AN EFFECT OF ANTIDIURETIC HORMONE ON THE FLOW OF BLOOD THROUGH THE VASA RECTA OF THE RAT KIDNEY

1966 ◽  
Vol 35 (2) ◽  
pp. 173-NP ◽  
Author(s):  
JULIA FOURMAN ◽  
G. C. KENNEDY
Keyword(s):  
Blood Flow ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Water Conservation ◽  
Rat Kidney ◽  
Renal Medulla ◽  
Countercurrent System ◽  
Vasa Recta ◽  
Collecting Ducts ◽  
Flow Through

SUMMARY The injection of a fluorescent dye which stained the vessel walls showed the pathway taken by the blood in the renal medulla in rats. The vasa recta stained in normal rats given water; they did not stain in dehydrated rats nor did they stain in rats given an antidiuretic dose of vasopressin in addition to water. The vasa recta stained in all rats with diabetes insipidus whether they were given water or dehydrated. These results suggest that antidiuretic hormone increases water conservation in the medulla by reducing blood flow through the countercurrent system as well as by increasing the permeability of the collecting ducts to water.

Acute effect of cyclosporin on inner medullary blood flow in normal and postischemic rat kidney

1990 ◽  
Vol 258 (5) ◽  
pp. F1139-F1144
Author(s):  
Y. Yagil
Keyword(s):  
Blood Flow ◽  
Rat Kidney ◽  
Electromagnetic Flowmeter ◽  
Renal Medulla ◽  
Acute Effect ◽  
Acute Administration ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Group 2 ◽  
Group 1

Acute cyclosporin A (CysA) nephrotoxicity has been attributed to intrarenal vasoconstriction. It has been previously demonstrated that CysA decreases whole kidney and cortical blood flow. The effect of CysA on medullary blood flow has not been adequately studied, despite the high susceptibility of structures in the renal medulla to ischemia and the common use of CysA after the kidney is subjected to transient ischemia. To determine its effects on medullary blood flow in the normal and postischemic kidney, CysA was administered acutely in anesthetized Munich-Wistar rats at doses ranging from 4 to 20 mg/kg. Total renal blood flow (TRBF) and glomerular filtration rate (GFR) were determined in normal kidneys (group 1) by standard clearance techniques before and after infusion of CysA. In animals subjected to 40-min unilateral renal ischemia (group 2) TRBF was measured with an electromagnetic flowmeter. Vasa recta blood flow was determined in both groups by fluorescence videomicroscopy. In group 1, infusion with 20 mg/kg CysA, but not with 4 or 8 mg/kg, increased renal vascular resistance (RVR) and decreased TRBF. GFR was not affected and filtration fraction increased. Vasa recta blood flow was not significantly altered. In group 2, 20 mg/kg CysA increased RVR and decreased TRBF. Vasa recta blood flow decreased significantly in the descending but not in the ascending vasa recta. These results suggest that, in the normal kidney, vasa recta blood flow in the renal medulla is not affected by acute administration of CysA, whereas in the postischemic kidney, CysA decreases blood flow preferentially in the descending vasa recta, in proportion to the decline in TRBF.

scholarly journals Urine concentrating mechanism: impact of vascular and tubular architecture and a proposed descending limb urea-Na+ cotransporter

2012 ◽  
Vol 302 (5) ◽  
pp. F591-F605 ◽  
Author(s):  
Anita T. Layton ◽  
William H. Dantzler ◽  
Thomas L. Pannabecker
Keyword(s):  
Blood Flow ◽  
Interstitial Fluid ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Renal Medulla ◽  
Fluid Composition ◽  
Vascular Bundles ◽  
Vasa Recta ◽  
Countercurrent Exchange ◽  
Thin Limb

We extended a region-based mathematical model of the renal medulla of the rat kidney, previously developed by us, to represent new anatomic findings on the vascular architecture in the rat inner medulla (IM). In the outer medulla (OM), tubules and vessels are organized around tightly packed vascular bundles; in the IM, the organization is centered around collecting duct clusters. In particular, the model represents the separation of descending vasa recta from the descending limbs of loops of Henle, and the model represents a papillary segment of the descending thin limb that is water impermeable and highly urea permeable. Model results suggest that, despite the compartmentalization of IM blood flow, IM interstitial fluid composition is substantially more homogeneous compared with OM. We used the model to study medullary blood flow in antidiuresis and the effects of vascular countercurrent exchange. We also hypothesize that the terminal aquaporin-1 null segment of the long descending thin limbs may express a urea-Na+ or urea-Cl− cotransporter. As urea diffuses from the urea-rich papillary interstitium into the descending thin limb luminal fluid, NaCl is secreted via the cotransporter against its concentration gradient. That NaCl is then reabsorbed near the loop bend, raising the interstitial fluid osmolality and promoting water reabsorption from the IM collecting ducts. Indeed, the model predicts that the presence of the urea-Na+ or urea- Cl− cotransporter facilitates the cycling of NaCl within the IM and yields a loop-bend fluid composition consistent with experimental data.

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.

Role of the renal medulla in volume and arterial pressure regulation

1997 ◽  
Vol 273 (1) ◽  
pp. R1-R15 ◽  
Author(s):  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Fluid Pressure ◽  
Regulatory System ◽  
Renal Medulla ◽  
Water Excretion ◽  
Vasa Recta ◽  
Pressure Natriuresis ◽  
Total Renal Blood Flow

The original fascination with the medullary circulation of the kidney was driven by the unique structure of vasa recta capillary circulation, which Berliner and colleagues (Berliner, R. W., N. G. Levinsky, D. G. Davidson, and M. Eden. Am. J. Med. 24: 730-744, 1958) demonstrated could provide the economy of countercurrent exchange to concentrate large volumes of blood filtrate and produce small volumes of concentrated urine. We now believe we have found another equally important function of the renal medullary circulation. The data show that it is indeed the forces defined by Starling 100 years ago that are responsible for the pressure-natriuresis mechanisms through the transmission of changes of renal perfusion pressure to the vasa recta circulation. Despite receiving only 5-10% of the total renal blood flow, increases of blood flow to this region of the kidney cause a washout of the medullary urea gradient and a rise of the renal interstitial fluid pressure. These forces reduce tubular reabsorption of sodium and water, leading to a natriuresis and diuresis. Many of Starling's intrinsic chemicals, which he named "hormones," importantly modulate this pressure-natriuresis response by altering both the sensitivity and range of arterial pressure around which these responses occur. The vasculature of the renal medulla is uniquely sensitive to many of these vasoactive agents. Finally, we have found that the renal medullary circulation can play an important role in determining the level of arterial pressure required to achieve long-term fluid and electrolyte homeostasis by establishing the slope and set point of the pressure-natriuresis relationship. Measurable decreases of blood flow to the renal medulla with imperceptible changes of total renal blood flow can lead to the development of hypertension. Many questions remain, and it is now evident that this is a very complex regulatory system. It appears, however, that the medullary blood flow is a potent determinant of both sodium and water excretion and signals changes in blood volume and arterial pressure to the tubules via the physical forces that Professor Starling so clearly defined 100 years ago.

Renal medullary blood flow: its measurement and physiology

1986 ◽  
Vol 64 (7) ◽  
pp. 873-880 ◽  
Author(s):  
W. A. Cupples
Keyword(s):  
Blood Flow ◽  
Renal Medulla ◽  
Vascular Bundles ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Countercurrent Exchange ◽  
Renal Medullary Blood Flow ◽  
Urinary Concentrating Ability ◽  
Velocity Tracking ◽  
Uptake Method

The vasculature of the mammalian renal medulla is complex, having neither discrete input nor output. There is also efficient countercurrent exchange between ascending and descending vasa recta in the vascular bundles. These considerations have hampered measurement of medullary blood flow since they impose pronounced constraints on methods used to assess flow. Three main strategies have been used: (i) indicator extraction; (ii) erythrocyte velocity tracking; and (iii) indicator dilution. These are discussed with respect to their assumptions, requirements, and limitations. There is a consensus that medullary blood flow is autoregulated, albeit over a narrower pressure range than is total renal blood flow. When normalized to gram tissue weight, medullary blood flow in the dog is similar to that in the rat, on the order of 1 to 1.5 mL∙min−1∙g−1. This is considerably greater than estimated by the radioiodinated albumin uptake method which has severe conceptual and practical problems. From both theoretical and experimental evidence it ssems that urinary concentrating ability is considerably less sensitive to changes in medullary blood flow than is often assumed.

scholarly journals Localization of 125I-atrial natriuretic factor (ANF)-binding sites in rat renal medulla. A light and electron microscope autoradiographic study.

1987 ◽  
Vol 35 (2) ◽  
pp. 149-153 ◽  
Author(s):  
C Bianchi ◽  
J Gutkowska ◽  
R Garcia ◽  
G Thibault ◽  
J Genest ◽  
...  
Keyword(s):  
Electron Microscope ◽  
Binding Sites ◽  
Atrial Natriuretic Factor ◽  
Renal Medulla ◽  
Microscopic Level ◽  
Electron Microscopic Level ◽  
Natriuretic Factor ◽  
Vasa Recta ◽  
Collecting Ducts ◽  
Atrial Natriuretic

Using light and electron microscope autoradiography in vivo, the localization of 125I-(Arg 101-Tyr 126) atrial natriuretic factor (ANF)-binding sites was studied in the renal medulla of rats. At the light microscopic level, the autoradiographic reaction was mainly distributed in patches in the outer medulla, and followed the tubular architecture in the innermost part of the inner medulla. At the electron microscopic level, binding sites were mainly found in the outer medullary descending vasa recta and inner medullary collecting ducts. These results suggest that, in rats, the renal medulla may participate in the natriuresis and diuresis produced by ANF through vascular and tubular effects; the former by changing medullary blood flow at the level of descending vasa recta and the latter by acting on electrolyte and water transport at the level of collecting ducts.

Distribution of capillary blood flow in rat kidney during postischemic renal failure

1986 ◽  
Vol 251 (3) ◽  
pp. H510-H519 ◽  
Author(s):  
F. Vetterlein ◽  
A. Petho ◽  
G. Schmidt
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Rat Kidney ◽  
Renal Medulla ◽  
Fluorescein Isothiocyanate ◽  
Artery Occlusion ◽  
Ischemic Insult ◽  
Renal Artery Occlusion ◽  
Tubular System ◽  
Intrarenal Blood Flow

Changes in distribution of intrarenal blood flow were studied in anesthetized rats during the acute phase of postischemic renal failure (1 h renal artery occlusion, 1 h reflow). Distribution of capillary plasma flow was determined by injecting fluorescein-isothiocyanate-globulin and lissamine-rhodamine-B200-globulin 1, 3, or 10 min prior to rapid freezing of the kidney. In histological sections it was possible to differentiate among the vessels perfused during the time of labeling because of their respective fluorescence. In these experiments all glomeruli became labeled within 1 min, although in contrast to the controls, the glomerular capillary network itself was not filled completely in the postocclusion organs. Incomplete labeling was far more pronounced, however, in the postglomerular network of the occlusion experiments. Due to this effect in the cortex and in the medulla, 11 and 58% of tissue, respectively, were found lying at a distance of more than 60 microns from the next vessel labeled after 1 min of dye circulation. In the control experiments there was no tissue within this distance. Prolonging the time of labeling up to 10 min caused little change in this pattern of distribution. In the occlusion experiments, the globulins were observed in nearly all Bowman spaces, but in less than half of the tubular lumina. The results strengthen the view that the ischemic insult leads primarily to disturbance of the postglomerular perfusion, which then results in trophic damage of the tubular system mainly within the renal medulla.

Autoregulation in vasa recta of the rat kidney

1983 ◽  
Vol 245 (1) ◽  
pp. F32-F40 ◽  
Author(s):  
H. J. Cohen ◽  
D. J. Marsh ◽  
B. Kayser
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Flow Velocity ◽  
Volume Expansion ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Extracellular Fluid ◽  
Vessel Diameter ◽  
Video Adaptation ◽  
Vasa Recta

Vasa recta blood flow autoregulation was studied by measuring flow velocity in individual vessels on the papilla surface with a video adaptation of the dual-slit erythrocyte velocity method. Vessel diameter did not vary with arterial pressure in the range of 60-150 mmHg, allowing the calculation of the ratio of flows in a single vessel at two pressures from the ratio of velocities. Flow velocity in single vasa recta increased with arterial pressure to 75 mmHg, remained constant in the range of 75-125 mmHg, and increased with higher pressures. In a second series of animals, whole kidney blood flow auto-regulated above 90 mmHg. Vasa recta and whole kidney flow patterns were not changed by extracellular fluid volume expansion. Volume expansion caused a greater increase in ascending than in descending vasa recta flow, reflecting the volume load from enhanced collecting duct reabsorption in diuresis. In a final series, Na excretion varied with arterial pressure in the range of 90-130 mmHg. Because vasa recta velocity remains constant within this range, pressure diuresis cannot be caused by the lack of autoregulation of vasa recta blood flow, at least to 130 mmHg.

Autoregulation of blood flow in renal medulla of the rat: no role for angiotensin II

1988 ◽  
Vol 66 (6) ◽  
pp. 833-836 ◽  
Author(s):  
W. A. Cupples ◽  
D. J. Marsh
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Lower Limit ◽  
Enzyme Inhibitor ◽  
Renal Medulla ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Upper Limit ◽  
Vasa Recta

Autoregulation of blood flow was assessed by a dual-slit technique in descending and ascending vasa recta of the exposed renal papillae of antidiuretic rats. There was complete autoregulation of blood flow in descending vasa recta. The lower limit of autoregulation was approximately 85 mmHg (1 mmHg = 133.3 Pa) and the upper limit was greater then 160 mmHg. Auto-regulation in ascending vasa recta was also good. To test the role of angiotensin II in this autoregulation, the converting enzyme inhibitor captopril was infused. Captopril had no effect on autoregulation of blood flow in either descending or ascending vasa recta. We conclude that blood flow in vasa recta of renal medulla is efficiently autoregulated and that this autoregulation is independent of angiotensin II

Interstitial water and solute recovery by inner medullary vasa recta

2000 ◽  
Vol 278 (2) ◽  
pp. F257-F269 ◽  
Author(s):  
Aurélie Edwards ◽  
Mark J. Delong ◽  
Thomas L. Pallone
Keyword(s):  
Interstitial Water ◽  
Renal Medulla ◽  
Recent Model ◽  
Generation Rate ◽  
Aquaporin 1 ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Collecting Ducts ◽  
Filtered Load ◽  
Small Solute

A recent model of volume and solute microvascular exchange in the renal medulla was extended by simulating the deposition of NaCl, urea, and water into the medullary interstitium from the loops of Henle and collecting ducts with generation rates that undergo spatial variation within the inner medullary interstitium. To build an exponential osmolality gradient in the inner medulla, as suggested by Koepsell et al. (H. Koepsell, W. E. A. P. Nicholson, W. Kriz, and H. J. Höhling. Pflügers Arch. 350: 167–184, 1974), the ratio of the interstitial area-weighted generation rate of small solutes to that of water must increase along the corticomedullary axis. We satisfied this condition either by holding the area-weighted generation rate of water constant while increasing that of NaCl and urea or by reducing the input rate of water with medullary depth. The latter case, in particular, yielded higher solute concentrations at the papillary tip. Assuming that the fraction of the filtered load recovered by inner medullary vasa recta for water, NaCl, and urea is 1%, 1%, and 40%, respectively, papillary tip osmolality is 1,470 mosmol/kgH2O when urea generation and NaCl generation per unit volume of interstitium increase exponentially and linearly, respectively. The inner medullary osmolar gradient also increases further when 1) medullary blood flow is reduced, 2) hydraulic conductivity of descending vasa recta (DVR) is lowered, and 3) vasa recta permeability to NaCl and urea is maximized. The coupling between water and small solute transport, resulting from aquaporin-1-mediated transcellular flux in DVR, also enhances tip osmolality.

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