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

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

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

Using a microcatheterization technique, the contribution of the collecting duct to the renal response to extracellular fluid volume expansion was studied in anesthetized rats. During intravenous infusion of Ringer solution (0.25 ml/min per 100 g body wt), urinary excretion of fluid, sodium, and potassium was 365 mul/min per g kidney wt (V), 52.6 mueq/min per g kidney wt (UNaV), and 3.86 mueq/min per g kidney wt (UKV), representing 23, 24, and 65% of filtered load, respectively. Analysis of collecting duct fluid from cortex and outer medulla indicated continued net reabsorption of ions and water in these nephron segments; in contrast, in inner medulla net secretion of Na, K, and fluid into the collecting duct was demonstrated. Addition of sodium and water was equivalent to approximately 10% of filtered load. It is concluded that under the stress of extreme intravenous fluid loading tubular secretion of salt and water into the inner medullary collecting duct contributes importantly to diuresis and natriuresis. The mechanism of such secretion remains undetermined.
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PMID:Secretion of salt and water into the medullary collecting duct of Ringer-infused rats. 111 77

The influence of avian atrial natriuretic factor (ANF) on renal function was examined in conscious saltwater-acclimated Pekin ducks undergoing a steady state diuresis maintained by iv infused isotonic avian Krebs-Ringer solution at a rate of 1.0 ml/min. Synthetic chicken ANF (chANF) was applied iv at doses of 10, 50, and 90 ng/min.kg BW for 10 min and caused dose-dependent transient increases in urine flow, osmolal excretion, glomerular filtration rate, effective renal plasma flow, and fractional water clearance at decreased urinary osmolality. Using receptor autoradiography, binding sites for [125I]Bolton-Hunter-labeled chANF [( 125I]BH-chANF) were localized in both the reptilian-type glomeruli and the collecting duct system throughout the duck kidney. A RRA for [125I]BH-chANF, established using an enriched kidney membrane fraction, indicated that unlabeled chANF and human ANF competitively displaced [125I]BH-chANF with comparable potencies. ANF-induced modulation of renal salt and water elimination via glomerular and tubular receptor interactions is consistent with the concept that this hormone has a physiological role in avian volume homeostasis.
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PMID:Modulation of kidney function in conscious Pekin ducks by atrial natriuretic factor. 131 Feb 79

Sodium absorption in distal tubule segments was stimulated by increasing the distal delivery via infusion of hypertonic saline. In these animals, and in control rats, electrolyte concentrations in thick ascending limb cells, light and dark cells of the collecting duct in the outer and inner stripe of the outer medulla and in cells of the proximal straight tubule (outer stripe only) were studied. The measurements were performed by electron microprobe analysis of freeze-dried cryosections of the outer medulla. In addition, organic osmolytes (glycerophosphorylcholine, betaine and myo-inositol) were measured by high performance liquid chromatography in cortex and outer medulla. Augmented delivery of sodium chloride to the distal tubule was associated with increased sodium concentrations of thick ascending limb cells both in the outer and inner stripe and of medullary collecting duct light and dark cells in the outer stripe. While the sum of organic osmolyte concentrations was 28% higher in the outer medulla of the salt-loaded animals compared with controls, this value was unchanged in the renal cortex. These findings indicate that the primary event underlying stimulation of sodium absorption along the thick ascending limb during increased distal sodium delivery is enhanced entry of sodium across the apical cell membrane. This would be expected to lead to higher cell sodium concentrations and stimulation of basolateral active Na-K-exchange. The enhanced transport activity of outer medullary tubules may be associated with increased interstitial tonicities and intracellular retention of organic osmolytes.
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PMID:Effect of increased distal sodium delivery on organic osmolytes and cell electrolytes in the renal outer medulla. 148 81

We selectively focus on two growth factors, epidermal growth factor (EGF) and insulin-like growth factor (IGF), and discuss their roles on regulation of renal function and associated diseases conditions, as well. EGF, 6 kD polypeptide, is derived by proteolysis from a large precursor (prepro EGF, 133 kD). Prepro EGF is a membrane-anchored protein and its mRNA is predominantly localized to distal tubules of mouse and rat kidneys. We immunohistochemically demonstrated the glomerular distribution of EGF and EGF-receptor in normal and nephritic human kidneys. The physiologic roles of EGF produced in the kidney are various; it is mitogenic for tubular epithelial cell, inhibits gluconeogenesis and salt and water reabsorption in the tubules, and effects on glomerular hemodynamics. Alteration of renal EGF expression is suggested in renal ischemic injury, renal hypertrophy and cystic renal disease. IGF-I, somatomedin-C, is produced in collecting duct, and glomerular cells, and exerts a variety of actions on kidney. IGF-I stimulates gluconeogenesis in renal tubules, and is mitogenic for mesangial cells. The administration of this growth factor increases glomerular filtration rate. Enhanced expression of renal IGF-I was observed in the uninephrectomized animals.
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PMID:[Growth factors: a regulator of renal function]. 149 47

Two populations of intercalated cells, type A and type B, are present in the rat cortical collecting duct (CCD). Type A cells are involved in proton secretion and contain an apical H(+)-adenosinetriphosphatase (ATPase) and a basolateral Cl(-)-HCO3- exchanger. Type B cells are believed to be involved in HCO3- secretion, which is mediated by a Cl(-)-HCO3- exchange process and is Cl- dependent. The aim of this study was to examine the morphological and immunocytochemical response of type B intercalated cells in the rat to increased delivery of Cl- to the CCD. This was accomplished by chronic infusion of a loop diuretic, bumetanide (30 mg.kg body wt-1.day-1), via an osmotic minipump, and simultaneous administration of 0.9% sodium chloride in the drinking water for 6 days. The kidneys were preserved by in vivo perfusion with a periodate-lysine-paraformaldehyde fixative and processed for horseradish peroxidase and protein A gold immunocytochemistry, using rabbit polyclonal antibodies against carbonic anhydrase II, proton ATPase, and band 3 protein. Chronic infusion of bumetanide in combination with a high salt intake was associated with significant changes in the intercalated cells. Type B cells were increased in size and exhibited numerous apical microvilli, increased basolateral membrane area, and marked cytoplasmic and basolateral labeling for H(+)-ATPase. In contrast, type A cells were small and had sparse apical microprojections. H(+)-ATPase immunolabeling was observed primarily over apical tubulovesicles, and there was decreased basolateral immunolabeling for band 3 protein and occasional labeling for band 3 in lysosome-like structures. These observations support the hypothesis that increased delivery of Cl- to the CCD is associated with stimulation of type B intercalated cells to secrete HCO3-. The observations in type A cells are consistent with the cells being in a resting or inactivated state.
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PMID:Immunocytochemical response of type A and type B intercalated cells to increased sodium chloride delivery. 153 33

In the following, factors will be discussed which regulate the ionic conductances of the luminal membrane of principal cells of the cortical collecting duct. Transport of sodium and potassium, which is mediated via selective sodium- and potassium-channels, is chronically or acutely adjusted to the needs of the salt balance by the hormones aldosterone and adiuretin. In addition, the potassium conductance and thus potassium secretion can be modified by the cellular pH, which results in a direct and reciprocal coupling between potassium and proton excretion in the cortical collecting duct.
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PMID:[Regulation of ion conductance in the cortical collecting duct]. 166 49

ANP stimulates a profound natriuresis and diuresis by a series of concerted actions along the nephron, including stimulation of glomerular filtration and inhibition of net salt and water reabsorption in the cortical and inner medullary collecting ducts. Several actions of ANP contribute to its natriuretic and diuretic effects in the collecting duct. These include reductions in aldosterone secretion, increases in hydrostatic pressures opposing Na+ reabsorption, possible stimulation of medullary washout, and direct inhibition of salt and water transport. In both CCD and IMCD, ANP antagonizes the hydroosmotic actions of vasopressin, which leads to diuresis. The mechanisms by which ANP inhibits response to vasopressin remain unclear, although in IMCD, cGMP can duplicate the response to ANP. In CCD, ANP can inhibit Na+ reabsorption via cGMP; the transport pathway regulated by ANP is unknown. In IMCD, ANP acting via cGMP inhibits a conductive Na+ or cation channel, which appears to be on the luminal membrane.
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PMID:Renal actions of atrial natriuretic peptide: regulation of collecting duct sodium and water transport. 213 59

Unilateral ureteral obstruction results in marked changes in renal function throughout the nephron, including impaired acid and potassium secretion and salt wastage. The nephron site believed responsible for the acidification defect is the collecting duct. It has been presumed, although not demonstrated, that the cellular mechanism for the acidification defect is both a decrease in transepithelial voltage and a decrease in activity of the proton pump located at the luminal membrane. The mechanism for the abnormalities in sodium handling are thought due to alterations in Na-K ATPase activity. Our laboratory has recently mapped the profile of the N-ethylmaleimide (NEM)-sensitive ATPase and Na-K ATPase in microdissected rat nephron, documenting their presence throughout much of the nephron. In animals with acute unilateral ureteral obstruction for 18 to 24 hours, we measured NEM-sensitive ATPase and Na-K ATPase activities in several nephron sites. In all nephron segments Na-K ATPase activity was markedly decreased. In the medullary collecting duct, NEM-sensitive ATPase activity was also markedly reduced in animals with acute ureteral obstruction; in the cortical collecting duct, activity fell significantly, but to a lesser degree than was observed in the medullary collecting duct. NEM-sensitive ATPase activity was unchanged from control in the proximal convoluted tubule and in the medullary thick ascending limb; in the cortical thick ascending limb enzyme activity increased. These results demonstrate a change in both Na-K ATPase and NEM-sensitive ATPase activities as a direct consequence of a defect known to result in salt wastage and an acidification defect in humans and animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enzyme activity in obstructive uropathy: basis for salt wastage and the acidification defect. 215 50


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