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)

This study was designed to determine the effect of acute hyperventilation on distal nephron hydrogen ion secretion. The blood PCO2 declined and stabilized rapidly when bicarbonate loaded rats were hyperventilated. In contrast, the urine PCO2 declined slowly, resulting in an early increase in the urine minus blood (U-B) PCO2 which could not be obliterated by carbonic anhydrase infusion. Within approximately 50 min, the U-B PCO2 in the hyperventilated and carbonic anhydrase infused rats approached zero. Consequently, equilibrium between collecting duct urine and arterial blood PCO2 was then presumed to exist. This provided the basis for the subsequent studies on a series of rats. The U-B PCO2 decreased from a control of 22+/-1 mm Hg (mean+/-SEM) to 11+/-2 mm Hg (mean+/-SEM) with hypocapnia, and rose again to its control value when the blood PCO2 returned to prehyperventilation values. This decline in U-B PCO2 with acute hyperventilation could not be attributed to changes in urine flow, phosphate, or bicarbonate excretion, suggesting, therefore, a decrease in distal nephron (probably collecting duct) hydrogen ion secretion with acute hyperventilation. Possible pitfalls in the interpretation of the UB PCO2 are illustrated.
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PMID:The effect of hyperventilation on distal nephron hydrogen ion secretion. 0 92

The purpose of this study was to investigate distal nephron hydrogen ion secretion in the intact animal. The rabbit was chosen as the experimental model because it produces acid urine containing little ammonium. Upon replacement of the usual rabbit diet with milk, plus administration of an acid load (10 mEq/kg), the urine pH fell consistently from very alkaline values (PH greater than 7.4) to 4.8 +/- 0.2. Despite the ability to achieve high urine-to-blood hydrogen ion concentration gradients, the U-B PCO2, an index of collecting duct hydrogen ion secretion, was virtually zero. In these studies, the urine bicarbonate and buffer concentration were comparable to those observed in dog, rat, and man in which a high U-B PCO2 gradient was achieved. The rabbits studied had low plasma potassium concentrations (less than 3 mEq/L). Since potassium deficiency has been implicated in impaired urine acidification, potassium was administered, and it resulted in an increase in collecting duct hydrogen ion secretion as evidenced by a further fall in minimum urine pH during acidemia and a prompt rise in the U-B PCO2 during alkali administration. In summary, rabbits had a very low but not absent rate of collecting duct hydrogen ion secretion. Potassium administration increased the rate of hydrogen ion secretion in a segment of the collecting duct in which hydrogen ion secretion is reflected by an increase U-B PCO2.
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PMID:Collecting duct hydrogen ion secretion in the rabbit: role of potassium. 2 38

Acute clearance studies were performed in normal subjects to assess the actions of the new diuretic, piretanide, on renal function. The drug increased both glomerular filtration rate and effective renal plasma flow in roughly proportionate amounts, so that filtration fraction did not change. In a dosage of 2 to 3 mg, it induced an increase in sodium excretion of almost 13% of filtered load, and there was an associated 2- to 3-fold increase in potassium excretion. The abstraction of solute-free water from the collecting duct was markedly reduced, but the drug induced no significant decline in the generation of free water. The rate of bicarbonate excretion, as well as that of titratable acid and ammonium, was increased approximately proportionately so that there was no increase in urinary pH or net hydrogen ion excretion. There was no phosphaturia, a unique finding, since all other drugs and maneuvers that cause a bicarbonate diuresis are also phosphaturic. Piretanide increased calcium excretion by approximately 19% of filtered load. The data suggest that the drug acts largely in the ascending limb of the loop of Henle and that it also affects the proximal tubule. Despite its sulfonamide structure, none of the drug's effects appear to be related to inhibition of carbonic anhydrase.
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PMID:Acute effects of piretanide in normal subjects. 3 85

1. The proposition that changes in renal calcium excretion during vasopressin administration are positively correlated with concurrent changes in urine hydrogen ion concentration was tested by administration of vasopressin into twelve conscious diuresing sheep receiving either alkalinizing or acidifying infusions. 2. Vasopressin-induced antidiuresis in sheep with alkaline urine was associated with significant increases in urinary pH and decreases in the rate of calcium excretion whereas antidiuresis in sheep with acid urine was associated with significant decreases in urinary pH and no consistent effect on calcium excretion. 3. Magnesium excretion increased during vasopressin administration in most experiments regardless of urinary pH changes. 4. Vasopressin administration did not significantly alter the rate of excretion of sodium, potassium, chloride and phosphate or the rates of sodium, potassium, chloride, inulin, para-aminohippurate and osmolal clearance in sheep with either acid or alkaline urine. Potassium excretion and clearance in sheep with alkaline ruine was higher than that of sheep with acid urine during vasopressin infusion. 5. The results support the hypothesis that changes in renal tubular hydrogen ion concentration or bicarbonate concentration caused by water reabsorption from the collecting duct and possibly the late distal tubule could be part of the explanation for changes in renal calcium excretion which occur during vasopressin-induced antidiuresis.
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PMID:Renal calcium and magnesium excretion during vasopressin administration into sheep with acid or alkaline urine. 4 39

Mucosal acidification to pH 6.5 reduced by 88% the oxytocin- (2.2 x 10(-8) M) elicited increase of water permeability in frog urinary bladder. Mucosal alkalinization (pH 10.5) increased by as much as 200% the response to the same concentration of oxytocin. These effects were not observed when supramaximal concentrations of oxytocin were imployed. Similar changes were found when the serosal pH was modified. The hydrosmotic responses elicited by serosal hypertonicity or cyclic AMP plus theophylline were also affected by mucosal or serosal changes of the hydrogen in concentration, suggesting an effect at a post-cyclic AMP level. Important interactions were found between luminal pH and serosal hypertonicity when experimental conditions were employed similar to those observed in the collecting duct of mammalian nephron. Freeze-fracture studies showed that the number of intramembranous aggregates of particles induced by ADH in the luminal membrane was reduced by mucosal acidification and augmented by an increase in medium pH.
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PMID:Influence of mucosal and serosal pH on antidiuretic action in frog urinary bladder. 4 16

Rapidly induced systemic alkalinization due to either sodium-lactate or sodium-bicarbonate infusion in prolonged-fasted subjects with steady-state ketoacidosis was associated with a decrease in urine pH. This decrease in urine pH from 5.50 to 5.20 was the result of a significant decrease in urinary ammonium excretion from 8.40 to 6.35 mEg/hr and was not accompanied by an increase in net acid excretion (11.3 vs. 10.6 mEg/hr). The decreased ammonium excretion is attributed to the raised pH of the proximal tubular fluid resulting in a less favorable pH gradient for gaseous ammonia entry. This would decrease gaseous ammonia generated in the loop of Henle for collecting duct buffering of secreted hydrogen ions.
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PMID:Mechanism for the paradoxical aciduria following alkali administration to prolonged-fasted patients. 23 93

Osteoclasts dissolve bone mineral by the vectorial secretion of hydrogen ion at their osseous attachment site. To accomplish this, the osteoclast employs a vacuolar H+ ATPase that is polarized to the specialized proton-secreting plasma membrane domain, the ruffled border. Physiologically and biochemically, they resemble the specialized proton-secreting intercalated cells of the renal collecting duct, which also use a polarized vacuolar H+ ATPase to effect transepithelial hydrogen ion transport. Studies on the mechanism of hydrogen ion transport by the kidney may therefore provide insights into the control of acid secretion by the osteoclast.
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PMID:The osteoclast as a unicellular proton-transporting epithelium. 131 97

Renal hydrogen ion excretion increases with chronic acid loads and decreases with alkali loads. We examined the mechanism of adaptation by analyzing vacuolar proton-translocating adenosine triphosphatase (H+ ATPase) 31-kD subunit protein and mRNA levels, and immunocytochemical distribution in kidneys from rats subjected to acid or alkali loads for 1, 3, 5, 7, and 14 d. Acid- and alkali-loaded rats exhibited adaptive responses in acid excretion, but showed no significant changes in H+ ATPase protein or mRNA levels in either cortex or medulla. In contrast, there were profound adaptive changes in the immunocytochemical distribution of H+ ATPase in collecting duct intercalated cells. In the medulla, H+ ATPase staining in acid-loaded rats shifted from cytoplasmic vesicles to plasma membrane, whereas in alkali-loaded rats, cytoplasmic vesicle staining was enhanced, and staining of plasma membrane disappeared. In the cortical collecting tubule, acid loading increased the number of intercalated cells showing enhanced apical H+ ATPase staining and decreased the number of cells with basolateral or poorly polarized apical staining. The results indicate that both medulla and cortex participate in the adaptive response to acid and alkali loading by changing the steady-state distribution of H+ ATPase, employing mechanisms that do not necessitate postulating interconversion of intercalated cells with opposing polarities.
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PMID:Expression and distribution of renal vacuolar proton-translocating adenosine triphosphatase in response to chronic acid and alkali loads in the rat. 182 94

Hydrogen ion secretion in the kidney is thought to be mediated in part by an N-ethylmaleimide (NEM)-sensitive proton-translocating adenosine triphosphatase (ATPase). This enzyme has been found throughout the nephron, but it has not been completely characterized enzymatically in the rat collecting duct. In the present study we characterized the NEM-sensitive ATPase from microdissected cortical (CCT) and medullary (MCT) collecting tubules of the rat nephron. At optimum conditions, NEM-sensitive ATPase activity was the same in both tubule segments: activity was 275.6 +/- 18.6 pmol/mm/h in the CCT and 280.3 +/- 35.2 pmol/mm/h in the MCT (n = 23, NS). ATP sensitivity was greater in CCT than in MCT, and in the former guanosine triphosphate was able to partially support enzyme activity. Maximal enzyme inhibition with NEM occurred at a lower concentration in CCT as compared to MCT. At pH 7.0 in MCT enzyme activity was approximately one half that seen at pH 7.4; in MCT and CCT, the pH optimum was 7.4. The temperature optimum in both segments was between 37 and 42 degrees C. Enzyme activity in CCT and MCT was linear to 30 min and proportional to tubule length. These results demonstrate that there are important differences in the NEM-sensitive ATPase isolated from two segments of rat collecting duct, and raise the possibility that enzyme heterogeneity may exist.
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PMID:Characterization of the N-ethylmaleimide-sensitive ATPase in rat cortical and medullary collecting tubule. 184 Feb 79

Reactive oxygen species (ROS) have been implicated in the pathogenesis of toxic, ischemic and immunologically-mediated renal injury. Although substantial evidence exists for the production of ROS by glomerular cells, little is known about production of these reactive oxygen metabolites by renal tubular cells. We examined the ability of cultured cells from different segments of the rabbit nephron to elaborate ROS. Under basal conditions, cells of the proximal tubule, cortical collecting duct, and papillary collecting duct produced superoxide anion and hydrogen peroxide. Exposure to opsonized zymosan or heat-aggregated gamma globulin significantly increased ROS production by all three tubular cell types. The production of superoxide anion and hydrogen peroxide was time dependent and increased with increasing concentrations of the stimulating factors. These experiments indicate that renal tubular cells have the potential to participate in renal injury via elaboration of highly-reactive oxygen metabolites.
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PMID:Production of reactive oxygen species by tubular epithelial cells in culture. 216 66


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