Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dive was carried out in the open sea to a depth of 850 fsw (26.7 ATA) for 6 days (DD 1--6) in the saturated mode, with personnel transfer capsule (PTC) excursions between 0 and 150 fsw and diver excursions between 0 and 50 fsw from the saturation base. Each diver had two excursion dives on alternate days. Although each PTC excursion lasted approximately 7 h, the actual time spent in the water averaged 10.5 min per diver. For 12 divers, daily excretion of water, electrolytes, aldosterone, and antidiuretic hormone (ADH) was studied, along with plasma composition (including prolactin), before, during, and after hyperbaric exposure. A significant increase in urine flow was observed on DD2--4 (1604 ml/day predive vs. 2300 ml/day on DD 4; P less than 0.05), after which the degree of diuresis decreased to about 1800 ml/day. Urine osmolality changed inversely with urine flow, with the lowest value of 532 mOsm/kg on DD 4. During the postdive period, both urine flow and urine osmolality returned to the predive level. The endogenous creatinine clearance was maintained at about 200 liters/day throughout the dive. The fractional excretion of Na+ remained unchanged while that of K+ increased significantly during hyperbaric exposure, thus decreasing the urinary Na+/K+ ratio. The fractional excretion of total osmotic substances showed a small hyperbaric exposure. Body weight decreased progressively during the initial 4 days of pressure exposure, equalling 2.6 kg on DD 4. These findings suggest that the observed diuresis may be accompanied by a net loss of body water. Neither the plasma prolactin level nor urinary excretion of aldosterone and ADHshowed any consistent change throughout the dive. It thus appears that, although there is a small osmotic component, the observed diuresis is primarily due to the ADH-independent inhibition of fre water reabsorption from the collecting duct by means of a mechanism yet to be identified.
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PMID:Urinary excretion of water and electrolytes during open-sea saturation diving to 850 fsw. 52 29

In anaesthesized dogs given large doses of ADH and DOC and subjected to acute left renal denervation, urine flow (V) and sodium excretion (UNaV) rose significantly in response to bilateral carotid artery clamping in both the intact (p less than 0.05) and the denervated kidney (p less than 0.001). This was associated with significant (p less than 0.05) increases of the tubular rejection fraction of sodium (TRFNa) while creatinine clearance (Ccr) remained unchanged. Following a second control period, carotid occlusion was repeated, while perfusion pressure in the left kidney was kept constant by aortic constriction. In this case the diuretic and natriuretic response in the right kidney occurred in the same fashion as previously, and no significant change in V, UNaV, or TRFNa was observed in the left kidney. The amount of free water reabsorbed in the collecting duct (TcH2O) was not consistently altered by carotid occlusion. It is concluded that acute renal denervation augments the pressure diuresis that follows carotid occlusion. The failure of carotid polyuria to occur when renal perfusion pressure is kept constant points to the importance of mechanical factors. Still, a wash-out of the medullary osmotic gradient seems to be an unlikely mechanism.
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PMID:Mechanism of carotid-occlusion diuresis. 75 93

During the past 5 years, we have identified idiopathic hypercalciuria in five of seven patients referred for evaluation of renal glycosuria between 1985 and 1991. The children, all boys, ranged in age from 6 to 12 years. Endocrine function was normal, and none of the patients had hyperparathyroidism, hypercalcemia, renal tubular acidosis, or other secondary causes of hypercalciuria. The calcium/creatinine ratio in a fasting urine specimen was elevated in all five children who had hypercalciuria, with a mean value (+/- SD) of 0.34 +/- 0.06 (normal, < 0.2). In one child who had renal colic with spontaneous passage of gravel-like material, the idiopathic hypercalciuria persisted after 1 week on a diet containing 2000 mg of sodium and 300 mg of calcium. On the basis of studies that examined the site along the nephron responsible for hypercalciuria in rats with streptozocin-induced diabetes, we speculate that in children with renal glycosuria, there is defective reabsorption of glucose and calcium in the straight portion of the proximal tubule or in the collecting duct. It is likely that a similar mechanism accounts for the idiopathic hypercalciuria in children with diabetes mellitus.
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PMID:Hypercalciuria in children with renal glycosuria: evidence of dual renal tubular reabsorptive defects. 841 May 29

Hypertrophic kidney growth in K depletion was analyzed morphometrically in rats fed a K-free diet for 18 days. K excretion decreased rapidly to less than 1% of control, creatinine clearance decreased, and urinary concentrating ability was impaired. Kidney weight in K-depleted rats was 30% higher than in controls. Growth of individual kidney zones was not uniform; hypertrophy of the inner stripe (IS) of the outer medulla was most prominent. Among tubules the most striking enlargement was seen in the outer medullary collecting duct (CD); hypertrophy and hyperplasia of both CD cells and intercalated (IC) cells occurred in the same proportion. In the IS, both luminal and basolateral membrane area per unit tubule length doubled in IC cells and increased 1.2- and 1.7-fold, respectively, in CD cells. Despite overall kidney growth, epithelial volume of thick ascending limb (TAL) per tubule length was unchanged in IS and cortex and only slightly increased in outer stripe. The increased membrane area of CD epithelium in the IS is consistent with previously reported increases in activity of enzymes involved in active reabsorption of K+ and Na+.
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PMID:Morphometric analysis of kidney hypertrophy in rats after chronic potassium depletion. 156 79

Urine cytology, plasma (P), and urinary (U) interleukin-2 (IL-2)* and IL-2 receptor (IL-2R) levels were evaluated as immunological monitoring techniques in 65 renal allograft recipients. Normal individuals showed normal urine cytology, IL-2(U) = 0, IL-2(P) = 0.4 +/- 0.1 ng/ml (mean +/- SEM) and IL-2R(P) = 318 +/- 26 U/ml. Stable transplants also showed normal urine cytology, no IL-2(U), IL-2(P) = 0.8 +/- 0.2 ng/ml, and IL-2R(P) = 326 +/- 29 U/ml. Rejection episodes (n = 21) were accompanied by cytologic changes, including lymphocyturia, exfoliation of immature tubular cells, platelet aggregates, and fibrin deposits. The corresponding lymphokine changes were IL-2(U) = 39.6 +/- 1.4 ng/ml, IL-2(P) = 79 +/- 21 ng/ml, and IL-2R = 1884 +/- 202 U/ml, all markedly increased. Successful treatment was associated with return of all parameters to normal; treatment failure was associated with continued abnormalities. Fourteen rejections unresponsive to Solumedrol (500 mg x 5 days) required OKT3 rescue (5 mg x 14 days). In the 11 that were reversed, onset of OKT3 therapy was characterized by markedly increased exfoliation of necrotic cellular debris, lymphocytes, and collecting duct cells. Interestingly, serum creatinine increases of 57.2 +/- 18.9% (range 25-90%) over pre-OKT3 levels were noted. Maximal changes occurred 48-72 hr after the first dose, followed by gradual return to normal. Rejections unresponsive to OKT3 (n = 3) showed no cytologic changes from the pretreatment mean creatinine increase of 13.2 +/- 2.7% (range 9-15%), and maximum change occurred 24 hr after the first dose. Rejections responsive to Solumedrol only (n = 4) showed gradual improvement of all parameters. Rejections treated with Solumedrol following failed OKT3 prophylaxis (n = 3) did not reverse and continued to show rejection associated cytologic changes and abnormal creatinines. Patients experiencing CsA toxicity (n = 12) showed mild creatinine elevations, normal or negative IL-2(P) and IL-2R(P) levels, and no IL-2(U). They showed distinctive cytologic changes consisting of swollen convoluted tubular cells with nuclear pyknosis and cytoplasmic vacuoles. Pretransplant IL-2(P) levels of patients who subsequently rejected were elevated, with 19/21 patients with preoperative IL-2 levels greater than 15 ng/ml having subsequent rejections. In contrast, pretransplant creatinine, urine cytology, and IL-2(U) levels showed no correlation to subsequent clinical course.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sequential determinations of urinary cytology and plasma and urinary lymphokines in the management of renal allograft recipients. 264 1

Renal tubular and glomerular function following ovine fetal urinary tract obstruction has been studied predominantly in anesthetized, exteriorized fetuses immediately after relief of obstruction. Since surgery and anesthesia may alter fetal cardiovascular and renal physiology, we developed a chronically catheterized, ovine model of unilateral fetal urinary tract obstruction to compare function of the unobstructed and obstructed kidneys repeatedly after relief of obstruction. Split renal function of the previously obstructed kidneys and unobstructed kidneys was measured serially in 7 fetal sheep after obstruction at 55 to 85 days per 147 days of gestation for 30 to 49 days. Seventy-five split clearances were determined on days 1, 2, 3 to 4 and 5 to 6 postoperatively. Not every fetus was studied each day. By 2-way ANOVA, renal function was stable on day 1 after surgery and did not change with time. Previously obstructed kidneys had lower creatinine clearance (0.16 versus 0.71 ml. per minute, p equals 0.0001), higher fractional sodium excretion (33.04 versus 6.02 per cent, p equals 0.0001) and higher urine sodium/creatinine ratio (4.80 versus 0.90 mEq. per mg., p equals 0.0001). Urine flow in the unobstructed kidneys did not differ significantly from that of the obstructed kidneys (0.122 versus 0.083 ml. per minute, p equals 0.35). Obstruction reduced kidney weight (4.7 versus 9.7 gm., p equals 0.0006), cortical thickness (-39 per cent) and nephrogenic zone (-59 per cent), and it increased collecting duct dilatation and medullary fibrosis. No cysts or dysplasia was noted. Fetal urinary tract obstruction for 39.7 days alters renal histology, glomerular function and tubular function. Renal function is stable by 1 day after catheterization and does not change from days 1 to 6 following relief of obstruction.
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PMID:Serial renal function in an ovine model of unilateral fetal urinary tract obstruction. 274 94

Na-K-ATPase activity was determined in seven nephron segments of five-week-old, spontaneously hypertensive rats (SHR) with or without continuous hydrochlorothiazide (HCTZ) treatment for seven days. For comparison, the effects of HCTZ treatment on Na-K-ATPase activity in the nephron segments of age-matched normotensive Wistar-Kyoto rats (WKY) were also determined. Na-K-ATPase activity in proximal convoluted tubule (PCT), medullary thick ascending limb (MTAL), cortical thick ascending limb (CTAL), distal convoluted tubule (DCT) and cortical collecting duct (CCD) was significantly lower in HCTZ-treated SHR compared to control (untreated) SHR. However, there was no significant difference in Na-K-ATPase activity in proximal straight tubule (PST) and medullary collecting duct (MCD) between HCTZ-treated and control SHR. HCTZ treatment also produced a significant decrease in blood pressure (BP) and creatinine clearance (CCr) in SHR. On the other hand, HCTZ treatment did not produce a significant change in Na-K-ATPase activity in PCT, PST, MTAL, CTAL and MCD, in BP or in CCr in WKY. However, HCTZ treatment produced a decrease in the enzyme activity in the DCT and an increase in the enzyme activity in the CCD in WKY. The decrease in Na-K-ATPase activity in almost all nephron segments from SHR may be due to a significant decrease in CCr produced by HCTZ. On the other hand, a decrease in Na-K-ATPase activity in the DCT with an increase in the enzyme activity in the CCD from WKY suggest that renal compensation to the natriuretic effect of HCTZ occurs by an increase in Na+ reabsorption in the CCD.
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PMID:Effects of hydrochlorothiazide on Na-K-ATPase activity along the rat nephron. 303 68

Circadian rhythms in the urinary excretion of eleven heavy metals and organic substances were examined under free, water-restrictive and water-loading conditions for 6 d (2 d for each of the three conditions) in twenty metal workers exposed to lead, zinc and copper. Circadian rhythms were found for all heavy metals and organic substances as well as for urinary flow (UF) rate, creatinine (Cn) and total urinary solutes (TUS). The Cn rhythm was significantly unparallel to the UF rhythm under the water-loading condition, indicating that the two rhythms were essentially different from each other. Circadian rhythms of the eleven urinary substances were then related to the Cn and UF rhythms, using profile analysis. The results indicated that the rhythms in the manganese, chromium, copper and beta-2-microglobulin excretion depend on the Cn rhythm, i.e. the rhythm of glomerular filtration; the rhythms in the hippuric acid, delta-aminolevulinic acid and TUS excretion are on the UF rhythm, i.e. the rhythm of reabsorption by the distal tubule and collecting duct. On the other hand, the rhythms in the lead, inorganic mercury, cadmium, zinc and coproporphyrin excretion were considered as reflecting complex renal excretory mechanisms.
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PMID:Circadian rhythms in the urinary excretion of heavy metals and organic substances in metal workers in relation to renal excretory mechanism: profile analysis. 335 May 98

Acetazolamide, furosemide, chlorothiazide, and amiloride are pharmacologic agents that act primarily in the proximal tubule, loop of Henle, early distal tubule and late distal tubule and collecting duct, respectively. In order to investigate the renal pathophysiology induced by amphotericin B, these diuretic agents were used as probes of discrete segments of the nephron in the neonatal rat. Six-day-old rats were treated with amphotericin B (20 mg/kg, sc) or the vehicle. Twenty-four hours later, when evidence of amphotericin B-induced renal pathophysiology is detectable, the responses to the diuretic agents were assessed in a 2-hr clearance test, during which creatinine clearance (CCr) and the fractional excretion (FE) of water and various components of the filtrate were determined. Amphotericin B induced alterations in basal function including azotemia, hypostenuria, increases FE water and electrolytes, and a decreased FE urea (although CCr was normal). The diuretic responses to furosemide, chlorothiazide, and amiloride were not altered, indicating that the functional viability of the respective tubular segments was not affected by amphotericin B treatment. Although the maximal response to acetazolamide also remained unchanged in amphotericin B-treated pups, there was an attenuation in the half-maximal response, reflecting an apparent shift in the sensitivity to acetazolamide. All of the diuretic agents elicited an increase in urea excretion in amphotericin B-treated pups such that FE urea approached control values. Additionally, the magnitude of this increase was proportional to the magnitude of the increase in water excretion induced by each diuretic agent. These results indicate a disruption of urea recycling in the nephron and support the hypothesis that amphotericin B acts to increase the permeability of the distal tubule to urea. Thus, results from this study demonstrate the usefulness of pharmacologic agents as functional probes in the characterization of specific components of renal pathophysiology.
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PMID:Pharmacologic probing of amphotericin B-induced renal dysfunction in the neonatal rat. 336 16

It has been hypothesized that urea from the final urine is recycled into the renal papilla through the pelvic epithelium. To test this hypothesis, samples of urine were collected by micropuncture proximally and distally through the intact, contracting ureter of the anesthetized rat. In 12 rats, in which urine flow was 5.89 +/- 0.67 microliter/min (a moderate antidiuresis), the ratio of proximal-to-distal urea concentration, corrected for water movement, was 0.93 +/- 0.03 (P less than 0.01 compared with unity), indicating that approximately 7% of urea in the urine emerging from the terminal collecting duct was reabsorbed by the time it reached the distal ureter. To assess the possible contribution of urea reabsorption by the ureter, the ureter was cannulated proximally and distally and perfused with urine of known composition at 6.26 +/- 0.10 microliter/min. In nine rats, the ratio of urea concentration in the perfusate collected from the distal end of the ureter to that in the perfusate entering the proximal end was 0.93 +/- 0.02 (P less than 0.01 compared with unity), indicating 7% reabsorption. Movement of solute across the ureteral epithelium was not restricted to urea. Potassium and creatinine were also reabsorbed [3.4 +/- 0.9 (P less than 0.01) and 3.5 +/- 1.2% (P less than 0.05), respectively], whereas sodium was secreted [9.2 +/- 2.3% (P less than 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urea flux in the ureter. 340 82


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