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

Recent studies suggest the presence of two populations of intercalated cells in the rabbit cortical collecting duct (CCD), one involved with hydrogen ion secretion and another that may play a role in bicarbonate secretion. The purpose of this study was to determine whether two populations of intercalated cells are present in the rat CCD and to establish their response to acute respiratory acidosis. Rats were studied during normal acid-base conditions and after 4-5 h of respiratory acidosis. In all animals light microscopy and transmission and scanning electron microscopy revealed two configurations of intercalated cells, type A with an extensive apical tubulovesicular membrane compartment and prominent surface microprojections and type B with a well-developed vesicular compartment and short sparse surface microprojections. By transmission electron microscopy, studs were present on the cytoplasmic face of the apical plasmalemma and tubulovesicular profiles of A cells. In respiratory acidosis there was a striking increase in apical microprojections and in the surface density of the apical membrane of type A cells similar to the response observed previously in intercalated cells in the outer medullary collecting duct (OMCD) studied under the same physiological conditions. No changes were observed in type B cells. Scanning electron microscopy revealed no change in the relative number of type A and type B cells in respiratory acidosis. We conclude that two distinct populations of intercalated cells exist in the rat CCD: type A, which resembles the intercalated cells in the OMCD, and type B. The response of type A cells to acute respiratory acidosis and the similarity between these cells and intercalated cells in the OMCD, which are believed to secrete hydrogen ion, suggest that the type A cells are involved in hydrogen ion secretion in the CCD.
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PMID:Effect of acute respiratory acidosis on two populations of intercalated cells in rat cortical collecting duct. 342 24

There is increasing evidence of acidification along the entire mammalian collecting duct including the inner medullary collecting duct (IMCD). Recent studies have provided morphologic evidence that the intercalated cells are involved in hydrogen ion secretion in the cortical and outer medullary collecting duct of the rat. In the present study we performed a quantitative and qualitative morphologic examination of the intercalated cells in the IMCD of the rat and compared the results to observations obtained from intercalated cells in the collecting duct in the inner stripe of the outer medulla (OMCDi). Kidneys of male rats were preserved by in vivo perfusion with glutaraldehyde and processed for morphologic evaluation. With light microscopy and scanning electron microscopy intercalated cells were found in the outer third of the IMCD (IMCD1) and accounted for 10% of the total cell population. They were absent in the terminal two-thirds of the IMCD. Examination of the intercalated cells using transmission electron microscopy revealed striking similarities between the cells of the IMCD1 and those in the OMCDi. In addition, no differences were found in the surface densities of the apical or basolateral plasma membranes or the volume densities of the mitochondria of the intercalated cells in the two regions. In light of the morphologic similarity with the intercalated cells of the OMCDi that are believed to be involved in hydrogen ion secretion, it is likely that the intercalated cells of the IMCD1 are also involved in the acidification of tubular fluid.
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PMID:Intercalated cells of the rat inner medullary collecting duct. 359 48

Enhanced renal acidification during chronic hypercapnia (CH) results in transient augmentation in net acid excretion (NAE) (adaptation phase) and persistent acceleration in renal bicarbonate reclamation (adaptation and steady-state phases). The mechanisms responsible for the return of NAE to control values despite persistent acidemia during the steady state phase of CH remain undefined. In addition, it remains unsettled whether the enhancement of renal ammoniagenesis known to occur during the adaptation phase of CH persists during the steady-state phase. Furthermore it is uncertain if the alteration in whole-kidney acidification observed in CH originates from augmentation in the acidification of both proximal and distal nephronal segments. To shed further light on these issues, observations on the profile of the urine acid-base moieties during the adaptive and steady-state phases of CH were carried out in dogs chronically exposed to hypercapnia (10% FiCO2) in an environmental chamber (13 days). Additionally, collecting duct hydrogen ion secretion (CDH+S) was evaluated by employing the U-B PCO2 in alkaline urine in intact unanesthetized dogs with either CH (10% FiCO2) or eucapnia. The balance studies demonstrated that NAE increased in early hypercapnia (4.84 meq/kg body weight, control 3.27 meq/kg body weight, p less than 0.05) and returned to baseline thereafter; by contrast, urine NH+4 which was augmented during the adaptation phase (3.71 meq/kg body weight, control 1.97 meq/kg body weight, p less than 0.05) remained elevated throughout (3.25 meq/kg body weight).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal acidification during chronic hypercapnia in the conscious dog. 371 50

Ammonium is the most important component of renal acid excretion. A reduced rate of ammonium excretion is the common feature of the group of diseases called distal renal tubular acidosis. We have presented an alternative approach to patients with distal acidification defects based upon the pathophysiology of these disorders. Accordingly, the purpose of this review is to describe a revised classification based on our current understanding of collecting duct hydrogen ion secretion and ammonium addition to the lumen of the distal nephron. We have subdivided these defects into four groups: disorders of the collecting duct proton pump (pump defects); failure to generate and/or maintain an appropriate electrical gradient to favor hydrogen ion secretion (voltage defects); back-leak of hydrogen ions across an abnormally permeable collecting duct membrane (gradient defects), and diminished availability of NH3 in this nephron segment (NH3 defects). These four subtypes can be identified by measuring the urine pH and PCO2 under appropriate circumstances and evaluating the renal excretion of ammonium and potassium.
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PMID:Distal renal tubular acidosis syndromes: a pathophysiological approach. 397 76

In this review, the distal nephron is considered to be that portion of the renal tubule commencing with the thick ascending limb of the loop of Henle and ending with the papillary collecting duct. The collecting duct, including its subdivisions in the cortex and medulla, originates from a different embryologic anlage than more proximal nephron segments, which may explain its morphologic and functional dissimilarities from the thick ascending limb and the distal convoluted tubule. This review summarizes selected aspects of the physiology of the distal nephron, with particular emphasis on the physiology of distal nephron transport of sodium, potassium, chloride and hydrogen ion. The pathophysiologic features of the following disorders of distal nephron function are reviewed: (1) pseudohypoaldosteronism, a heterogenous group of disorders in which the signs and symptoms are suggestive of aldosterone deficiency, but in which aldosterone levels are supernormal and administration of exogenous mineralocorticoid is not ameliorative; (2) pseudohyperaldosteronism (Liddle syndrome), a familial disorder in which the clinical manifestations closely resemble those resulting from an aldosterone-producing adenoma of the adrenal gland (primary aldosteronism), but in which the measured rate of aldosterone secretion and excretion is greatly subnormal; (3) Bartter syndrome and related syndromes of renal potassium wasting; (4) type 1 renal tubular acidosis (classic, distal); (5) type 4 renal tubular acidosis (hyperkalemic). Reference citations are generally to articles reporting recent advances in these areas and to review articles that contain comprehensive bibliographies.
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PMID:Disorders of distal nephron function. 627 92

The purpose of these studies was to clarify the basis of the relationship between the urine bicarbonate concentration and the urine minus blood PCO2 difference in alkaline urine (U-B PCO2) and hence shed light on factors that influence hydrogen ion secretion in the collecting duct in vivo. The U-B PCO2 was used to monitor this latter parameter. In dogs with a normal extracellular fluid (ECF) volume, the U-B PCO2 was not primarily influenced by the urine bicarbonate concentration but rather it was related to the rate of sodium excretion. The U-B PCO2 could be abolished by amiloride when the urine bicarbonate concentration was less than 60 mm. At higher urine bicarbonate concentrations, there was a linear correlation between the U-B PCO2 and the urine bicarbonate concentration in normovolemic dogs given amiloride, but the absolute values were lower than they were in normovolemic animals not treated with amiloride. In the dogs with an expanded ECF volume, the U-B PCO2 was lower than it was in the normovolemic animals, and the U-B PCO2 was nor directly related to the urine bicarbonate concentration and not influenced by the rate of sodium excretion. Amiloride had little influence on the U-B PCO2 under these conditions. These results are interpreted to suggest that the magnitude of collecting duct hydrogen ion secretion is determined primarily by the electrical gradient generated by sodium reabsorption in normovolemic dogs and by the intracellular and lumenal hydrogen ion concentrations when the ECF volume is expanded or when active sodium reabsorption is inhibited by amiloride.
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PMID:Studies on the regulation of hydrogen ion secretion in the collecting duct in vivo: evaluation of factors that influence the urine minus blood PCO2 difference. 628 30

The purpose of these studies was to elucidate the mechanism whereby collecting duct hydrogen ion secretion was augmented by acidemia. The urine minus blood PCO2 difference in alkaline urine (U-B PCO2) was used to evaluate this parameter. In dogs with a normal ECF volume, the U-B PCO2 factored was high, and there was no significant relationship between the U-B PCO2 factored for the urine bicarbonate concentration and the blood hydrogen ion concentrations unless amiloride, an agent that abolishes the transtubular potential difference, was present. In this latter case, the U-B PCO2 was a linear function of the urine bicarbonate concentration, and the U-B PCO2 factored for the urine bicarbonate concentration was directly proportional to the blood hydrogen ion concentration. To extend the pH range considerably, we used lysine to induce bicarbonaturia in dogs with an expanded ECF volume. Amiloride now caused only a small decrease in the U-B PCO2 at any urine bicarbonate concentration, and furthermore, it did not influence the linear relationship between the U-B PCO2 factored for the urine bicarbonate concentration and the blood hydrogen ion concentration. These results suggests that acidemia stimulates collecting duct hydrogen ion secretion by a mechanism that appears to be independent of the amiloride-sensitive component of the U-B PCO2. We speculate that the mechanism might involve an increased intracellular hydrogen ion concentration during acidemia.
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PMID:Studies on the mechanism whereby acidemia stimulates collecting duct hydrogen ion secretion in vivo. 628 31

The effect of acute respiratory acidosis (ARA) on inner medullary collecting duct (IMCD) acidification was studied and the results were compared with previously obtained data by our laboratory in rats with acute metabolic acidosis (AMA). We employed the microcatheterization technique to directly measure pH and PCO2 with glass-membrane electrodes, and fluid samples were obtained for measurement of bicarbonate, phosphate, and ammonium. Arterial pH was 7.18 +/- 0.01 and PCO2 was 88 +/- 2 mmHg. The IMCD data were analyzed as a function of IMCD length (approximately 6 mm). pH decreased from 5.78 +/- 0.07 to 5.27 +/- 0.03 and PCO2 increased from 55 +/- 4 to 75 +/- 2 mmHg between origin and tip. Bicarbonate delivery decreased from 154 +/- 34 to 25 +/- 3 nmol/min but no change was noted in acid phosphate, ammonium, or net acid addition along the IMCD. However, net acid excretion was not different from that found previously in AMA. We conclude that during ARA acidification is augmented prior to, but not along, the IMCD. In contrast, during AMA we previously found that IMCD plays a major regulatory role in urinary acidification, accounting for about 50% of the excreted hydrogen ion.
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PMID:Effect of respiratory acidosis on acidification by the medullary collecting duct. 640 6

The renal medulla can play an important role in acid excretion by modulating both hydrogen ion secretion in the medullary collecting duct and the medullary PNH3. The purpose of these experiments was to characterize the intrarenal events associated with ammonium excretion in acute acidosis. Cortical events were monitored in two ways: first, the rates of glutamine extraction and ammoniagenesis were assessed by measuring arteriovenous differences and the rate of renal blood flow; second, the biochemical response of the ammoniagenesis pathway was examined by measuring glutamate and 2-oxoglutarate, key renal cortical metabolites in this pathway. There were no significant differences noted in any of these cortical parameters between acute respiratory and metabolic acidosis. Despite a comparable twofold rise in ammonium excretion in both cases, the urine pH, PNH3, and the urine minus blood PCO2 difference (U-B PCO2) were lower during acute hypercapnia. In these experiments, the urine PCO2 was 34 mmHg (1 mmHg = 133.322 Pa) lower than that of the blood during acute respiratory acidosis while the U-B PCO2 was 5 +/- 3 mmHg in acute metabolic acidosis. Thus there were significant differences in medullary events during these two conditions. Although the urine pH is critical in determining ammonium excretion in certain circumstances, these results suggest that regional variations in the medullary PNH3 can modify this relationship.
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PMID:Importance of medullary events in ammonium excretion: studies in acute respiratory and acute metabolic acidosis. 640 34

The outer medullary collecting duct which is composed of both principal and intercalated cells is involved in hydrogen ion secretion. In the turtle urinary bladder stimulation of hydrogen ion secretion is associated with ultrastructural changes in the mitochondria-rich cells, suggesting that membrane and possibly a proton pump are being transferred from apical tubulovesicular structures and inserted into the apical plasma membrane. Since the intercalated cells resemble the mitochondria-rich cells, this study was initiated to determine whether or not similar changes occur in the outer medullary collecting duct during chronic metabolic acidosis. Rats received ammonium chloride in their drinking water for 15 days and as a daily gavage for 3 days before sacrifice. Control rats received regular tap water. After collection of physiologic data the kidneys were fixed by in vivo perfusion with glutaraldehyde and processed for electron microscopy. No changes were observed in the principal cells. Morphometric analyses of the intercalated cells in both the outer and inner stripe revealed a significant increase in the surface density of the apical plasma membrane concomitant with a striking depletion of the tubulovesicular structures in the apical plasma region of the cell with chronic metabolic acidosis. These findings suggest that in response to chronic metabolic acidosis membrane, possibly containing a proton pump, is transported from the tubulovesicular membrane compartment to the apical plasma membrane of the intercalated cell.
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PMID:Response of intercalated cells of rat outer medullary collecting duct to chronic metabolic acidosis. 647 8


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