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Biomedical subjects

S F Wen

Publications and source records attributed to S F Wen.

52 records · Page 3Linked to original sources
PubMed1978

Sodium transport in dogs with acute remnant and glomerulonephritic kidneys.

The nephron site responsible for the different patterns of sodium excretion in response to extracellular volume expansion observed in dogs with bilateral acute remnant kidneys, acute NTN, and normal kidneys was studied with clearance and micropuncture techniques. Mean kidney GFR's in the remnant and NTN kidneys were similar at 14 and 15 ml/min, respectively, compared to 28 ml/min for the normal kdineys. However, SNGFR's were normal in the remnant kidneys but markedly reduced in dogs with NTN. Mean absolute sodium excretion was similar for the remnant and normal kidneys both during the control phase and after volume expansion. Because of the reduced GFR, FENa of the remnant kidneys was significantly higher in each situation. In contrast, mean absolute sodium excretion was markedly less in dogs with NTN than in normal dogs both before and after volume expansion. Although FENa during the control phase was similar to that in normal dogs, it increased significantly less with volume expansion. Despite these differences in urinary sodium excretion, the percent sodium reabsorption at the end of the proximal convoluted tubule was similar in all three groups. In addition, volume expansion depressed proximal SFENa to the same degree in each group. Therefore the different patterns of urinary FENa were the result of differences in fractional sodium reabsorption by the nephron segments distal to the proximal convoluted tubule. Decreased distal delivery of sodium secondary to the reduced SNGFR also contributed to the decreased sodium excretion in acute NTN.

Animals↗
PubMed1976

Acute effect of nephrotoxic serum on renal sodium transport in the dog.

In order to study the tubular mechanism for salt retention in acute proliferative glomerulonephritis, clearance and micropuncture experiments were performed on nine volume-expanded dogs before and after injection of sheep anti-dog glomerular basement membrane (GBM) antibodies (nephrotoxic sera [NTS]). Histologic sections obtained two hours after NTS injection following completion of the functional studies demonstrated infiltration of glomerular tufts by polymorphonuclear leukocytes, swelling of both glomerular endothelial and mesangial cells and the mesangial matrix, and linear anti-GBM antibody deposits along the glomerular capillaries. There was an almost immediate reduction in glomerular filtration rate (GFR), filtration fraction, urine flow and absolute and fractional sodium excretion; arterial blood pressure and renal plasma flow were not significantly altered. Micropuncture studies revealed no change in fractional sodium reabsorption in the proximal tubule despite a fall in single nephron GFR. A proportional reduction in single nephron and kidney GFR coupled with an unchanged intrarenal distribution of blood flow following NTS suggests a relatively uniform effect on both superficial and deep nephrons. In contrast to the well-preserved glomerulotubular balance in the proximal tubule, fractional distal sodium reabsorption was significantly increased as reflected by the decreased fractional urinary sodium excretion. We conclude that salt retention and low fractional urinary sodium excretion observed in acute glomerulonephritis could be primarily due to reduced distal delivery of sodium which leads to increased fractional sodium reabsorption in the nephron segments distal to the proximal convoluted tubule.

Animals↗
PubMed1976

Electrolyte transport in remnant kidney of the dog: effect of furosemide.

Micropuncture studies were performed in 26 dogs with a unilateral remnant kidney to examine its response to modest extracellular volume expansion and furosemide administration in the presence (Stage II) and absence (Stage III) of an intact contralateral kidney. During hydropenia in 15 Stage II dogs, proximal and distal transport of sodium and potassium was comparable to that of normal dogs (Stage I). Following 3% volume expansion, fractional proximal reabsorption was reduced similarly in Stages I and II. Although a slightly greater reduction in fractional loop reabsorption of sodium in Stage II after volume expansion was not significant, it was significantly greater with furosemide administration. In 11 Stage III dogs, proximal fractional reabsorption was depressed during hydropenia, and the loop sodium response to both volume expansion and furosemide administration was exaggerated. In contrast, greater increase in distal potassium secretion was demonstrated mainly in Stage III but not in Stage II remnant kidneys both before and after the diuretic maneuvers. The observations of exaggerated sodium response to furosemide by the remnant kidney in both Stages II and III but greater potassium response only in Stage III suggest that independent factors are responsible for these adaptations when functioning renal mass is reduced.

Animals↗
PubMed1976

Micropuncture studies of glucose transport in the dog: mechanism of renal glycosuria.

Clearance and micropuncture studies were performed in 23 dogs without glucose loading to examine the tubule mechanism of renal glycosuria. Studies were carried out in three groups of animals before and after 10% extracellular volume expansion, and administration of maleic acid in low dose at 150 mumol/kg and in high dose at 300 mumol/kg. Specific hexokinase methods were used for the determination of glucose in tubule fluid and urine. Under control conditios, glucose reabsorption occurred predominantly in the proximal tubule. In all three groups, proximal tubule reabsorption of both sodium and glucose was inhibited in the second phase, showing a good correlation between the two. In contrast, fractional urinary glucose excretion remained unchanged after volume expansion and low-dose maleic acid, indicating reabsorption of virtually all the increased glucose load at a further "distal" site. On the other hand, significant glycosuria developed after high-dose maleic acid that was a result of reduced glucose reabsorption in the distal nephron, in addition to the proximal effect. It was concluded that distal glucose transport plays a significant role in regulating urinary glucose excretion and maintains renal thershold for glucose,

Aminohippuric Acids↗
PubMed1974

Micropuncture studies of phosphate transport in the proximal tubule of the dog. The relationship to sodium reabsorption.

Micropuncture studies were performed in the dog to examine the relationship between sodium and phosphate transport in the proximal tubule. In hydropenic, thyroparathyroidectomized animals, administration of parathyroid extract, saline, or acetazolamide resulted in a fall in proximal tubule fluid-to-plasma (TF/P) inulin ratio as well as a rise in tubule fluid-to-plasma ultrafilterable (TF/UF) phosphate ratio. A correlation was found between the changes in fractional reabsorption of sodium and phosphate but the phosphate changes were generally greater than those of sodium. Also, a high distal phosphate delivery in the face of low fractional excretion of phosphate in the urine in thyroparathyroidectomized dogs suggests significant phosphate reabsorption in the distal nephron. On the other hand, calcium chloride infusion to saline-loaded, normal dogs to suppress endogenous parathyroid hormone reduced proximal TF/UF phosphate without change in TF/P inulin, while both parameters remained unchanged in saline-loaded, thyroparathyroidectomized dogs after calcium infusion. An increase in proximal TF/UF phosphate associated with unchanged TF/P inulin was also demonstrated by administration of highly purified parathyroid hormone to saline-loaded, thyroparathyroidectomized dogs. It was concluded that although proximal tubule phosphate transport is generally closely related to that of sodium, the two can dissociate under certain experimental conditions, especially under the influence of parathyroid hormone. These observations also indicate that the effect of parathyroid hormone on proximal tubule phosphate transport is not solely dependent upon its effect on sodium transport.

Absorption↗
PubMed1974

The effect of vasopressin on phosphate transport in the proximal tubule of the dog.

Recollection micropuncture study was performed in 11 thyroparathyroidectomized dogs during antidiuresis to determine the effect of continuous vasopressin infusion at 50 mU/kg/h on proximal tubule phosphate and sodium transport. The animals were divided into two groups according to changes in mean arterial blood pressure. In the first group (five dogs) with increased blood pressure and glomerular filtration rate (GFR), mean proximal tubule fluid-to-plasma inulin ratio fell significantly from 1.69 to 1.53, whereas it remained unchanged at 1.60 in the second group (six dogs) with no change in blood pressure. In contrast, mean proximal tubule fluid-to-plasma ultrafilterable phosphate ratio increased consistently in both groups, regardless of blood pressure changes. Since natriuresis as well as phosphaturia were observed in all animals, the sodium effect of vasopressin in the distal nephron must be mainly responsible for the natriuresis. It was concluded that vasopressin, when given in the doses employed, inhibits phosphate transport in the proximal tubule and sodium reabsorption in the distal nephron. An additional effect on proximal tubule sodium reabsorption appears to be related to the rise in blood pressure and GFR secondary to vasopressin administration.

Animals↗
PubMed1973

Micropuncture studies of sodium transport in the remnant kidney of the dog. The effect of graded volume expansion.

Proximal and distal tubule micropuncture studies were performed to examine the response to graded extracellular volume (ECV) expansion in 10 normal dogs (stage I), 11 dogs with a unilateral remnant kidney (stage II), and 7 dogs with a remnant kidney after removal of the contralateral kidney (stage III). Before ECV expansion in stage III, there was a suggestive reduction in proximal tubule as well as loop fractional reabsorption of sodium. After ECV expansion to 3% body weight proximal tubule reabsorption was depressed in all groups of animals, while little further inhibition was observed in this segment with additional expansion to 10% body weight. In contrast, the fraction of filtered sodium remaining in the distal tubule rose progressively in all three groups after graded ECV expansion, suggesting that the graded natriuretic response found in the final urine was largely due to a similar response in the loop of Henle rather than that in the proximal tubule. The distal tubule response of the remnant kidney in both stages II and III was greater than that in stage I. These data indicate that although enhanced sodium excretion per nephron in chronic renal failure may be related to uremia, its exaggerated response to ECV expansion is due, at least in part, to certain as yet unidentified intrarenal factors consequent to reduction in functioning renal mass.

Animals↗
PubMedDate not supplied

Chronic reduction in renal mass: micropuncture studies of response to volume expansion and furosemide.

Chronic nephron loss is compensated by functional adaptations which preserve electrolyte homeostasis. The response to volume expansion and diuretics was tested in dogs. Three phase recollection micropuncture studies were performed to assess the response of the remnant kidney in various stages of renal failure to furosemide administration (10 mg/Kg) and graded volume expansion (3 percent and 10 percent body weight). After the diuretic maneuvers, mean fractional excretion of sodium, potassium and water rose progressively in normal dogs (Stage I), with a greater increase in the remnant kidneys in the presence (Stage II) and absence (Stage III) of the contralateral kidney. Proximal and distal TF/P (Inulin) ratios were depressed after 3 percent volume expansion. However, proximal TF/P (Inulin) was not further lowered after 10 percent volume expansion and furosemide administration, while distal TF/P (Inulin) ratios were progressively depressed. The distal TF/P (Inulin) ratios in Stage III were significantly lower than in Stage II under analogous conditions. Our results suggest that the adaptive increase in the response of sodium transport by the remnant kidney to the diuretic maneuvers occurs in the loop of Henle, both in the azotemic and the non-azotemic stage. Adaptation of potassium excretion, as revealed by distal micropuncture, took place in the azotemic Stage III. Chronic functional adaptation for electrolyte transport occurs even before azotemia in the distal nephron and includes the proximal tubule with azotemia.

Adaptation, Physiological↗
PubMedDate not supplied

A recombinant adenoviral vector expressing full-length human retinoblastoma susceptibility gene inhibits human tumor cell growth.

As a prelude to considering retinoblastoma (RB) gene therapy for cancer, a series of human tumor cell lines with either full-length, mutated, or undetectable RB protein were treated with recombinant adenovirus encoding RB (ACNRB). Both RB protein expression and the cytotoxic and antiproliferative effects of ACNRB treatment were evaluated. While the transgene expression of a reporter virus encoding the beta-galactosidase enzyme (rAd-beta-gal) varied among cell lines, the reintroduction and expression of the RB gene resulted in a pronounced inhibition of cellular proliferation in RB-altered cell lines. An antiproliferative response was observed with control adenovirus treatment in some cell lines. ACNRB treatment did not cause detectable cytotoxicity in either RB+ or RB-altered cells. Dose-dependent cytostasis was observed in RB- cell lines. In vivo tumor suppression was observed in a breast xenograft model subsequent to the treatment of established tumors with ACNRB. These data support a role for RB gene therapy of tumors with RB mutations and provide a basis for the further evaluation of ACNRB gene therapy of human cancer.

Adenoviridae↗