scholarly journals Hyperfiltration and inner stripe hypertrophy may explain findings by Gamble and coworkers

2010 ◽  
Vol 298 (4) ◽  
pp. F962-F972 ◽  
Author(s):  
Anita T. Layton ◽  
Thomas L. Pannabecker ◽  
William H. Dantzler ◽  
Harold E. Layton
Keyword(s):  
Mathematical Model ◽  
Boundary Conditions ◽  
Transport Properties ◽  
Flow Rate ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Supplemental Feeding ◽  
Duct System ◽  
Flow Rates

Simulations conducted in a mathematical model were used to exemplify the hypothesis that elevated solute concentrations and tubular flows at the boundary of the renal outer and inner medullas of rats may contribute to increased urine osmolalities and urine flow rates. Such elevated quantities at that boundary may arise from hyperfiltration and from inner stripe hypertrophy, which are correlated with increased concentrating activity (Bankir L, Kriz W. Kidney Int. 47: 7–24, 1995). The simulations used the region-based model for the rat inner medulla that was presented in the companion study (Layton AT, Pannabecker TL, Dantzler WH, Layton HE. Am J Physiol Renal Physiol 298: F000–F000, 2010). The simulations were suggested by experiments which were conducted in rat by Gamble et al. (Gamble JL, McKhann CF, Butler AM, Tuthill E. Am J Physiol 109: 139–154, 1934) in which the ratio of NaCl to urea in the diet was systematically varied in eight successive 5-day intervals. The simulations predict that changes in boundary conditions at the boundary of the outer and inner medulla, accompanied by plausible modifications in transport properties of the collecting duct system, can significantly increase urine osmolality and flow rate. This hyperfiltration-hypertrophy hypothesis may explain the finding by Gamble et al. that the maximum urine osmolality attained from supplemental feeding of urea and NaCl in the eight intervals depends on NaCl being the initial predominant solute and on urea being the final predominant solute, because urea in sufficient quantity appears to stimulate concentrating activity. More generally, the hypothesis suggests that high osmolalities and urine flow rates may depend, in large part, on adaptive modifications of cortical hemodynamics and on outer medullary structure and not entirely on an extraordinary concentrating capability that is intrinsic to the inner medulla.

Correction of age-related polyuria by dDAVP: molecular analysis of aquaporins and urea transporters

2003 ◽  
Vol 284 (1) ◽  
pp. F199-F208 ◽  
Author(s):  
Sophie Combet ◽  
Nancy Geffroy ◽  
Véronique Berthonaud ◽  
Bernhard Dick ◽  
Laurent Teillet ◽  
...  
Keyword(s):  
Flow Rate ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Adult Rats ◽  
Age Related ◽  
Adult Kidney ◽  
Old Rats

Senescent female WAG/Rij rats exhibit polyuria without obvious renal disease or defects in vasopressin plasma level or V2 receptor mRNA expression. Normalization of urine flow rate by 1-desamino-8-d-arginine vasopressin (dDAVP) was investigated in these animals. Long-term dDAVP infusion into 30-mo-old rats reduced urine flow rate and increased urine osmolality to levels comparable to those in control 10-mo-old rats. The maximal urine osmolality in aging rat kidney was, however, lower than that in adult kidney, despite supramaximal administration of dDAVP. This improvement involved increased inner medullary osmolality and urea sequestration. This may result from upregulation of UT-A1, the vasopressin-regulated urea transporter, in initial inner medullary collecting duct (IMCD), but not in terminal IMCD, where UT-A1 remained low. Expression of UT-A2, which contributes to medullary urea recycling, was greatly increased. Regulation of IMCD aquaporin (AQP)-2 (AQP2) expression by dDAVP differed between adult and senescent rats: the low AQP2 abundance in senescent rats was normalized by dDAVP infusion, which also improved targeting of the channel; in adult rats, AQP2 expression was unaltered, suggesting that IMCD AQP2 expression is not regulated by dDAVP directly. Increased AQP3 expression in senescent rats may also be involved in improved urine-concentrating capacity owing to higher basolateral water and urea reabsorption capacity.

Renal Function in Unanaesthetized River Lampreys (Lampetra FluviatilisL.): Effects of Anaesthesia, Temperature and Environmental Salinity

1983 ◽  
Vol 105 (1) ◽  
pp. 351-362 ◽  
Author(s):  
A. J. MCVICAR ◽  
J. C. RANKIN
Keyword(s):  
Renal Function ◽  
Flow Rate ◽  
Ventilation Rate ◽  
Urine Flow ◽  
The Body ◽  
Urine Flow Rate ◽  
Flow Rates ◽  
Gill Ventilation ◽  
Daily Excretion ◽  
The Mean

1. Improved estimates of urine flow rates of lampreys in various salinities were obtained by the collection of urine for periods of up to 48 h from minimally-stressed, unanaesthetized fish, following catheterization of the urinogenital papilla. 2. The mean urine flow rate of freshwater lampreys was 200.7 ±14.3 ml kg−1 day−1. 3. Urine flow in freshwater lampreys was correlated with spontaneous changes in gill ventilation rate. MS222 anaesthesia reduced both ventilation and urine flow rates, but pronounced effects were only observed at concentrations greater than those needed to induce light anaesthesia (50–55 mg 1−1). Urine flow rate in unanaesthetized fish was extremely sensitive to rapid (6°Ch−1) changes in temperature and Q10 (6–16°C) was approximately 5. 4. Urine flow rate decreased rapidly as the osmotic difference between the body fluids and environment approached zero, and the rate of flow in 30% seawater lampreys was only 7.6% that of freshwater fish. 5. There was no evidence for an effect of environmental calcium concentration on branchial osmotic permeability. 6. Extensive tubular reabsorption of ions occurred in freshwater lampreys. The total daily excretion rate of sodium ions generally decreased in salinities hyperosmotic to the plasma, indicating enhanced reabsorption, but secretion of magnesium and sulphate ions was greatly increased. Urine osmolarity was significantly increased in lampreys in hyperosmotic salinities. 7. Present data compare favourably with data obtained previously from anaesthetized animals, indicating that renal function in lampreys is not significantly impaired by light MS222 anaesthesia.

Potassium transport in the distal tubule and collecting duct of the rat

1975 ◽  
Vol 229 (5) ◽  
pp. 1403-1409 ◽  
Author(s):  
HJ Reineck ◽  
RW Osgood ◽  
TF Ferris ◽  
JH Stein
Keyword(s):  
Flow Rate ◽  
Collecting Duct ◽  
Distal Tubule ◽  
Potassium Transport ◽  
Distal Convoluted Tubule ◽  
Potassium Excretion ◽  
Flow Rates ◽  
Urinary Potassium ◽  
Potassium Secretion ◽  
Tubular Flow

Because of recent conflicting results, micropuncture studies were performed to clarify the respective role of the distal convoluted tubule and collecting duct in the regulation of urinary potassium excretion. Five groups of Sprague-Dawley rats were studied: group I, hydropenia (n = 10); group II, Ringer loading (n = 7); group III, acute KC1 loading (n = 6); group IV, mannitol diuresis (n = 6); group V, KC1 infusion during mannitol diuresis (n = 7). Early and late distal tubules were identified with intravenous injections of lissamine green. In each animal net secretion of potassium occurred along the distal convoluted tubule, and a direct relationship between distal tubular flow rate and potassium secretion was observed. The magnitude of potassium secretion at high distal tubular flow rates was dependent on the model studied. Potassium transport beyond the distal tubule was evaluated by comparing end distal potassium delivery and fractional potassium excretion. At low urinary flow rates net reabsorption was observed, whereas at higher flow rates no net transport occurred. Thus, flow rate along the collecting duct may be a major determinant of urinary potassium excretion.

scholarly journals Mechanoregulation of BK channel activity in the mammalian cortical collecting duct: role of protein kinases A and C

2009 ◽  
Vol 297 (4) ◽  
pp. F904-F915 ◽  
Author(s):  
Wen Liu ◽  
Yuan Wei ◽  
Peng Sun ◽  
Wen-Hui Wang ◽  
Thomas R. Kleyman ◽  
...  
Keyword(s):  
Flow Rate ◽  
Collecting Duct ◽  
Bk Channel ◽  
Slow Flow ◽  
Cortical Collecting Duct ◽  
Flow Rates ◽  
Calphostin C ◽  
Flow Stimulation ◽  
Slow Flow Rate ◽  
Stimulation Of

Flow-stimulated net K secretion ( JK) in the cortical collecting duct (CCD) is mediated by an iberiotoxin (IBX)-sensitive BK channel, and requires an increase in intracellular Ca2+ concentration ([Ca2+]i). The α-subunit of the reconstituted BK channel is phosphorylated by PKA and PKC. To test whether the BK channel in the native CCD is regulated by these kinases, JK and net Na absorption ( JNa) were measured at slow (∼1) and fast (∼5 nl·min−1·mm−1) flow rates in rabbit CCDs microperfused in the presence of mPKI, an inhibitor of PKA; calphostin C, which inhibits diacylglycerol binding proteins, including PKC; or bisindolylmaleimide (BIM) and Gö6976, inhibitors of classic and novel PKC isoforms, added to luminal (L) and/or basolateral (B) solutions. L but not B mPKI increased JK in CCDs perfused at a slow flow rate; a subsequent increase in flow rate augmented JK modestly. B mPKI alone or with L inhibitor abolished flow stimulation of JK. Similarly, L calphostin C increased JK in CCDs perfused at slow flow rates, as did calphostin C in both L and B solutions. The observation that IBX inhibited the L mPKI- and calphostin C-mediated increases in JK at slow flow rates implicated the BK channel in this K flux, a notion suggested by patch-clamp analysis of principal cells. The kinase inhibited by calphostin C was not PKC as L and/or B BIM and Gö6976 failed to enhance JK at the slow flow rate. However, addition of these PKC inhibitors to the B solution alone or with L inhibitor blocked flow stimulation of JK. Interpretation of these results in light of the effects of these inhibitors on the flow-induced elevation of [Ca2+]i suggests that the principal cell apical BK channel is tonically inhibited by PKA and that flow stimulation of JK in the CCD is PKA and PKC dependent. The specific targets of the kinases remain to be identified.

Does a high concentration of calcium in the urine cause an important renal concentrating defect in human subjects?

2000 ◽  
Vol 98 (3) ◽  
pp. 313-319 ◽  
Author(s):  
George S. S. LAM ◽  
John R. ASPLIN ◽  
Mitchell L. HALPERIN
Keyword(s):  
Flow Rate ◽  
Human Subjects ◽  
Collecting Duct ◽  
Urine Volume ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Ionized Calcium ◽  
High Concentration ◽  
History Of ◽  
Medullary Collecting Duct

The objective of this study was to evaluate the hypothesis that a high concentration of ionized calcium in the lumen of the medullary collecting duct causes an osmole-free water diuresis. The urine flow rate and osmolality were measured in normal human subjects, as well as in patients with a history of nephrolithiasis who excreted more than 5 mmol of calcium per 24 h. There was an inverse relationship between the concentration of calcium in the urine and the 24 h urine volume both in normal subjects and in patients with a history of nephrolithiasis. When the concentration of calcium in the urine was greater than 5 mmol/l, the urine volume was less than 1 litre per day in the majority of subjects. After 16 h of water deprivation, when the concentration of calcium in the urine was as high as 17 mmol/l (ionized calcium 7.4 mmol/l), urine osmolality was 1258 mOsm/kg of water and the urine flow rate was 0.30 ml/min. We conclude that, although a calcium receptor may be present in the lumen of the medullary collecting duct in human subjects, an extremely high concentration of urinary total and ionized calcium does not cause a clinically important defect in the renal concentrating process.

Renal medullary plasma flow rate and reabsorption of salt and water from inner medullary collecting duct

1987 ◽  
Vol 65 (12) ◽  
pp. 2415-2421 ◽  
Author(s):  
W. A. Cupples ◽  
H. Sonnenberg
Keyword(s):  
Blood Flow ◽  
Sodium Chloride ◽  
Angiotensin Ii ◽  
Flow Rate ◽  
Plasma Flow ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Renal Circulation ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

It has been proposed that medullary washout secondary to increased blood flow will limit maximal urine osmolality and reabsorption of salt and water from the inner medullary collecting duct. We have tested this prediction. The function of the inner medullary collecting duct was examined by microcatheterization. Acetylcholine was infused directly into the renal circulation, captopril was infused intravenously, and angiotensin II was infused into the renal circulation in rats which also received captopril. Medullary plasma flow rate, measured by dye–dilution in parallel experiments, was not significantly increased by acetylcholine; it was increased 30% (p < 0.02) by systemic infusion of captopril, and was returned to control by angiotensin II. Acetylcholine increased both urine flow rate and sodium excretion (p < 0.01, p < 0.001, respectively), while captopril increased only sodium excretion (p < 0.025). Angiotensin II blocked the natriuresis due to captopril. None of the treatments altered urine osmolality (p > 0.4 in all cases). Acetylcholine increased the loads of water, sodium, chloride, and total solute delivered to the inner medullary collecting duct. Angiotensin II reduced delivery of water and solutes compared with captopril alone. None of the treatments affected load dependency of reabsorption of water, sodium, chloride, or total solute in the inner medullary collecting duct. We conclude that there is, at most, a weak interaction between medullary blood flow and reabsorption from the inner medullary collecting duct.

scholarly journals Improvement of marina design technology using hydrodynamic models

2013 ◽  
Vol 6 (1) ◽  
pp. 63-72
Keyword(s):  
Mathematical Model ◽  
Flow Field ◽  
Flow Rate ◽  
Small Dimension ◽  
Water Circulation ◽  
Minor Importance ◽  
Hydrodynamic Models ◽  
Design Technology ◽  
Flow Rates ◽  
General Behavior

Á mathematical model is applied to calculate the water circulation in the marina of Latsi in Cyprus. The flow field in the marina shows the general behavior of coastal, wind driven flows, being strongly influenced by the characteristics of the entrance of the marina. The small dimension and the location of the entrance do not permit the inflow or outflow of significant flow rates, thus resulting to long flushing times. The use of two openings has been investigated. Computations show that the first opening plays a very important role, while the effect of the second opening is only of local and minor importance. This behavior is due to the orientation and the position of these openings with respect to the entrance. The use of the first opening results to a significant increase of the flow-rate passing through the inner part of the marina, which increases the magnitude of the velocities and reduce the flushing times. The use of the second opening leads to a significant short-circuiting path of the flow between the opening and the entrance. The first opening has been proposed for construction.

Decreased vasopressin-mediated renal water reabsorption in rats with chronic aldosterone-receptor blockade

2000 ◽  
Vol 278 (2) ◽  
pp. F246-F256 ◽  
Author(s):  
Thomas E. N. Jonassen ◽  
Dominique Promeneur ◽  
Sten Christensen ◽  
Jørgen S. Petersen ◽  
Søren Nielsen
Keyword(s):  
Collecting Duct ◽  
Water Channel ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Receptor Blockade ◽  
Water Reabsorption ◽  
Aldosterone Receptor ◽  
Duct Ligation ◽  
Urine Production ◽  
Daily Urine

Previous studies have suggested that mineralocorticoids are needed for a normal action of vasopressin on collecting duct osmotic water permeability. However, the mechanisms behind this are unknown. To investigate if aldosterone-receptor blockade influences vasopressin type 2 receptor (V2)-mediated renal water reabsorption and the renal expression of the vasopressin-regulated water channel aquaporin-2 (AQP2), rats were treated with the aldosterone-receptor antagonist canrenoate (20 mg/day iv) for 4 wk. Daily urine flow was increased significantly by 44%, and urine osmolality was decreased by 27% in canrenoate-treated rats. Acute V2-receptor blockade (OPC-31260, 800 μg ⋅ kg−1 ⋅ h−1) was performed under conditions in which volume depletion was prevented. In control rats, OPC-31260 induced a significant increase in urine flow rate (V, +25%) and free water clearance ([Formula: see text], −29%). In canrenoate-treated rats, the effect of OPC-31260 was significantly reduced, and semiquantiative immunoblotting demonstrated a significant reduction (45%) in AQP2 expression. Because rats with common bile duct ligation (CBL) have a reduced vasopressin-mediated water reabsorption compared with normal rats (V: −24%;[Formula: see text]: −28%, and 86% downregulation of AQP2), the effect of canrenoate combined with OPC-31260 was tested. Canrenoate treatment of CBL rats significantly increased daily urine flow, decreased urine osmolality, and impaired the aquaretic response to OPC-31260 (V: −23%;[Formula: see text]: −31%) with maintained suppression of the renal AQP2 expression. Thus canrenoate treatment of normal and CBL rats showed 1) increased urine production, 2) reduced aquaretic effect of acute V2-receptor blockade, and 3) a marked reduction in AQP2 expression. This strongly supports the view that aldosterone plays a significant role for vasopressin-mediated water reabsorption.

Postnatal maturation of potassium transport in rabbit cortical collecting duct

1994 ◽  
Vol 266 (1) ◽  
pp. F57-F65 ◽  
Author(s):  
L. M. Satlin
Keyword(s):  
Flow Rate ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Flow Rates ◽  
Postnatal Maturation ◽  
Significant Linear Correlation ◽  
Potassium Secretion ◽  
Tubular Flow ◽  
Neonatal Kidney

Clearance studies in newborns demonstrate low rates of urinary excretion of potassium, suggesting that the neonatal kidney contributes to the conservation of potassium necessary for growth. Because the cortical collecting duct (CCD) is a primary site for potassium secretion in the adult, we sought to examine the transport capacity of this segment for potassium during postnatal maturation. CCDs isolated from rabbits of various ages (5-6 animals/age group) were microperfused in vitro with solutions simulating plasma. The concentrations of potassium in samples of collected fluid, measured by helium glow photometry, were used to calculate net transport. At a flow rate of approximately 1.6 nl.min-1 x mm-1 net potassium secretion was absent at birth, first became evident at 4 wk of age (-11.08 +/- 2.39 pmol.min-1 x mm-1), and increased sharply thereafter to reach mature rates (-23.08 +/- 3.47 pmol.min-1 x mm-1; P < 0.05) by 6 wk of age. To determine whether low distal tubular flow rates limit net potassium secretion in the neonate, we perfused CCDs at two or more flow rates in the 0.5–5 nl.min-1 x mm-1 range. In CCDs taken from animals > or = 6 wk of age, potassium secretion showed a significant linear correlation with flow rate (y = -10.0x - 7.45; r = 0.87; n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)

A mathematical model of rat collecting duct I. Flow effects on transport and urinary acidification

2002 ◽  
Vol 283 (6) ◽  
pp. F1237-F1251 ◽  
Author(s):  
Alan M. Weinstein
Keyword(s):  
Mathematical Model ◽  
Flow Rate ◽  
Collecting Duct ◽  
Osmotic Gradient ◽  
Acid Excretion ◽  
Urinary Ph ◽  
Model Calculations ◽  
Luminal Flow ◽  
High Flows ◽  
Net Acid Excretion

A mathematical model of the rat collecting duct (CD) has been developed by concatenating previously published models of cortical (Weinstein AM. Am J Physiol Renal Physiol 280: F1072–F1092, 2001); outer medullary (Weinstein AM. Am J Physiol Renal Physiol 279: F24–F45, 2000); and inner medullary segments (Weinstein AM. Am J Physiol Renal Physiol 274: F841–F855, 1998). Starting with end-distal tubular flow rate and composition, plus interstitial solute profiles, the model predicts urinary solute flows, including the buffer concentrations required to assess net acid excretion. In the model CD, the interstitial corticomedullary osmotic gradient provides the basis for the flow effect on the transport of several solutes. For substances that have an interstitial accumulation and that can have diffusive secretion (e.g., urea and NH[Formula: see text]), enhanced luminal flow increases excretion by decreasing luminal accumulation. For substances that are reabsorbed (e.g., K+ and HCO[Formula: see text]), and for which luminal accumulation can enhance reabsorption, increasing luminal flow again increases excretion by decreasing luminal solute concentration. In model calculations, flow-dependent increases in HCO[Formula: see text] and NH[Formula: see text] approximately balance, so net acid excretion is little changed by flow, albeit at a higher urinary pH. The model identifies delivery flow rate to the CD as a potent determinant of urinary pH, with high flows blunting maximal acidification. At even modestly high flows (9 nl · min−1 · tubule−1, with 6% of filtered Na+ entering the CD), the model cannot achieve a urinary pH <5.5 unless the delivered HCO[Formula: see text]concentration is extremely low (<2 mM). Nevertheless, simulation of Na2SO4 diuresis does yield both an increase in net acid excretion and a decrease in urinary HCO[Formula: see text](i.e., a decrease in pH) despite the increase in urinary flow. This model should provide a tool for examining hypotheses regarding transport defects underlying distal renal tubular acidosis.

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