge
Keyword(s):  
Salivary Gland ◽  
Thyroid Gland ◽  
Vasoactive Intestinal Peptide ◽  
Reference Sample ◽  
Conscious State ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Radioactive Microsphere ◽  
Anesthetized Rats

In rats anesthetized with ketamine and pentobarbital (KET/PB), vasoactive intestinal peptide (VIP) increases vascular conductance (VC) in the salivary gland, pancreas, and thyroid gland, whereas no changes in VC are observed in a number of other organs. Because anesthesia may alter the responsiveness of physiological systems, we compared the effects of VIP on organ VC in conscious or anesthetized rats. Chronically catheterized rats were studied in the conscious state or 30 min after induction of anesthesia with KET/PB, isoflurane, or Inactin. Blood flows were measured by the reference sample version of the radioactive microsphere (MS) technique using two MS injections (141Ce-MS/85Sr-MS). Mean arterial blood pressure was monitored and used in the calculation of VC. Organ VCs were similar under basal conditions in conscious and anesthetized rats. VIP infusion caused systemic hypotension and increased VCs in the salivary gland, pancreas, and thyroid gland, and these responses were largely unaffected by anesthesia. These results indicate that the anesthetics used do not alter basal VC or the responsiveness of the vasculature to exogenous VIP.

Dissociation between skeletal muscle microvascular Po2and hypoxia-induced microvascular inflammation

2003 ◽  
Vol 94 (6) ◽  
pp. 2323-2329 ◽  
Author(s):  
Sidharth Shah ◽  
Julie Allen ◽  
John G. Wood ◽  
Norberto C. Gonzalez
Keyword(s):  
Blood Flow ◽  
Microvascular Blood Flow ◽  
Phosphorescence Quenching ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Systemic Hypoxia ◽  
Individual Contributions ◽  
Microvascular Inflammation ◽  
Quenching Method ◽  
The Individual

Systemic hypoxia (SHx) produces microvascular inflammation in mesenteric, cremasteric, and pial microcirculations. In anesthetized rats, SHx lowers arterial blood pressure (MABP), which may alter microvascular blood flow and microvascular Po2(PmO2) and influence SHx-induced leukocyte-endothelial adherence (LEA). These experiments attempted to determine the individual contributions of the decreases in PmO2, venular blood flow and shear rate, and MABP to the hypoxia-induced increase in LEA. Cremaster microcirculation of anesthetized rats was visualized by intravital microscopy. PmO2was measured by a phosphorescence-quenching method. SHx [inspired Po2of 70 Torr for 10 min, MABP of 65 ± 3 mmHg, arterial Po2(PaO2) of 33 ± 1 Torr] and cremaster ischemia (MABP of 111 ± 7 mmHg, PaO2of 86 ± 3 Torr) produced similar PmO2: 7 ± 2 and 6 ± 2 Torr, respectively. However, LEA increased only in SHx (1.9 ± 0.9 vs. 11.2 ± 1.1 leukocytes/100 μm, control vs. SHx, P < 0.05). Phentolamine-induced hypotension (MABP of 55 ± 4 mmHg) in normoxia lowered PmO2to 26 ± 6 Torr but did not increase LEA. Cremaster equilibration with 95% N2-5% CO2during air breathing (PaO2of 80 ± 1 Torr) lowered PmO2to 6 ± 1 Torr but did not increase LEA. On the other hand, when cremaster PmO2was maintained at 60–70 Torr during SHx (PaO2of 35 ± 1 Torr), LEA increased from 2.1 ± 1.1 to 11.1 ± 1.5 leukocytes/100 μm ( P < 0.05). The results show a dissociation between PmO2and LEA and support the idea that SHx results in the release of a mediator responsible for the inflammatory response.

Ouabain-sensitive and -insensitive K-ATPases in rat nephron: effect of K depletion

1995 ◽  
Vol 268 (6) ◽  
pp. F1141-F1147 ◽  
Author(s):  
M. Younes-Ibrahim ◽  
C. Barlet-Bas ◽  
B. Buffin-Meyer ◽  
L. Cheval ◽  
R. Rajerison ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Collecting Duct ◽  
Proximal Tubules ◽  
Lower Sensitivity ◽  
Mammalian Kidney ◽  
Henle's Loop ◽  
Collecting Ducts ◽  
Straight Tubules ◽  
K Depletion ◽  
Higher Sensitivity

Because a ouabain-sensitive H-K-adenosinetriphosphatase (H-K-ATPase) has been identified recently in the amphibian bladder, we evaluated whether such an ATPase might exist also in the mammalian kidney, along with the ouabain-insensitive H-K-ATPase previously described in the collecting duct. For this purpose, we searched for an Na-independent, K-stimulated, ouabain- and Sch-28080-inhibitable ATPase activity in single segments of rat nephron. Ouabain-sensitive K-stimulated ATPase activity was detected in the absence of Na+ in rat proximal convoluted and straight tubules and in medullary and cortical thick ascending limbs of Henle's loop but not in collecting ducts. This K-ATPase differs from Na-K-ATPase by 1) its absence of requirement for Na, 2) its sensitivity to Sch-28080, 3) its higher sensitivity to ouabain, and 4) its absence in the collecting duct. It differs from the collecting duct H-K-ATPase by 1) its distribution along the nephron, 2) its sensitivity to ouabain, and 3) its lower sensitivity to Sch-28080. Furthermore, in rats fed a K-depleted diet for 2 wk, ouabain-sensitive K-ATPase activity was markedly reduced in both proximal tubules and thick ascending limbs, whereas collecting duct H-K-ATPase was upregulated.

Return of the secretory kidney

2002 ◽  
Vol 282 (1) ◽  
pp. F1-F9 ◽  
Author(s):  
Jared J. Grantham ◽  
Darren P. Wallace
Keyword(s):  
Glomerular Filtration ◽  
Extracellular Fluid ◽  
Fluid Secretion ◽  
Proximal Tubules ◽  
Renal Tubules ◽  
Functional Elements ◽  
Dry Land ◽  
Fluid Reabsorption ◽  
Collecting Ducts ◽  
Urine Formation

The evolution of the kidney has had a major role in the emigration of vertebrates from the sea onto dry land. The mammalian kidney has conserved to a remarkable extent many of the molecular and functional elements of primordial apocrine kidneys that regulate fluid balance and eliminate potentially toxic endogenous and xenobiotic molecules in the urine entirely by transepithelial secretion. However, these occult secretory processes in the proximal tubules and collecting ducts of mammalian kidneys have remained underappreciated in the last half of the twentieth century as investigators focused, to a large extent, on the mechanisms of glomerular filtration and tubule sodium chloride and fluid reabsorption. On the basis of evidence reviewed in this paper, we propose that transepithelial salt and fluid secretion mechanisms enable mammalian renal tubules to finely regulate extracellular fluid volume and composition day to day and maintain urine formation during the cessation of glomerular filtration.

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