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Biomedical subjects

W E Yarger

Publications and source records attributed to W E Yarger.

30 records · Page 2Linked to original sources
PubMed1976

Renal function in experimental cystic disease of the rat.

The administration of diphenylamine to rats induces an acquired form of cystic disease. In order to examine the early changes in this model of experimental cystic disease prior to the development of the more severe structural alterations, clearance, micropuncture, and morphologic studies were performed in rats fed DPA for 3 to 6 weeks. A significant defect in maximal urine concentrating ability (Umax) was manifest by the second week and averaged 50% of control values. Further studies were undertaken to examine the cause of the defect in Umax. Whole-kidney glomerular filtration rate (GFR), single-nephron GFR, end-proximal TF/Pinulin, glucose and bicarbonate reabsorption were all normal, indicating normal function of the proximal tubule. Free water clearance and free water reabsorption were not significantly different in DPA-treated rats as compared to controls, suggesting normal function of the ascending limb of the loop of Henle and collecting duct. Morphologic examination revealed gross cysts in less than 10% of the kidneys but structural changes were consistently demonstrated in the collecting ducts of DPA-treated rats. These studies indicate that the decrease in Umax in DPA-treated animals is the result of a defect located at the terminal portion of the collecting duct.

Animals↗
PubMed1975

Post-obstructive diuresis: a varied syndrome.

A prospective study was undertaken to define the clinical features, natural history and etiology of post-obstructive diuresis. Studied in detail were 8 patients with a massive diuresis after relief of urinary tract obstruction. We found that urea mediated osmotic diuresis, natriuresis owing to elimination of retained sodium from the obstructed phase, tubular defects in sodium reabsorption, renal unresponsiveness to antidiuretic hormone and iatrogenic factors may play varying roles in each individual diuresis. Overzealous fluid replacement should be avoided.

Adult↗
PubMed1975

Lanthanum permeability of tight junctions along the collecting duct of the rat.

The permeability of the tight junctions (zonulae occludentes) was evaluated along the entire length of the collecting duct of the rat using a lanthanum tracer technique. Nine rats with hereditary hypothalamic diabetes insipidus were studied using standard micropuncture and clearance techniques. Glomerular filtration rate (GFR) estimated from inulin clearance, urine and plasma osmolality (U/Posm) and urine flow rate (V) were determined in eight of nine animals. During either sustained diuresis (five animals) or vasopressin-induced antidiuresis (four animals), individual surface convolutions of distal convoluted tubules or early cortical collecting ducts were preserved for ultrastructural examination by intraluminal microperfusion with a glutaraldehyde-formaldehyde fixative followed by a second microperfusion with a lanthanum tracer. Mean GFR during diuresis was 6.31 plus or minus se 0.63 ml/min/kg of body wt and v=797 plus or minus se 108 mul/min/kg or 13.6 plus or minus se 2.2% of the filtered load of water. After administration of exogenous vasopressin, V fell to 311 plus or minus 157 mul/min/kg or 5.2 plus or minus se 3.8% of the filtered load of water and U/Posm rose from 0.658 plus or minus se 0.043 to 2.124 plus or minus 0.454. Tight junctions of cortical and outer medullary segments of the collecting duct resisted lanthanum penetration. Tight junctions of the inner medullary and papillary segments of the collecting duct were freely permeable to lanthanum suggesting the presence of a paracellular shunt pathway for solute and water movement. The results were independent of the presence or absence of vasopressin. Physiological studies have previously demonstrated that cortical and outer medullary segments of the collecting duct have a low urea permeability while inner medullary and papillary segments of the collecting duct have a relatively high urea permeability. The possibility is suggested that urea movement across the inner medullary and papillary segments of the collecting duct may occur, at least in part, via a paracellular pathway formed by the nonoccluding tight junction and the lateral intercellular space.

Animals↗
PubMed1975

The pathogenesis of post-obstructive diuresis. The role of circulating natriuretic and diuretic factors, including urea.

To investigate the pathogenesis of post-obstructive diuresis, a state of functional "anuria" during ureteral obstruction was created in awake rats by (a) bilateral obstruction (BO); (b) unilateral obstruction and contralateral nephrectomy (UO-Nx); or (c) unilateral obstruction and continuous i.v. reinfusion of urine from the intact contralateral kidney (UO-reinf). These groups were compared with unilaterally obstructed (UO) and sham-operated control (sham) rats. After release of obstruction of 24 h duration, mean urine flows (V) and sodium excretion rates (UNaV) were significantly elevated above those of sham rats in BO, UO-Nx, and UO-reinf animals, but slightly decreased in UO rats. Glomerular filtration rates were comparably depressed in UO, BO, UO-Nx, and UO-reinf rats. These results suggest that post-obstructive diuresis is due to one or more circulating diuretic factors that are normally excreted in the urine, and which, when retained )as in BO or UO-Nx rats) or returned to the circulation (as in UO-reinf rats), exert a diuretic affect. In additional experiments, UO rats infused with urea exhibited post-obstructive diuresis, if extracellular volume contraction was prevented. This result suggests that urea may be an important diuretic factor in post-obstructive diuresis, but does not exclude possible roles for other humoral factors. The intact kidney of UO-reinf rats displayed a massive unilateral diuresis and natriuresis, further suggesting the presence of potent diuretic factors in the urine. A marked increase in the fractional excretion of glomerular filtrate (V/GFR) by the intact kidney suggests that this diuresis may be attributable, in part, to impaired proximal reabsorption.

Aminohippuric Acids↗
PubMed1972

A micropuncture study of postobstructive diuresis in the rat.

In order to investigate the syndrome of postobstructive diuresis, clearance and micropuncture studies were carried out in rats after relief of 24 hr of bilateral (BUL) or unilateral (UUL) ureteral ligation. In rats with BUL, a striking diuresis and natriuresis occurred when the obstruction to one kidney (the experimental kidney) was relieved. The results were not influenced by administration of vasopressin or d-aldosterone. Whole kidney clearances of inulin and p-aminohippuric acid (PAH) in the experimental kidney were reduced to 10% and 20% of normal, respectively. Superficial nephron inulin and PAH clearances were also reduced, but only to 40% and 45%, respectively. These findings suggest a heterogeneity of nephron function in which deep nephrons were functioning poorly or not at all. To investigate the site of impaired tubular reabsorption in the surface nephrons, absolute and fractional water reabsorption was measured. Absolute reabsorption was found to be decreased all along the nephron. Fractional reabsorption in proximal tubules was normal, as indicated by an average endproximal tubular fluid per plasma inulin (TF/P(In)) of 2.16 vs. 2.30 in controls. TF/P(In) was markedly decreased in distal tubules (2.91 vs. 8.02) and final urine (5.56 vs. 263). These observations indicate that the major sites of impaired sodium reabsorption leading to the diuresis were beyond the proximal tubule.Rats with 24 hr of UUL did not demonstrate a comparable natriuresis or diuresis either spontaneously when the obstruction was relieved or after i.v. infusion of urea. A major difference between the BUL and UUL rats was that prerelease intrarenal hydrostatic pressure was markedly elevated (30.1 mm Hg) in the former but was below normal free-flow values (9.2 mm Hg) in the latter. Thus, elevation of intrarenal pressure during the period of obstruction may be causally related to the natriuresis and diuresis which occurs after the obstruction is relieved.

Aminohippuric Acids↗
PubMed1971

A microperfusion study of sucrose movement across the rat proximal tubule during renal vein constriction.

Constriction of the renal vein has been shown to inhibit net sodium and water reabsorption by the rat proximal tubule. The mechanism is unknown but might be the result of inhibition of the active sodium pump induced by changes in the interstitial fluid compartment of the kidney, or to enhanced passive backflux of sodium and water into the cell or directly into the tubular lumen. Since passive movement of solutes across epithelial membranes is determined in part by the permeability characteristics of the epithelium, an increase in the permeability of the proximal tubule during venous constriction would suggest that enhanced passive flux is involved in the inhibition of reabsorption. In the present experiments, isolated segments of rat proximal convoluted tubules were microperfused in vivo with saline while the animals were receiving (14)C-labeled sucrose intravenously. In normal control animals, no sucrose was detected in the majority of the collected tubular perfusates. In rats with renal vein constriction (RVC), however, sucrose consistently appeared in the tubular perfusates. The rate of inflow of sucrose correlated with the length of the perfused segment, estimated by fractional water reabsorption. In another group of animals with renal vein constriction, inulin-(14)C was given intravenously and the proximal tubules similarly microperfused. Inulin did not appear in the majority of collected perfusates in these animals. These observations indicate that a physiological alteration in the permeability of the proximal tubule occurs during RVC. Such an increase in permeability is consistent with the view that enhanced passive extracellular back-flux plays a role in the reduction of net sodium and water reabsorption in this experimental condition.

Animals↗