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Biomedical subjects

N Bank

Publications and source records attributed to N Bank.

At least 55 records · Page 3Linked to original sources
PubMed1983

Selective deep nephron hyperfiltration in uninephrectomized spontaneously hypertensive rats.

Studies were carried out to determine the effect of uninephrectomy (UNX) on single nephron hemodynamics and proteinuria in the spontaneously hypertensive rat (SHR). Four groups were studied: two-kidney SHR and normotensive WKY controls; SHR + UNX and WKY + UNX. UNX was performed at age 8 to 10 weeks. Blood pressure and protein excretion were measured periodically, and micropuncture experiments of cortical nephrons were carried out at age 32 to 40 weeks. Systolic blood pressure was not significantly different between SHR and SHR + UNX. Protein excretion increased markedly in the SHR + UNX 6 months after UNX, as compared with the other three groups. In cortical nephrons, single nephron glomerular filtration rate (SNGFR) and plasma flow entering the glomeruli (SNPF) was lower in SHR + UNX than in WKY + UNX. Glomerular hydraulic pressure (PG) during stopped flow was closely comparable in all groups, rising only 2 mm Hg after UNX. SNGFR was measured in juxtamedullary (JM) nephrons 2 months after UNX, a stage before heavy proteinuria developed. We found that JM SNGFR was approximately 50% higher in SHR + UNX than in WKY + UNX. The observations suggest that following ablation of renal mass, superficial cortical glomeruli are not exposed to excessively high pressure or flow rates in the SHR. In contrast, JM glomeruli undergo a disproportionate rise in SNGFR, presumably associated with excessively high PG and/or blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Role of tubular obstruction in acute renal failure due to gentamicin.

Gentamicin sulfate was administered by intraperitoneal injection to male Sprague-Dawley rats in a dose of 100 to 120 mg/kg/day for 4 to 5 days to induce severe nephrotoxicity. In comparison to controls, inulin clearance was markedly decreased (2.87 +/- 0.31 vs. 8.65 +/- 0.31 ml/min/kg, P less than 0.001) as was urinary osmolality (462 +/- 36 vs. 1196 +/- 46, P less than 0.001). Surface tubules appeared heterogeneous. Some were plugged by whitish debris, whereas others were markedly dilated (I.D. = 41.5 +/- 2 mu). All other tubules were moderately dilated (I.D. = 28.8 vs. 20 mu). The microinfusion of tubules with cellular debris with an isotonic "equilibrium" solution resulted in a rise in intratubular pressure to as high as 60 to 80 mm Hg, compared with 13 to 15 mm Hg in normal rats. In better functioning nephrons, free-flow pressure (FFP) was increased significantly (16.0 +/- 0.5 vs. 10.2 +/- 0.1 mm Hg, P less than 0.001). Paired measurements of single nephron glomerular filtration rate (SNGFR) in these nephrons, made while monitoring intratubular pressure (ITP), revealed a rise in SNGFR when ITP was lowered from the initially high level to 10 mm Hg. Comparable changes in SNGFR were induced in normal rats by varying ITP from 10 to 15 mm Hg. The data suggest that in severe gentamicin nephrotoxicity, many cortical nephrons may be contributing very little to excretory function, presumably because of intratubular obstruction. The less impaired nephrons have reduced SNGFR, due in part to increased free-flow pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1982

Studies of the urinary acidification defect induced by lithium.

Experiments were carried out in rats and isolated turtle bladders to study the defect in H+ transport induced by LiCl. After 3-4 days of intraperitoneal LiCl, rats developed urinary findings of "distal" renal tubular acidosis. Proximal tubular fluid pH measured in situ by glass microelectrodes was higher in lithium-treated rats than in acidotic controls. Proximal fluid total CO2 [tCO2] was also higher, and the fraction of tCO2 leaving the proximal tubule was 14 vs. 7% (P less than 0.001). Impaired acidification was also apparent beyond distal convoluted tubules, as judged by normal distal tCO2 reabsorption but increased HCO3(-) in the urine. During NaHCO3 loading, the proximal defect was ameliorated but not the distal. Turtle bladder studies showed that mucosal lithium inhibits H+ secretion secondary to reducing transepithelial electrical potential, presumably by hyperpolarization of the luminal membrane. A similar mechanism may be responsible for lithium's effect on the distal nephron. Inhibition of proximal tubular HCO3(-) reabsorption is probably not attributable to electrical potential changes but might be due to interference of luminal membrane Na+ entry by Li+ and reduced (Na+ + Li+)-H+ exchange.

Acid-Base Equilibrium↗
PubMed1980

Diuretics stimulate H+ secretion in turtle urinary bladder.

The effect of various diuretics on H+ secretion was studied in the isolated short-circuited urinary bladder of the turtle. Mucosal (urinary) chlorothiazide stimulated H+ secretion promptly, from 1.33 +/- 0.24 to 3.03 +/- 0.25 mueq/h (P less than 0.001). The effect was rapidly reversible upon washout of the drug, H+ returning to control levels, 1.37 +/- 0.26 mueq/h (P less than 0.001). Similar effects were observed with mucosal hydrochlorothiazide and mucosal ethacrynic acid/cysteine. Stimulation of H+ secretion occurred in the presence or the absence of exogenous CO2, in the presence or absence of mucosal Na+ and during inhibition of Na+ transport by ouabain. There was no stimulation of H+ secretion by uncomplexed ethacrynic acid or by mucosal furosemide. The nondiuretic sulfonamide, sulfasoxizole, and the nonsulfonamide buffer, borate, had no effect on H+ SECRETION. These observations indicate that the stimulatory effect of diuretics on H+ secretion is not related to active sodium transport, transepithelial electrical potential, or the buffering capacity of the drugs. Since the transepithelial pH gradient at which active H+ secretion was abolished was identical for chlorothiazide-treated tissues (2.68 pH U) as for control tissues (2.65 pH U, NS), the data suggest that the protonmotive force of the H+ pump was unaffected by the diuretic. This observation, plus the rapid onset and reversibility of the drugs, is consistent with an effect on the mucosal membrane to increase H+ conductance (K). The findings raise the possibility that direct enhancement of renal H+ secretion may play a role in the metabolic alkalosis induced by some diuretics.

Animals↗
PubMed1979

A micropuncture study of renal sodium retention in nephrotic syndrome in rats: evidence for increased resistance to tubular fluid flow.

Micropuncture studies were carried out in surface nephrons of rats with nephrotoxic-serum (NTS)-induced nephrotic syndrome during a period of active sodium and water retention. It was found that hydrostatic pressure and tubular diameter were increased in the proximal tubules (13.4 +/- 0.2 vs. 10.4 +/- 0.2 mm Hg; 31.3 +/- 0.9 vs. 18.4 +/- 0.7 mu), whereas pressure and tubular diameter were normal in the distal tubules. Single nephron glomerular filtration rate (SNGFR) was decreased and fractional reabsorption of fluid was markedly increased in the proximal tubules (74.1 vs. 61.7%). The increased pressure gradient between the proximal and distal tubules suggests a condition of increased resistance to flow between the proximal and distal tubules. Microinfusion of proximal tubules with an isotonic "equilibrium" solution led to little or no rise in intratubular pressure in normal rats but it led to a significant rise in nephrotic rats. When proximal tubules of normal rats were infused with a solution containing 100 mg/100 ml albumin, pressure rose to levels observed in nephrotic rats. The mechanism of the increased resistance to flow appeared to be related, therfore, to the presence of protein in the tubular fluid. Sodium retention in the nephrotic animals might be attributed to the reduction in GFR. In other types of renal disease in animals and man with comparable or greater reductions in GFR, sodium retention does not occur, however, and fractional excretion of sodium in the urine is increased in proportion to the reduction in GFR. Thus, the rise in proximal fractional reabsorption secondary to impaired fluid flow could be an important factor in the sodium retention of this disease.

Animals↗
PubMed1978

The effect of normalization of serum complement and anti-DNA antibody on the course of lupus nephritis: a two year prospective study.

A prospective study was carried out in 25 patients with systemic lupus erythematosis (SLE) on the effect of normalizing serum complement (CH50) and anti-DNA antibodies on the course of lupus nephritis. In 16 of the 25 patients, CH50 was maintained within the normal range for two years. Urinary protein excretion increased or remained low in all 16. Repeat renal biopsies were performed in 10 of these 16, and disclosed either stabilization of glomerular disease or diminution. In the nine patients in whom CH50 could not be normalized with tolerated doses of drugs, urinary protein excretion increased or remained increased. Repeat renal biopsies in six of these nine patients were carried out and showed worsening of glomerular disease in five. No clear-cut correlation was found between urinary protein excretion or renal disease and the serum levels of anti-DNA antibody. We conclude from these observations that continuous normalization of CH50 by drug therapy in patients with SLE is associated with stabilization or diminution of lupus nephritis.

Antibodies↗
PubMed1978

A micropuncture study of renal phosphate transport in rats with chronic renal failure and secondary hyperparathyroidism.

Micropuncture studies were carried out in rats to determine changes in tubular transport of phosphate which occur in chronic renal failure and secondary hyperparathyroidism. Rats underwent subtotal nephrectomy (NX) and were fed a low calcium, high phosphorus diet for 3--4 wk. Other groups consisted of normal control animals, normal rats infused with sodium phosphate to raise filtered load of phosphate, subtotal NX rats parathyroidectomized (PTX) on the day of experiment, and normal PTX rats infused with sodium phosphate. It was found that filtered phosphate/nephron is markedly increased in subtotal NX rats due to high single nephron filtration rates, proximal tubular fluid plasma phosphate ratios are less than 1.0, and fractional reabsorption of phosphate is decreased in the proximal tubule. More phosphate was present in the final urine than in surface distal convoluted tubules. Acute PTX in subtotal NX rats resulted in a striking increase in proximal phosphate reabsorption, and urinary phosphate became approximately equal to that remaining in surface distal tubules. Phosphate loading in normal rats reduced fractional reabsorption in the proximal tubule, but urinary phosphate was not greater than that at the end of surface distal tubules. Acute PTX in normal phosphate-loaded animals had no significant effect on proximal tubular phosphate reabsorption. These observations suggest that phosphate homeostasis in chronic renal failure is acheived by inhibition of proximal phosphate reabsorption, counteracting a greatly enhanced intrinsic capacity for reabsorption. In addition, the large amount of urinary phosphate is consistent either with secretion by the collecting ducts or with a disproportionately high contribution by deep nephrons. The changes in phosphate transport are mediated by parathyroid hormone and are completely abolished by acute removal of the hormone.

Acid-Base Equilibrium↗
PubMed1978

Use of diuretics in treatment of hypertension secondary to renal disease.

Eleven patients with hypertension secondary to renal disease were treated with hydrochlorothiazide or furosemide plus other drugs to normalize blood pressure. Creatinine clearance fell during the initial treatment period, but then either remained constant or rose toward pretreatment levels in spite of continued therapy. Plasma renin activity was low-normal to subnormal in eight of the 11 patients prior to therapy and did not rise significantly with therapy. Aldosterone excretion was within the normal range prior to treatment and remained normal or increased moderately with treatment. This study demonstrates that diuretics effectively reduce blood pressure in patients with hypertension secondary to renal disease without producing severe volume depletion or clinically significant reduction in renal function. The low renin levels are consistent with other evidence that hypertension in these patients is related to salt and water retention.

Adult↗
PubMed1977

Diagnosis of lupus nephritis by skin immunofluorescence, in the absence of extrarenal manifestations of systemic lupus erythematosus.

Six patients with glomerulonephritis were found to have granular deposits of complement and/or immunoglobulins at the dermalepidermal junction of normal skin. No patient had extrarenal clinical manifestations of systemic lupus erythematosus (SLE). The only serologic test suggestive of SLE was a positive antinuclear antibody (ANA) reaction; results of complement and antinative deoxyribonucleic acid (DNA)-antibody tests were repeatedly normal. The patients with glomerulonephritis had a favorable initial response to therapy with prednisone with or without azathioprine. These patients may represent a variant of SLE in which the diagnosis can only be established by a direct immunofluorescence test of normal skin. Alternatively, they may constitute a separate new clinical entity. Because of the favorable response to therapy, we suggest that skin immunofluorescence be performed in patients who present with unexplained glomerulonephritis and a positive ANA.

Adolescent↗
PubMed1976

Effect of intraluminal bicarbonate and chloride on fluid absorption by the rat renal proximal tubule.

In order to study mechanisms of fluid transport in the rat renal proximal convoluted tubule, the effects of large variations in intraluminal HCO3- and Cl- concentrations were measured by microperfusion techniques. No differences in rates of fluid transport were found when intraluminal HCO3- was varied from 4 to 30 mEq/liter and Cl- from 146 to 120 mEq/liter. Inhibition of H+ secretion with benzolamide had no effect on fluid absorption when little or no HCO3- was present in the lumen, but did reduce fluid transport when 25 mEq of HCO3- was present. If several different mechanisms are responsible for proximal fluid transport, such as nonelectrogenic active NaHCO3 transport, passive chloride diffusion and active sodium transport linked to H+ secretion, the above observations imply that they all operate at approximately the same rate, since the dominant driving force would have been different with each perfusion solution. The data seem more compatible with the view that active sodium transport is the major driving force for fluid absorption in the proximal tubule, that this is not linked to H+ secretion and that anions modify the rate of absorption only to the degree that they are able to accompany sodium across the epithelium. An additional observation was that absorption of isotonic NaCl was very slow in short segments of tubule, as compared to HCO3--containing perfusion solutions. Although the mechanism is uncertain, these data suggest that a finite amount of intraluminal HCO3- is necessary for optimal proximal fluid transport.

Animals↗
PubMed1976

Effect of stretch on passive transport in toad urinary bladder.

In order to gain further information about the effect of stretch on the urinary bladder of the toad, transepithelial movement of radioactive sucrose, chloride, and urea was measured across bladder sacs during acute changes in the internal volume. Short-circuit current (SCC) and total tissue conductance (Kt) were also measured in each experiment. It was found that sudden large increases or smaller graded increases in volume resulted in a consistent fall in the tracer permeability (P*) of all three isotopes. However, this fall was due entirely to the larger area term in the calculation of P* rather than any real change in isotope movement. When total diffusion (TD) of each isotope was calculated by a method that eliminated the changes in surface area, it was apparent that stretch produced no significant effects on the transepithelial movement of any of these three molecules. Large stretch also resulted in parallel increases in SCC and Kt in most bladders. We conclude from these observations that the intercellular pathway for sucrose and chloride and the transcellular pathway for urea are unaltered by degrees of stretch that enhance SCC and sodium transport. By inference, the observed increases in Kt appear to represent changes in specific active pathway conductance (Ka), and may relate importantly to the changes in sodium transport.

Animals↗
PubMed1976

A micropuncture study of the effect of parathyroid hormone on renal bicarbonate reabsorption.

Renal micropuncture and clearance experiments were carried out in rats to study the effect of parathyroid hormone (PTH) on renal tubular HCO-/3 reabsorption. The rats were studied during an initial period of parathyroid deficiency (acute thyroidparathyroidectomy, TPTX) and during infusion of large amounts of bovine PTH. Under normal acid-base conditions, PTH administration to TPTX rats caused a significant rise in proximal tubular fluid HCO-/3 concentration (TFHCO-/3), a decrease in fluid reabsorption, and a fall in proximal HCO-/3 reabsorption from 94.0 to 88.2% (P less than 0.01). In control experiments with mannitol infusion, a comparable reduction in proximal fluid reabsorption occurred without any significant effect on intraluminal HCO-/3 concentration. During acute intravenous HCO-/3 loading, PTH inhibited proximal HCO-/3 reabsorption. However, no change in whole kidney HCO-/3 reabsorption was observed in these experiments or in the animals studied under normal acid-base conditions. The findings are consistent with the view that PTH inhibits proximal tubular HCO-/3 reabsorption with normal or high filtered loads of HCO-/3, but distal segments of the nephron are able to reabsorb the excess delivered from the proximal tubule. Measurements of urinary ammonium and titratable acid indicate that net acid excretion (NH+/4 + TA -- HCO-/3) increases significantly after PTH administration. These results do not provide support for the view that PTH excess causes metabolic acidosis by reducing renal acid excretion.

Acidosis↗
PubMed1975

A micropuncture study of renal salt and water retention in chronic bile duct obstruction.

The mechanism of sodium retention by the kidney in rats with ligation of the common bile duct was studied with micropuncture techniques. 10-14 days after bile duct ligation, rats showed positive sodium balance and ascites formation. Measurements of renal blood flow and glomerular filtration rate yielded values that were not different from those in normal control animals. Likewise, single nephron filtration rte of surface nephrons was the same in the experimental rats as in the controls. Sodium reabsorption, however, was markedly increased in the proximal convoluted tubule, as well as in segments beyond the proximal convolutions. Single nephron filtration fraction, calculated from measurements of efferent arteriolar and arterial hematocrits, was significantly elevated in the cortical nephrons, even though whole kidney filtration fraction was the same as in normal rats. The calculated protein concentration of cortical peritubular blood was higher in the bile duct-ligated rats than in the normal controls. The observations are consistent with the view that sodium retention is the result of enhanced reabsorption primarily by cortical nephrons. The enhanced reabsorption can be accounted for by relative cortical ischemia due to efferent arteriolar vasoconstriction with the consequent elevation of peritubular colloid oncotic pressure.

Animals↗
PubMed1975

The behavior of carbenicillin as a nonreabsorbable anion.

In order to study the mechanism of hypokalemic alkalosis which occurs in some patients being treated with disodium carbenicillin, renal clearance experiments were carried out in rats and observations were made on electrical changes in isolated toad bladders. In rats maintained on a sodium-free diet, intravenous infusion of carbenicillin at 40 mg. per hour resuited in an immediate diuresis characterized by a striking increase in K and NH4 excretion, and progressive acidification of the urine. In a control group of rats, also prepared with a sodium free diet, intravenous infusion of mannitol resulted in a comparable diuresis, but no significant changes in K and NH4 excretion, and no acidification of the urine. The urinary changes in the carbenicillin-treated rats could not be accounted for by any alterations in blood electrolytes, acid-base values, or glomerular filtration rate (GFR). Isonatric, isohydric substitution of carbenicillin for chloride in the mucosal bathing media of toad bladders mounted in Ussing chambers resulted in a reversible increase in electrical potential (PD) and resistance (R) without a comparable change in short-circuit current (SCC). Substitution in the serosal medium resulted in a reversal of polarity of PD and SCC in 4 of 9 experiments, a finding best explained by more rapid movement of chloride from M leads to S than carbenicillin movement from S leads to M (a chloride diffusion potential). The observations in both the rat and toad bladder experiments are consistent with the view that carbenicillin behaves as a nonreabsorbable anion. Hypokalemic alkalosis in patients receiving this drug can thus be attributed to increased electrical negativity of the distal nephron with subsequent enhancement of K and H secretion.

Acid-Base Equilibrium↗