UNIPROT:P41181 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

Query: UNIPROT:P41181 (collecting duct)
5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The alligator excretes a persistently alkaline urine despite consuming an acid-residue diet. The amount of bicarbonate excreted is greater than the amount filtered, evidencing tubular secretion of bicarbonate. The parallel urinary excretion of ammonium maintains external acid balance. To investigate putative renal mechanisms responsible for the concurrent excretion of large quantities of ammonium bicarbonate, we used acridine orange fluorescence methodology in microvesicles prepared from the proximal tubule brush border to assess the activity of the Na+-H+ antiporter, and histochemical methods (cobalt sulfide precipitation) to assess carbonic anhydrase localization. We found no evidence for the presence of a functioning Na+-H+ antiporter, the protein known to be responsible for the majority of bicarbonate reabsorption in mammals; Na+-H+ exchange in vesicles from the alligator kidney failed to exhibit saturation kinetics, showed no affinity for lithium, and was not inhibited by amiloride. Sensitive histochemical techniques failed to reveal carbonic anhydrase activity anywhere in the proximal tubule but detected an abundance of enzyme activity in the basolateral membranes and nuclei of distal tubular cells. In the connecting segment and collecting duct, cells without carbonic anhydrase alternated with cells containing carbonic anhydrase; in the latter, the enzyme was localized to the basolateral and luminal membranes, the nucleus and, to a lesser extent, throughout the cytoplasm. We conclude that the proximal tubule of the alligator kidney is devoid of the machinery necessary for the transport of large amounts of bicarbonate. The principal site at which bicarbonate is added to the final urine appears to be the distal tubule, at which site carbonic anhydrase is widespread.
...
PMID:Transport and histochemical studies of bicarbonate handling by the alligator kidney. 253 23

To evaluate the role of increased thick ascending limb Na+-K+-ATPase activity in rats undergoing hypertonic salt loading, the following groups of rats were studied: 1) control rats, 2) rats receiving an oral hypertonic Na load for 7 days, and 3) rats receiving the same oral Na load as in group 2 plus a daily injection of 10 mg/100 g of furosemide ip for 7 days. Salt loading (group 2) was associated with increased glomerular filtration rate (GFR) and hence an increased filtered load of sodium. Plasma aldosterone levels were markedly decreased. Na+-K+-ATPase was unchanged in the proximal tubule [convoluted (PC) and straight (PS)], increased in the thick ascending limb of Henle's loop [outer medullary (OMTAL) and cortical (CTAL)] and decreased in the distal nephron [distal convoluted tubule (DCT) and cortical collecting duct (CCD)]. The renal corticomedullary gradient of solutes was markedly increased in the salt-loaded group. Salt loading plus furosemide for 7 days (group 3) was associated with severe dehydration and hypernatremia. GFR as well as plasma aldosterone levels were unchanged compared with control. Na+-K+-ATPase was significantly increased in the proximal tubule (PC and PS), markedly decreased in the thick ascending limb of Henle's loop (OMTAL and CTAL), increased in the DCT and unchanged in the CCD. The increase in the corticomedullary gradient caused by salt loading per se was abolished by treatment of salt-loaded rats with furosemide. These results indicate that treatment with furosemide prevents the preservation of water balance and of normal body fluid tonicity in rats undergoing hypertonic Na loading.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Inhibition of thick ascending limb Na+-K+-ATPase activity in salt-loaded rats by furosemide. 253 44

Endothelin, a potent vasoconstrictor released by vascular endothelial cells, can induce natriuresis in vivo. These studies examined the regulation of Na+ transport by endothelin in suspensions of rabbit proximal tubule (PT) and inner medullary collecting duct (IMCD) cells. Endothelin reduced oxygen consumption (QO2) by 18 +/- 1% in IMCD cells but did not alter QO2 in PT cells. In IMCD cells, endothelin inhibited QO2 half maximally at approximately 5 x 10(-12) M. Several lines of evidence indicate that endothelin reduces QO2 by inhibiting the Na(+)-K(+)-ATPase. 1) Endothelin gave no further inhibition of QO2 after ouabain and blunted the stimulatory effect of amphotericin B on QO2 (+29 +/- 4% in absence of endothelin, 0 +/- 5% in presence of endothelin; n = 6 preparations, P less than 0.001). 2) Endothelin inhibited ouabain-sensitive 86Rb+ uptake by 46.6 +/- 8.6% at 10 s and by 35.4 +/- 5.3% at 30 s without altering uptake at 60 min. 3) Addition of endothelin to IMCD cells induced a net K+ efflux with an initial rate of 32.2 +/- 4.8 nmol.min-1.mg protein-1, consistent with inhibition of the Na(+)-K(+)-ATPase. In contrast to the response observed in intact cells, in permeabilized IMCD cells endothelin did not inhibit ouabain-sensitive ATPase. Several observations indicated that prostaglandin E2 (PGE2) mediates endothelin inhibition of Na(+)-K(+)-ATPase activity. 1) The response to endothelin was blocked by ibuprofen in assays of QO2, net K+ flux, and 86Rb+ uptake. 2) Endothelin and PGE2 gave equivalent, nonadditive inhibition of ouabain-sensitive 86Rb+ uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Endothelin, a peptide inhibitor of Na(+)-K(+)-ATPase in intact renaltubular epithelial cells. 255 68

In the present study we have examined ten cases of the chromophobe type renal cell carcinoma. This type of tumor is distinguished from the other carcinomas of the kidney with light cytoplasm (formerly called "hypernephroid") by (a) a positive Hale's iron colloid stain of the cytoplasm, (b) the occurrence of numerous invaginated vesicles within the cytoplasm that resemble the invaginated vesicles of intercalated cells of the collecting duct system, and (c) a positive immunoreaction of both the plasma membrane and the cytoplasm with antibodies to the epithelial membrane antigen (EMA) and carbonic anhydrase C (CAC), respectively. Unlike oncocytomas, which also express CAC and EMA, the chromophobe renal cell carcinoma does not express the erythrocyte anion exchanger band 3. These findings strongly indicate that chromophobe renal cell carcinomas as well as oncocytomas of the kidney are histogenetically related to the two populations of intercalated cells of the collecting duct system. Thus, both tumors represent examples of renal tumors which disprove the broadly accepted hypothesis that all epithelial tumors of the kidney are histogenetically related to the proximal tubule.
...
PMID:The human chromophobe cell renal carcinoma: its probable relation to intercalated cells of the collecting duct. 256 18

The present study quantitated the effects of extracellular volume expansion on sodium and water excretion in 118 anesthetized dogs. The animals received a priming injection of 10 ml kg-1 Ringer solution i.v. which was followed by a constant Ringer solution infusion at a rate of 0.25 ml.min-1.kg-1 until the end of the experiment. Fifteen minutes after the start of the constant infusion the renal parameters were examined in 11 subsequent 15 min periods (the total time was 3 hours). Volume expansion produced no significant change in arterial blood pressure, glomerular filtration rate (GFR), plasma sodium and potassium concentration or, haematocrit, but did reduce the CPAH from 284 ml.min-1 to 218 ml.min-1 (the data were calculated for 100 gram wet kidney weight). There were constant significant increases in the urinary excretion rate from 0.84 ml.min-1 to 4.06 ml.min-1 and the 39% of the infused water was excreted during the experiment. Volume expansion also caused a significant increase in sodium excretion during the three first periods from 120 mumol.min-1 to 329 mumol.min-1 followed by a small but significant decrease. The sodium excretion at the end of the experiment was 221 mumol.min-1 and the 23% of the infused sodium was excreted in the course of the experiment. The increase of the water excretion during the volume expansion was associated with fall of the urine osmolality and the urine because hypoosmotic as compared to the plasma. We have provided evidence that vasopressin was not involved in the control of water excretion in our experiments. It is concluded that neither filtered sodium nor decreased aldosterone secretion can account for the increase in sodium excretion that occurs after Ringer solution loading in the dog. It has been proposed that a decrease in plasma protein concentration may decrease passive sodium reabsorption due to oncotic forces in the proximal tubule. The Ringer solution diuresis elicits a rise in medullary blood flow, thereby causing a washout of medullary sodium. This might dissipate the osmotic force for the back-diffusion of water from the collecting duct. Our studies indicate that the response of the diluting segments of the distal nephron to increased delivery of sodium depends upon the presence or absence of volume expansion. However the increase of the distal tubular loading activates the tubuloglomerular feedback which increases the proximal tubular reabsorption. Based on these assumptions our studies provide further evidence that the tubuloglomerular feedback regulates the blood pressure in the peritubular capillaries in the cortex around the proximal tubules.
...
PMID:The effect of Ringer solution induced extracellular volume expansion on kidney function. 260 31

Growth hormone (GH) exerts a variety of metabolic and anabolic effects on skeletal and soft tissues including kidney. Some of these actions are mediated directly, whereas others result from GH-dependent synthesis and release of polypeptide growth factors designated insulin-like growth factors (IGFs). Receptors for GH are present in proximal tubule and GH directly stimulates gluconeogenesis at this site. IGF receptors are found in glomerulus and proximal tubule. Mechanisms for signal transduction by GH and IGFs have been characterized using proximal tubular basolateral membranes. IGFs regulate metabolic and transport processes in cultured glomerular mesangial cells and in isolated proximal tubular cells. IGF I is synthesized in cultured mesangial cells and is produced in a GH-dependent manner in cortical and medullary collecting duct. Evidence has accumulated that IGF I of renal origin functions as a paracrine growth factor in the settings of GH-induced hypertrophy and compensatory hypertrophy of the kidney, and in the setting of proximal tubular regeneration following ischemic injury. IGFs are embryonal mitogens and IGF II may act as a transforming agent for Wilms' tumor. Further characterization of the GH-IGF axis in kidney will provide additional insights into the roles of these peptides as regulators of renal function, growth, and development.
...
PMID:The growth hormone-insulin-like growth factor axis in kidney. 267 42

PGE2 synthesis was measured along the nephron of Brattleboro (DI) rats, lacking ADH, and control LE rats, using an enzyme immunoassay. Experiments were performed in vitro, in the absence of exogenous arachidonic acid, using microdissected tubular segments. The effect of a chronic treatment of dDAVP was tested on three ADH sensitive tubular segments, medullary thick ascending limb (MTAL), medullary collecting tubule (OMCD) and papillary collecting duct (IMCD). No difference in PGE2 synthesis was present between LE and DI in glomerulus and tubular segments up to OMCD. In both strains, values were low in the proximal tubule and the loop of Henle, and gradually increased along the collecting tubule. In IMCD, PGE2 synthesis was much higher in DI (12.8 +/- 2.0 pg per 30 min per mm tubular length) than in LE (3.8 +/- 0.5, LE vs. DI p less than 0.001). In MTAL and OMCD, dDAVP treatment did not affect PGE2 synthesis. In IMCD, dDAVP reduced PGE2 synthesis to values (5.3 +/- 0.8 pg per 30 min per mm tubular length), which were not significantly different from those of LE. Neither oxytocin, which has been shown to be elevated in DI rats, nor furosemide, that reduced papillary osmolarity to values comparable to those of DI rats, were able to increase PGE2 synthesis in IMCD of LE rats. The mechanism of the increase in PGE2 synthesis in IMCD of DI rats, and of the inhibitory effect of dDAVP is yet unknown; it may participate to compensate for the lack of ADH in the Brattleboro rat.
...
PMID:Antidiuretic hormone reduces the high PGE2 synthesis in papillary collecting duct of DI rats. 279 42

1. Lithium clearance measurements were made in 72 patients with chronic nephropathy of different aetiology and moderate to severely reduced renal function. 2. Lithium clearance was strictly correlated with glomerular filtration rate, and there was no suggestion of distal tubular reabsorption of lithium or influence of osmotic diuresis. 3. Fractional reabsorption of lithium was reduced in most patients with glomerular filtration rates below 25 ml/min. 4. Calculated fractional distal reabsorption of sodium was reduced in most patients with glomerular filtration rates below 50 ml/min. 5. Lithium clearance data were independent of whether renal disease was of primarily glomerular or tubular origin and, further, were not influenced by long-term conventional antihypertensive treatment. 6. It is concluded that, even with a reduced kidney function, the data are compatible with the suggestion that lithium clearance may be a measure of the delivery of sodium and water from the renal proximal tubule. With this assumption it was found that adjustment of the sodium excretion in chronic nephropathy initially takes place in the distal parts of the nephron (loop of Henle, distal tubule and collecting duct). With more severe impairment the proximal tubule also becomes involved in the adjustment.
...
PMID:Lithium clearance in chronic nephropathy. 280 95

Renal kallikrein is synthetized in the distal nephron and secreted in urine. Studies on the microdissected nephron and on the whole kidney using immunohistochemistry indicate that kallikrein is produced at the level of the distal part of the distal tubule and in some species in the cells of the initial part of the collecting duct. Urinary kinins are formed at these same sites. The renal tubule contains high levels of kininases, able to inactivate kinins, but the kininases are located mainly up-stream the sites of kinin production, i.e. in the glomerulus and in the proximal tubule. A kininase activity is however also found in the medullary collecting duct. This collecting duct kininase activity might contribute to the control of kinin levels in kidney and urine. The physiological role of the renal kallikrein kinin system is not completely understood. There is some evidence for a role of urinary kinins in water and solute transferrence in the distal nephron. Also kinin production in the renal interstitium and/or circulation may contribute to the control of renal blood flow. In the isolated perfused rat kidney vasoconstricted by angiotensin II for example, the high molecular weight kininogen is hydrolyzed to release kinins and induces a vasodilatation. The kallikrein-kinin system therefore might play a role in kidney function by antagonizing the vascular effect of angiotensin II in the renal circulation and the maintenance renal blood flow.
...
PMID:[Kallikrein-kinin system, the kidney and arterial pressure]. 283 86

The distribution of vacuolar H+ATPase in rat kidney was examined by immunocytochemistry using affinity-purified antibodies against the 31-, 56-, and 70-kD subunits of the bovine kidney proton pump. Proximal convoluted tubules were labeled over apical plasma membrane invaginations, and in the initial part of the thin descending limb, apical and basolateral plasma membranes were moderately stained. Thick ascending limbs and distal convoluted tubules were apically stained although the intensity was greater in the distal convoluted tubule. Collecting duct principal cells were virtually unlabeled, but intercalated cells had intense staining with an apical, basolateral or diffuse pattern in the cortex, and exclusively apical staining in the medulla. These results (a) show the presence of an H+ATPase in the apical plasma membrane of the proximal tubule that may contribute to H+ transport in this segment; (b) provide direct evidence that the intercalated cell contains most of the H+ATPase detectable in the collecting duct, supporting its proposed role in H+ transport; (c) demonstrate that subpopulations of cortical intercalated cells have opposite polarities of an H+ATPase, consistent with the presence of both proton- and bicarbonate-secreting cells; and (d) suggest a role for the H+ATPase in acid/base regulation or H+ transport in segments other than the collecting duct and the proximal tubule.
...
PMID:Localization of a proton-pumping ATPase in rat kidney. 290 51

<< Previous 1 2 3 4 5 6 7 8 9 10