THE OSMOTIC GRADIENT IN KIDNEY MEDULLA: A RETOLD STORY

2002 ◽  
Vol 26 (4) ◽  
pp. 278-281 ◽  
Author(s):  
S. Kurbel ◽  
K. Dodig ◽  
R. Radić
Keyword(s):  
Hydrostatic Pressure ◽  
Osmotic Gradient ◽  
Interstitial Pressure ◽  
Kidney Medulla ◽  
Limited Space ◽  
Vasa Recta

This article is an attempt to simplify lecturing about the osmotic gradient in the kidney medulla. In the model presented, the kidneys are described as a limited space with a positive interstitial hydrostatic pressure. Traffic of water, sodium, and urea is described in levels (or horizons) of different osmolarity, governed by osmotic forces and positive interstitial pressure. In this way, actions of the countercurrent multiplier in nephron tubules and of the countercurrent exchanger in vasa recta are integrated in each horizon. We hope that this approach can help students to better accept conventional presentations in their textbooks.

Renal interstitial pressure in mineralocorticoid escape

1985 ◽  
Vol 249 (3) ◽  
pp. F396-F399 ◽  
Author(s):  
J. C. Burnett ◽  
J. A. Haas ◽  
M. S. Larson
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Hydrostatic Pressure ◽  
Arterial Pressure ◽  
Filtration Rate ◽  
Interstitial Pressure ◽  
Peritubular Capillary ◽  
Renal Interstitium ◽  
Vasa Recta ◽  
Peritubular Capillaries

Studies were performed in normal and DOCA-treated rats to determine renal hydrostatic pressures within superficial peritubular capillaries, the vasa recta, and renal interstitium during mineralocorticoid escape to test the hypothesis that mineralocorticoid escape is associated with elevated renal interstitial hydrostatic pressure. Fractional sodium excretion was greater in the DOCA-treated rats (3.20 +/- 0.51%) compared with control rats (1.23 +/- 0.12%) with no difference in glomerular filtration rate and renal blood flow between the two groups. Superficial peritubular capillary hydrostatic pressure (13.4 +/- 0.6 vs. 8.3 +/- 0.3 mmHg), vasa recta hydrostatic pressure (13.8 +/- 0.5 vs. 9.0 +/- 0.4 mmHg), renal interstitial hydrostatic pressure (9.8 +/- 0.4 vs. 4.5 +/- 0.4 mmHg), and arterial pressure (145 +/- 6 vs. 120 +/- 7 mmHg) were greater in the DOCA-treated compared with the control rats. These studies establish that mineralocorticoid escape is characterized by high renal interstitial hydrostatic pressure.

UT-B1 proteins in rat: tissue distribution and regulation by antidiuretic hormone in kidney

2002 ◽  
Vol 283 (5) ◽  
pp. F912-F922 ◽  
Author(s):  
M.-M. Trinh-Trang-Tan ◽  
F. Lasbennes ◽  
P . Gane ◽  
N. Roudier ◽  
P. Ripoche ◽  
...  
Keyword(s):  
Antidiuretic Hormone ◽  
Brain Cortex ◽  
Rat Kidney ◽  
Cross Reactivity ◽  
Ependymal Cells ◽  
Kidney Medulla ◽  
Vasa Recta ◽  
Cell Processes ◽  
Rat Tissue

UT-B1 is the facilitated urea transporter of red blood cells (RBCs) and endothelial cells of descending vasa recta in the kidney. Immunoblotting with a polyclonal antibody against the C-ter sequence of rat UT-B1 revealed UT-B1 as both nonglycosylated (29 kDa) and N-glycosylated (47.5 and 33 kDa) proteins in RBC membranes, kidney medulla, brain, and bladder in rat. In testis, UT-B1 was expressed only as a nonglycosylated protein of 47.5 kDa. Immunocytochemistry confirmed that the location of UT-B1 is restricted to descending vasa recta. In brain, UT-B1 protein was found in astrocytes and ependymal cells. Cell bodies and perivascular end feet of astrocytes were labeled in brain cortex, whereas astrocyte cell processes were labeled in corpus callosum. Flow cytometry analysis of RBCs revealed a good cross-reactivity of the antibody with mouse and human UT-B1. UT-B1 protein expression in rat kidney medulla was downregulated greatly by long-term [deamino-Cys1,d-Arg8]vasopressin infusion and moderately by furosemide treatment. This study discloses an uneven distribution of UT-B1 protein within astrocytes and the regulation of renal UT-B1 protein by antidiuretic hormone.

The Renal Pelvis: Machinery That Concentrates Urine in the Papilla

Physiology ◽  
2003 ◽  
Vol 18 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Terry M. Dwyer ◽  
Bodil Schmidt-Nielsen
Keyword(s):  
Renal Pelvis ◽  
Collecting Duct ◽  
Osmotic Gradient ◽  
Elastic Recoil ◽  
Vasa Recta ◽  
Rhythmic Contractions

Two decades ago, Bodil Schmidt-Nielsen and Bruce Graves documented the rhythmic contractions of the renal pelvis in a remarkable video, visually demonstrating how peristaltic waves empty the papilla and how the subsequent elastic recoil draws water from the collecting duct and into the tethered-open ascending vasa recta. Thus a periodic hydrostatic gradient generates an axial osmotic gradient. This review recapitulates the video and offers a link to figures and scenes digitized from the original tape.

Change in extra-alveolar perimicrovascular pressure with lung inflation

1984 ◽  
Vol 57 (3) ◽  
pp. 772-776 ◽  
Author(s):  
A. C. Jasper ◽  
H. S. Goldberg
Keyword(s):  
Hydrostatic Pressure ◽  
Volume Change ◽  
Transpulmonary Pressure ◽  
Pressure Change ◽  
Dry Mass ◽  
Interstitial Pressure ◽  
Autologous Plasma ◽  
Lung Inflation ◽  
Pulmonary Arterial ◽  
Over Time

In eight isolated dog lobes, we examined the change in extra-alveolar perimicrovascular hydrostatic pressure (Pis) due to lung inflation. The vasculature was filled with autologous plasma. Pulmonary arterial and venous lines were connected to a common plasma reservoir. Perimicrovascular volume change (delta Vis), compliance (Cis), and the microvascular filtration coefficient (Kf) were derived from the change in lobe mass over time following a step increase in vascular pressure (Piv). Initially, transpulmonary pressure (PL) was 5 cmH2O and Piv = 0 cmH2O. At constant Piv, two sequential 5-cmH2O increases in PL increased Vis; division of delta Vis by Cis yielded the change in Pis attributable to lung inflation. Cis was 0.035 +/- 0.018 g X cmH2O–1 X g dry mass-1 (mean +/- SD) at PL = 15 cmH2O. Kf was 0.019 +/- 0.023 g X min-1 X cmH2O–1 X g dry mass-1. With inflation from PL = 5 to PL = 10 cmH2O, Pis = -2.15 +/- 1.76 cmH2O; from PL = 10 to PL = 15 cmH2O, Pis = -2.25 +/- 1.50 cmH2O. This perimicrovascular pressure change is very close to the perihilar interstitial pressure change reported by others. Such near equality suggests that the stress of lung inflation is very uniformly applied to the interstitial continuum.

UT-B1 urea transporter is expressed along the urinary and gastrointestinal tracts of the mouse

2005 ◽  
Vol 288 (4) ◽  
pp. R1046-R1056 ◽  
Author(s):  
N. Lucien ◽  
P. Bruneval ◽  
F. Lasbennes ◽  
M.-F. Belair ◽  
C. Mandet ◽  
...  
Keyword(s):  
Plasma Membranes ◽  
Cell Types ◽  
Tissue Expression ◽  
Northern Blotting ◽  
Urea Transporter ◽  
Kidney Medulla ◽  
Vasa Recta ◽  
Mouse Tissues ◽  
Preferred Species ◽  
Umbrella Cells

Selective transporters account for rapid urea transport across plasma membranes of several cell types. UT-B1 urea transporter is widely distributed in rat and human tissues. Because mice exhibit high urea turnover and are the preferred species for gene engineering, we have delineated UT-B1 tissue expression in murine tissues. A cDNA was cloned from BALB/c mouse kidney, encoding a polypeptide that differed from C57BL/6 mouse UT-B1 by one residue (Val-8-Ala). UT-B1 mRNA was detected by RT-PCR in brain, kidney, bladder, testis, lung, spleen, and digestive tract (liver, stomach, jejunum, colon). Northern blotting revealed seven UT-B1 transcripts in mouse tissues. Immunoblots identified a nonglycosylated UT-B1 protein of 29 kDa in most tissues and of 36 and 32 kDa in testis and liver, respectively. UT-B1 protein of gastrointestinal tract did not undergo N-glycosylation. Immunohistochemistry and in situ hybridization localized UT-B1 in urinary tract urothelium (papillary surface, ureter, bladder, and urethra), prominently on plasma membranes and restricted to the basolateral area in umbrella cells. UT-B1 was found in endothelial cells of descending vasa recta in kidney medulla and in astrocyte processes in brain. Dehydration induced by water deprivation for 2 days caused a tissue-specific decrease in UT-B1 abundance in the urinary bladder and the ureter.

Role of renal interstitial hydrostatic pressure in the pressure diuresis response

1989 ◽  
Vol 256 (1) ◽  
pp. F63-F70 ◽  
Author(s):  
J. Garcia-Estan ◽  
R. J. Roman
Keyword(s):  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Capsule ◽  
Interstitial Pressure ◽  
Renal Perfusion Pressure ◽  
Residual Response

The present study examines the role of renal interstitial hydrostatic pressure (RIHP) in the pressure-diuretic and -natriuretic response. The relationships between RIHP, sodium excretion, and renal perfusion pressure (RPP) were determined in antidiuretic and volume-expanded (VE) rats with an intact or decapsulated kidney. RIHP was measured by use of the implanted capsule technique. RIHP increased significantly from 7.5 +/- 0.8 to 12.0 +/- 1.4 mmHg in VE animals and from 3.3 +/- 0.4 to 5.2 +/- 0.7 mmHg in antidiuretic rats after RPP was varied from 100 to 150 mmHg. The pressure-natriuretic response of the antidiuretic rats was blunted compared with that observed in the VE rats. Decapsulation of the kidney in VE rats lowered RIHP and reduced, but did not eliminate, the pressure-natriuretic response. To determine whether this residual response was related to changes in interstitial pressure in the medulla, cortical (CIHP) and medullary interstitial hydrostatic pressures (MIHP) were simultaneously measured in VE rats with an intact or decapsulated kidney. In control rats CIHP and MIHP were similar at all levels of RPP studied. In rats with the renal capsule removed MIHP was higher than CIHP and rose significantly from 6.7 +/- 0.8 to 9.2 +/- 0.8 mmHg when RPP was varied from 100 to 150 mmHg. These results indicate that pressure diuresis and natriuresis is accompanied by changes in RIHP and the response is modulated by the basal level of RIHP. These findings suggest that changes in MIHP may serve as an intrarenal signal for this response.

scholarly journals Three-dimensional architecture of inner medullary vasa recta

2006 ◽  
Vol 290 (6) ◽  
pp. F1355-F1366 ◽  
Author(s):  
Thomas L. Pannabecker ◽  
William H. Dantzler
Keyword(s):  
Collecting Duct ◽  
Rat Kidney ◽  
Three Dimensional ◽  
Osmotic Gradient ◽  
Graphical Modeling ◽  
Vasa Recta ◽  
Countercurrent Exchange ◽  
Modeling Software ◽  
Specific Proteins ◽  
Thin Limb

The manner in which vasa recta function and contribute to the concentrating mechanism depends on their three-dimensional relationships to each other and to tubular elements. We have examined the three-dimensional architecture of vasculature relative to tubular structures in the central region of rat kidney inner medulla from the base through the first 3 mm by combining immunohistochemistry and semiautomated image acquisition techniques with graphical modeling software. Segments of descending vasa recta (DVR), ascending vasa recta (AVR), descending thin limb (DTL), ascending thin limb (ATL), and collecting duct (CD) were identified with antibodies against segment-specific proteins associated with solute and water transport (urea channel B, PV-1, aquaporin-1, ClC-K1, aquaporin-2, respectively) by immunofluorescence. Results indicate: 1) DVR, like DTLs, are excluded from CD clusters that we have previously shown to be the organizing element for the inner medulla; 2) AVR, like ATLs, are nearly uniformly distributed transversely across the entire inner medulla outside of and within CD clusters; 3) DVR and AVR outside CD clusters appear to be sufficiently juxtaposed to permit good countercurrent exchange; 4) within CD clusters, about four AVR closely abut each CD, surrounding it in a highly symmetrical fashion; and 5) AVR abutting each CD and ATLs within CD clusters form repeating nodal interstitial spaces bordered by a CD on one side, one or more ATLs on the opposite side, and one AVR on each of the other two sides. These relationships may be highly significant for both establishing and maintaining the inner medullary osmotic gradient.

scholarly journals Axial compartmentation of descending and ascending thin limbs of Henle's loops

2013 ◽  
Vol 304 (3) ◽  
pp. F308-F316 ◽  
Author(s):  
Kristen Y. Westrick ◽  
Bradley Serack ◽  
William H. Dantzler ◽  
Thomas L. Pannabecker
Keyword(s):  
Blood Vessels ◽  
Water Permeability ◽  
Collecting Duct ◽  
Osmotic Gradient ◽  
Loop Length ◽  
Vasa Recta ◽  
Pass Through ◽  
Solute Gradient ◽  
Radial Organization

In the inner medulla, radial organization of nephrons and blood vessels around collecting duct (CD) clusters leads to two lateral interstitial regions and preferential intersegmental fluid and solute flows. As the descending (DTLs) and ascending thin limbs (ATLs) pass through these regions, their transepithelial fluid and solute flows are influenced by variable transepithelial solute gradients and structure-to-structure interactions. The goal of this study was to quantify structure-to-structure interactions, so as to better understand compartmentation and flows of transepithelial water, NaCl, and urea and generation of the axial osmotic gradient. To accomplish this, we determined lateral distances of AQP1-positive and AQP1-negative DTLs and ATLs from their nearest CDs, so as to gauge interactions with intercluster and intracluster lateral regions and interactions with interstitial nodal spaces (INSs). DTLs express reduced AQP1 and low transepithelial water permeability along their deepest segments. Deep AQP1-null segments, prebend segments, and ATLs lie equally near to CDs. Prebend segments and ATLs abut CDs and INSs throughout much of their descent and ascent, respectively; however, the distal 30% of ATLs of the longest loops lie distant from CDs as they approach the outer medullary boundary and have minimal interaction with INSs. These relationships occur regardless of loop length. Finally, we show that ascending vasa recta separate intercluster AQP1-positive DTLs from descending vasa recta, thereby minimizing dilution of gradients that drive solute secretion. We hypothesize that DTLs and ATLs enter and exit CD clusters in an orchestrated fashion that is important for generation of the corticopapillary solute gradient by minimizing NaCl and urea loss.

Alveolar pressure in fluid-filled occluded lung segments during permeability edema

1983 ◽  
Vol 55 (4) ◽  
pp. 1098-1102
Author(s):  
J. P. Kohler ◽  
C. L. Rice ◽  
G. S. Moss ◽  
J. P. Szidon
Keyword(s):  
Oleic Acid ◽  
Hydrostatic Pressure ◽  
Pulmonary Edema ◽  
Intravenous Injection ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Base Line ◽  
Interstitial Pressure ◽  
Alveolar Pressure ◽  
Permeability Pulmonary Edema

In a model of increased hydrostatic pressure pulmonary edema Parker et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 267-276, 1978) demonstrated that alveolar pressure in occluded fluid-filled lung segments was determined primarily by interstitial fluid pressure. Alveolar pressure was subatmospheric at base line and rose with time as hydrostatic pressure was increased and pulmonary edema developed. To further test the hypothesis that fluid-filled alveolar pressure is determined by interstitial pressure we produced permeability pulmonary edema-constant hydrostatic pressure. After intravenous injection of oleic acid in dogs (0.01 mg/kg) the alveolar pressure rose from -6.85 +/- 0.8 to +4.60 +/- 2.28 Torr (P less than 0.001) after 1 h and +6.68 +/- 2.67 Torr (P less than 0.01) after 3 h. This rise in alveolar fluid pressure coincided with the onset of pulmonary edema. Our experiments demonstrate that during permeability pulmonary edema with constant capillary hydrostatic pressures, as with hemodynamic edema, alveolar pressure of fluid-filled segments seems to be determined by interstitial pressures.

Mechanism of natriuresis during intrarenal infusion of prostaglandins

1984 ◽  
Vol 247 (3) ◽  
pp. F475-F479 ◽  
Author(s):  
J. A. Haas ◽  
T. G. Hammond ◽  
J. P. Granger ◽  
E. H. Blaine ◽  
F. G. Knox
Keyword(s):  
Blood Flow ◽  
Hydrostatic Pressure ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Prostaglandin Analogue ◽  
Similar Increase ◽  
Interstitial Pressure

Intrarenal infusion of the natural prostaglandin PGE2 increases renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. A newly synthesized prostaglandin analogue, 4-3-[3-[2-(1-hydroxycyclohexyl)- ethyl]-4-oxo-2-thiazolidinyl]propyl benzoic acid, increases renal blood flow without increasing sodium excretion. To investigate the role of renal interstitial hydrostatic pressure in this dissociation, comparisons were made between PGE2 and the prostaglandin analogue. Intrarenal infusion of PGE2 increased renal blood flow, renal interstitial hydrostatic pressure, and urinary sodium excretion. Following a similar increase in renal blood flow with intrarenal infusion of prostaglandin analogue, renal interstitial hydrostatic pressure and urinary sodium excretion were not changed. To determine whether increases in urinary sodium excretion due to PGE2 infusion are causally related to the increase in renal interstitial hydrostatic pressure rather than to the increase in renal blood flow, responses to PGE2 were obtained in the absence of increases in interstitial pressure. When renal interstitial hydrostatic pressure was held constant, urinary sodium excretion did not change although there was a marked increase in renal blood flow. We conclude that increased renal interstitial hydrostatic pressure is necessary to produce an increase in urinary sodium excretion with prostaglandin-mediated renal vasodilation.

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