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 functions of a kidney, whether normal or cystic, can be conceptualized in terms of anatomy (glomerulus, proximal tubule, loop of Henle, distal convolution, and collecting duct), activity (volume regulation, dilution and concentration, acid-base regulation, potassium excretion, transport of organic molecules, and calcium and phosphate excretion), and the integration of anatomic organization to meet functional demand. Our discussion of renal cystic disorders follows this conceptual outline. For discussions of normal renal physiology, the reader is referred to any one of several recent, excellent reviews (1-3). Systematic evaluation of renal function in cystic diseases of the kidney (medullary sponge kidney, medullary cystic disease, and polycystic kidney disease) has only rarely been performed. The available information suggests that the earliest detectable lesions consist primarily of tubular dysfunction. With time, however, significant reduction of glomerular filtration occurs and the resultant accumulation of uremic toxins dominates the clinical picture in polycystic and medullary cystic disease. Significant changes in glomerular function are unusual in medullary sponge kidney. This review represents an attempt to summarize the large body of literature that has accumulated on functional abnormalities in these disorders, and to point out those areas where further investigations are needed.
 ...
PMID:Functional abnormalities in renal cystic diseases. 0 65

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.
 ...
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.
 ...
PMID:Acute effects of piretanide in normal subjects. 3 85

Potassium depletion (KD) causes renal chloride-wasting. To investigate the effects of KD on renal tubular reabsorption of chloride, balance, clearance, micropuncture, and microinjection studies were performed on potassium-depleted rats. KD was produced by omitting potassium from the diet and by administration of DOCA on days 2 and 3; rats were studied on days 9 to 12. Diets were chloride-free in both control and KD groups. In the KD group, balance experiments confirmed greater chloride depletion and continued chloride-wasting, and clearance studies showed an increased FECl. Muscle potassium was reduced by 27% as compared to control. Whole kidney and single nephron GFR were reduced in KD rats to 72 and 74% of control. Fractional (6 +/- 6% vs. 22 +/- 4%, P less than 0.05) and absolute chloride reabsorption in the proximal tubule was not different. Fractional reabsorption of delivered chloride was reduced in the loop of Henle (92 +/- 0.8% in KD vs. 95 +/- 0.7% in control, P less than 0.02). Transtubular chloride ratio (0.28 +/- 0.02 vs. 0.21 +/- 0.02, P less than 0.02) was increased at the early distal tubule. Fractional delivery of chloride (8 +/- 0.9 vs. 5 +/- 0.5%, P less than 0.02), and fluid (26 +/- 1 vs. 22 +/- 1%, P less than 0.05) were also increased in KD at the early distal tubule. Recovery of chloride 36 injected into late distal tubules was 88 +/- 1% on a normal chloride intake, 62 +/- 2% in chloride depletion, and 88 +/- 2% in potassium and chloride depletion. Thus, KD depresses chloride reabsorption in the proximal tubule and in the loop of Henle, and it decreases chloride 36 efflux from the collecting duct.
 ...
PMID:Effects of potassium depletion on renal tubular chloride transport in the rat. 3 45

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.
 ...
PMID:Renal calcium and magnesium excretion during vasopressin administration into sheep with acid or alkaline urine. 4 39

General features of the processes that contribute to renal potassium excretion are understood from clearance, stop-flow, micropuncture, and in vitro microperfusion experiments. However, the complex architecture of the kidney has made it difficult to examine individual nephron segments in all parts of the kidney. Accordingly, the extent to which distinguishable nephron populations, such as superficial and deep, may differ in their contributions to overall potassium excretion are not known. Also, the nature of transport processes across the successive segments of the nephrons (including not only the underlying cellular mechanisms, but even the direction of transport) is not known for all segments in any one nephron population. Excreted potassium is derived both from filtered potassium that escapes reabsorption and from secreted potassium. The filtered portion is large in amphibians and may be larger than generally recognized in mammals. The remainder is secreted primarily by distal nephron segments (distal tubule and cortical collecting duct). Potassium is also secreted into descending limbs of Henle loops; apparently this fraction is recycled from collecting ducts, and so does not represent an additional quantity of potassium transferred from blood to tubule fluid. Systemic factors that affect potassium excretion (potassium intake, sodium chloride intake, mineralocorticoid hormone levels, acid-base balance, and diuretic treatments) do so by modifying the net uptake of potassium from blood to cell and by altering the rate of fluid flow through the distal nephron. Under most circumstances, the distal nephron in the cortex appears to secrete potassium and the medullary collecting duct reabsorbs potassium. Although it is clear that successive nephron segments transport potassium in different ways, evidence to date does not indicate that potassium is handled differently by superficial nephrons compared to nephrons whose glomeruli lie in the deeper levels of the cortex.
 ...
PMID:Renal potassium transport: contributions of individual nephron segments and populations. 36 78

Micropuncture techniques were employed to evaluate the effects of unilateral ureteral obstruction (UUO) of 18 h duration on the function of the terminal collecting duct in weanling rats 90-120 min following release of obstruction. In control animals and after release of UUO, water and sodium reabsorption continued along the terminal segment of the collecting duct. Fractional delivery of water (FRH2O) and sodium (FRNa) to this segment was increased after release of UUO. A significantly greater amount of the FRH2O and FRNa was reabsorbed along the terminal collecting duct following release of obstruction than in controls. Potassium was not consistently reabsorbed or secreted in either group. Following release of UUO, the osmolality of collecting duct fluid was lower than in controls, but was not different from the osmolality of fluid obtained from the bend of the loop of Henle. The results suggest that the permeability to water and the reabsorptive capacity of the collecting duct are not altered by acute obstruction.
 ...
PMID:Effect of acute ureteral obstruction on terminal collecting duct function in the weanling rat. 42 68

Potassium transport along the inner medullary collecting duct (IMCD) was evaluated by the microcatheterization technique in Charles River CD (cesarean derived) rats 7-9 days after sham operation (S) or uninephrectomy (UNPX). The fraction of filtered potassium (TF/P)K/In) as a function of IMCD length was analyzed by linear regression. In 13 S rats there was a significant correlation and slope (P less than 0.001) and (TF/P)K/In increased from 14% at the beginning of the IMCD to 25% in the urine. IMCD potassium secretion accounted for about half of the excreted potassium. In the UNPX rats a significant correlation and slope was also obtained (P less than 0.001); (TF/P)K/In at the beginning of IMCD was 24% and increased to 36% in the urine. No difference in slope was noted between the groups. There was a slightly greater absolute potassium secretion after UNPX (0.77 +/- 0.03 S vs. 0.93 +/- 0.04 mueq/min UNPX), but this did not account for most of the difference in potassium excretion noted. We conclude that net potassium secretion occurs along the IMCD in S and UNPX rats. After UNPX, there is significantly greater potassium delivery to the IMCD and a greater kaluresis. The increased kaluresis cannot be accounted for primarily by increased potassium secretion along the IMCD.
 ...
PMID:Potassium secretion along the inner medullary collecting duct. 42 70

Juxtamedullary (JM) nephron and collecting duct function was studied after a two-thirds reduction in renal mass in the young rat. The glomerular filtration rate of JM nephrons was twofold greater in the remnant kidney (RK) group than in controls, but this increase was proportional to the increase measured in surface nephrons. Despite an increase in absolute reabsorption, delivery of sodium and water to the end of the proximal tubule of superficial nephrons and to the bend of Henle's loop of JM nephrons was increased. This was a consequence of an increase in filtered load and a decrease in fractional reabsorption. Potassium handling in surface nephrons was similar to that of sodium and water. In deep nephrons of the RK group, potassium delivery to the bend was increased as a consequence of increased filtered load. The terminal portion of the collecting duct has a role in this adaptive response to a reduction in renal mass. In rats with a RK, reabsorption of water occurred along this segment; however, when the amount reabsorbed was related to delivery, fractional water reabsorption was only 30% of controls. Changes in sodium handling were more profound. In the group with the RK, sodium reabsorption was not detectable along this segment. Thus, while 40% of delivered sodium was reabsorbed in controls, in the remnant kidney group the mean was not different from zero (-1.7%).
 ...
PMID:Response of deep nephrons and the terminal collecting duct to a reduction in renal mass. 44 83

The functional expression of papillary necrosis was investigated with a model of drug-induced papillary necrosis. Bromoethylamine hydrobromide (BEA) administration to rats uniformly resulted in the development of papillary necrosis. All studies were performed 24 hours after BEA administration with the exception of the electrolyte balance studies, which were performed during the 72 hours after the induction of papillary necrosis. GFR was not different between BEA-treated and sham rats. BEA-treated rats had a significantly lower maximal urine osmolality and free water reabsorption than did sham rats. Renal tissue concentrations of sodium, potassium, and water were not different between BEA-treated and sham rats. During water diuresis, free water clearance was not significantly different between the two groups. During sodium bicarbonate administration, maximal bicarbonate reabsorption and urine-blood Pco2 gradient (at comparable urine bicarbonate concentrations) were not significantly different between the two groups. During sodium sulfate infusion, there was no difference in minimum urine pH, ammonium excretion, and net acid excretion between chronically acidotic BEA-injected and sham rats. In rats on "zero" sodium intake, BEA administration resulted in a significant increase in urine flow and sodium excretion, whereas sham rats remained in sodium balance. In rats with restriction of both sodium and chloride, BEA administration resulted in a significant wastage of sodium, chloride, and calcium. There was no difference in potassium excretion between BEA-treated and sham rats during hydropenia, bicarbonate administration, sodium sulfate infusion, or ingestion of a normal potassium diet. When potassium intake was restricted to "zero," BEA-treated rats developed potassium wastage; when potassium intake was increased to 21 mEq/day, BEA-treated rats had a significantly lower potassium excretion than did sham rats. These findings may result from alterations in collecting duct transport, but damage to deep medullary structures may also contribute.
 ...
PMID:Functional characterization of drug-induced experimental papillary necrosis. 51 89


1 2 3 4 5 6 7 8 9 10 Next >>