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)

Lithium carbonate, useful in the treatment of manic-depressive disorders, can produce nephrogenic diabetes insipidus. The drug, therefore, has been used to facilitate renal waster excretion when severe hyponatremia occurs in the syndrome of inappropriate antidiuretic hormone secretion. Symptomatic dilutional hyponatremia developed in a patient with pulmonary carcinoma whom we treated. Lithium carbonate was administered and renal sodium wasting, hypovolemia, and hypotension occurred. Hyperkalemia was also observed, and since adrenal steroid levels were not decreased, impairment of distal tubular function was suggested. Lithium carbonate blocks antidiuretic hormone effect by decreasing collecting duct cyclic adenosine monophosphate generation. These observations suggest that more generalized inhibitory effects on renal tubular function may also result from its use. An alternative drug, demeclocycline, may be preferable.
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PMID:Severe sodium depletion syndrome during lithium carbonate therapy. 93 81

Medullary collecting duct function was studied by direct microcatheterization techniques in rats undergoing postobstructive diuresis. Significant net addition of water and sodium to the duct was demonstrated during postobstructive diuresis after relief of 24-h bilateral ureteral ligation. This striking abnormality in function was associated with reduced delivery of sodium and water to the collecting duct compared to sham-operated controls. To examine the role of circulating factors in this phenomenon, another group of rats was studied that underwent 24 h of total urine reinfusion into the femoral vein. Natriuresis and diuresis were similar to the postobstructive group, but absolute collecting duct reabsorption of sodium and water was normal. The natriuresis and diuresis in rats with urine reinfusion resulted from increased delivery of fluid and sodium to the medullary collecting duct. A third group of rats was studied with 24-h unilateral ureteral ligation as well as urine reinfusion from the contralateral normal kidney. Without urine reinfusion there was no diuresis-natriuresis but with urine reinfusion the diuresis and natriuresis after relief of unilateral obstruction was similar to that after relief of bilateral obstruction. Moreover, net addition of sodium and no significant water reabsorption were demonstrated in the medullary collecting duct of such animals. The results indicate that (a) the medullary collecting duct is the critical nephron segment affected by ureteral obstruction, since postobstructive diuresis occurred despite reduced delivery of fluid from the more proximal nephron; (b) the net addition of sodium to the medullary collecting duct observed during postobstructive diuresis is probably a direct effect of obstruction, since it was found during postobstructive diuresis after relief of bilateral or unilateral ureteral ligation, but not with urine reinfusion alone; and (c) blood-borne factors are important in the development of postobstructive natriuresis and diuresis, and probably act by increasing the fraction of filtered sodium and water delivered from the proximal and distal tubule to the collecting duct.
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PMID:The role of the medullary collecting ducts in postobstructive diuresis. 93 94

The microcatheterization technique was used to study reabsorption of fluid, sodium, and potassium in the medullary collecting duct in chronically deoxycorticosterone acetate (DOCA)-treated and salt-loaded rats, as well as in normal and chronically salt-deprived (NaD) rats, before and after infusion of donor blood (33% of estimated circulating volume). Before expansion, urinary sodium excretion was highest in DOCA rats, intermediate in normal, and lowest in low salt rats. Significant collecting duct reabsorption was found in NaD, normal, and DOCA groups. In contrast to sodium, no net transport of potassium was found in any series. During intravascular expansion, increased renal excretion of fluid and sodium was observed uniformly in both DOCA and normal groups, whereas a diuretic response was found in five of seven rats, and a natriuretic response in four of seven rats of the NaD group. Natriuresis of DOCA rats was significantly greater than that of either normal or responding NaD rats. Diuresis and natriuresis in all three series were assocaited with complete inhibition of fluid and sodium reabsorption from the lumen of the medullary collecting duct, whereas such reabsorption persisted in nonresponding low salt rats. Increased sodium excretion in DOCA rats in comparison to the other two series could be explained by enhanced intratubular delivery of the ion to the medullary collecting system. I conclude that the renal response to acute blood volume expansion is due primarily to complete inhibition of both fluid and sodium reabsorption in the medullary collecting duct, but that differences in tubular delivery may modify the resulting diuresis and natriuresis.
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PMID:Collecting duct function in deoxycorticosterone acetate-escaped, normal, and salt-deprived rats. Response to hypervolemia. 93 14

The effects of furosemide were studied on isolated dog kidneys in the absence and in the presence of vasopressin. In the latter condition, furosemide did not modify renal blood flow and glomerular filtration rate while both parameters were decreased by the drug in the absence of vasopressin, as they were also reduced by vasopressin alone. This would indicate direct vasoactive effects of furosemide, depending on the previous tone of the vasculature. In the absence of vasopressin, furosemide decreased free water clearance through inhibition of sodium reabsorption in the ascending limb of Henle's loop. On the other hand, in the presence of vasopressin, furosemide increased free water clearance, presumably through reduction of water reabsorption in the collecting duct by enhanced distal tubular flux.
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PMID:Interactions between furosemide and vasopressin on hemodynamics and on water excretion by the isolated dog kidney. 94 35

The effects of acute hypercalcemia on hemodynamics and on water and sodium excretion were studied on the blood-perfused isolated dog kidney. This model advantageously eliminates various factors which modify medullary osmolality and intrarenal hemodynamics, as well as collecting duct permeability. Calcium ion directly inhibits sodium reabsorption in the proximal tubule and in the ascending limb of Henle's loop, leading to increased sodium excretion rate and to decreased free water generation. The vasoconstrictive action of calcium, leading to decreased glomerular filtration rate, may mitigate the strong natriuretic effect of this ion.
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PMID:Effects of hypercalcemia on water and sodium excretion by the isolated dog kidney. 94 13

A gel filtration fraction of urine from patients with chronic renal disease (natriuretic factor) has been shown previously to cause natriuresis in rats and to inhibit sodium transport in the isolated toad bladder. The effect of this fraction on transtubular potential difference and sodium transport was examined on the isolated perfused cortical collecting tubule of the rabbit. A rapid inhibition of potential difference from -22.5 mV to -12 mV (P less than 0.001) was observed when the fraction was applied to the peritubular surface. This effect was accompanied by a decrease in net sodium flux from 6.29 to 3.21 pmol/cm per s (P less than 0.001). Unidirectional fluxes using isotopic sodium revealed that the inhibition of net sodium transport was due to a decrease in flux from the lumen to the peritubular surface, i.e., an inhibition of active sodium transport. There was no change in sodium flux in the reverse direction. These changes were all rapidly reversed by removal of the fraction from the peritubular surface. The addition of the fraction to the lumen had no effect on potential difference or net sodium flux. Control studies using the same fraction from the urine of normal subjects had no effect on any of the parameters studies. Where both a uremic and a normal fraction were sequentially applied to the peritubular surface of the same tubule, inhibition of potential difference was obtained only with the former. In the light of evidence implicating the collecting duct fraction from normal animals, the data are consistent with the view that the natriuretic factor may be biologically important in the regulation of sodium balance via it's regulatory role in active sodium transport in the collecting tubule.
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PMID:On the influence of the natriuretic factor from patients with chronic uremia on the bioelectric properties and sodium transport of the isolated mammalian collecting tubule. 95 87

It has been suggested that collecting duct sodium transport was inhibited by extracellular volume expansion. To directly evaluate this possibility, micropuncture of the papillary collecting duct of young rats was performed during hydropenia and Ringer loading. The possibility of heterogeneity of nephron function was evaluated during Ringer and hyperoncotic albumin loading by comparing the delivery of sodium to the end of the distal tubule of superficial nephrons with papillary base delivery. During hydropenia (n = 14), sodium delivery to the base averaged 0.95% of the filtered sodium load and reabsorption along the collecting duct was noted from base to tip in each collection pair averaging 0.80% of the filtered load. During Ringer loading, sodium delivery to the base was markedly greater than in hydropenia, 11.8 vs. 0.95% of the filtered load (P less than 0.001). Yet, sodium reabsorption was also much greater, 6 vs. 0.8% (P less than 0.001). In 13 paired collections, during Ringer loading, sodium delivery to the papillary base, 12.2% of the filtered load, was consistently greater than late distal tubular delivery from superficial nephrons. 8% (P less than 0.005). In contrast, reabsorption of sodium from late distal tubule to papillary base was found during albumin infusion, 6.2 vs. 3.1% (P less than 0.001). Therefore, these studies demonstrate that: (a) the delivery of sodium to and reabsorption along the papillary collecting duct were markedly greater during Ringer loading than in hydropenia; (b) the amount of sodium delivered to the papillary base was greater than the delivery to the end of the distal tubule of superficial nephrons during Ringer loading, suggesting that deeper nephrons deliver more sodium to the collecting duct in this setting; and (c) the difference in sodium excretion between Ringer loading and hyperoncotic albumin infusion is due to events occurring between the late distal tubule of superficial nephrons and the base of the papillary collecting duct.
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PMID:Direct measurement of papillary collecting duct sodium transport in the rat. Evidence for heterogeneity of nephron function during Ringer loading. 96 83

After the adrenal glands are removed without their capsules, so-called adrenal enucleation, rats initially retain sodium, and, after adrenal regeneration, escape from salt retention. To define the renal mechanisms involved in this alteration in salt handling, we have utilized clearance and micropuncture techniques in three groups of saline-expanded rats that were sham-operated (S), enucleated (AE), or escaped after adrenal regeneration (E.) Sodium excretion was clearly blunted after AE, 5.5 mueq/min vs. 20.5 for S and 18.7 for E. Although glomerular filtration rate (GFR) and filtered load of sodium were lower in AE rats, the delivered load of sodium beyond the late distal tubule was not different among the groups: 0.30 neq/min for AE, 0.42 for S, and 0.40 for E. This was a consequence of strikingly greater sodium reabsorption in the loop of Henle and distal tubule in both the S and E rats. In the collecting duct over 50% of the delivered sodium was reabsorbed by the AE rats while over 30% of the excreted sodium was added in this tubular segment in the other groups. These data demonstrate that the impaired natriuresis after adrenal enucleation appears to be due to striking differences in collecting duct function. Since adrenal regeneration in the escape animals reverses this sodium retention, the effect is probably related to some alteration in adrenal hormone production. Sodium excretion in markedly expanded normal rats also appears to be determined by the net addition of sodium in the collecting duct.
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PMID:Effect of adrenal enucleation on sodium excretion in the rat. 99 85

This review focuses on the segmental handling of sodium during alterations in extracellular fluid volume. There is abundant evidence that proximal tubular sodium reabsorption is inhibited by Ringer loading but there are also unequivocal data demonstrating that inhibition of a more distal nephron segment is required for a maximal natriuretic response. From the evidence at hand presently, it would seem that, of the distal nephron segments, only the collecting duct is inhibited by expansion of the extracellular volume per se.
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PMID:Effect of alterations in extracellular fluid volume on segmental sodium transport. 108 91

A large body of evidence has accumulated which demonstrates that sodium transport in some distal nephron segment is altered in response to changes in extracellular fluid volume. Sodium reabsorption in the loop of Henle and distal tubule is directly related to delivery rate and is not inhibited by volume expansion. In contrast, recent studies have shown that Ringer loading causes a greater natriuretic response than hyperoncotic albumin because of diminished collecting duct sodium transport in the former model. Additional studies in animals with different basal extracellular fluid volumes and in DOCA-escape rats indicate further that the collecting duct is an important regulator of sodium balance. Although the factors that modulate sodium transport in the collecting duct are not clear, it is postulated that the local release of prostaglandins may be of major importance.
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PMID:Role of the collecting duct in the regulation of sodium balance. 109 51


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