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)

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.
 ...
PMID:Influence of mucosal and serosal pH on antidiuretic action in frog urinary bladder. 4 16

In anaesthesized dogs given large doses of ADH and DOC and subjected to acute left renal denervation, urine flow (V) and sodium excretion (UNaV) rose significantly in response to bilateral carotid artery clamping in both the intact (p less than 0.05) and the denervated kidney (p less than 0.001). This was associated with significant (p less than 0.05) increases of the tubular rejection fraction of sodium (TRFNa) while creatinine clearance (Ccr) remained unchanged. Following a second control period, carotid occlusion was repeated, while perfusion pressure in the left kidney was kept constant by aortic constriction. In this case the diuretic and natriuretic response in the right kidney occurred in the same fashion as previously, and no significant change in V, UNaV, or TRFNa was observed in the left kidney. The amount of free water reabsorbed in the collecting duct (TcH2O) was not consistently altered by carotid occlusion. It is concluded that acute renal denervation augments the pressure diuresis that follows carotid occlusion. The failure of carotid polyuria to occur when renal perfusion pressure is kept constant points to the importance of mechanical factors. Still, a wash-out of the medullary osmotic gradient seems to be an unlikely mechanism.
 ...
PMID:Mechanism of carotid-occlusion diuresis. 75 93

Prolactin was shown to activate adenylate cyclase in broken cellular enzyme preparations from rat renal medulla. Likewise, vasopresin was effective on this enzyme system. Parathyroid hormone was similarly active in the renal cortex. The simultaneous administration of vasopressin and prolactin to medullary kidney slices did not result in an additive effect in stimulating medullary adenyl cyclase. Audioradiographic techniques revealed a selective and prolonged localization of intravenously injected 125I-prolactin to the thick limb of the loop of Henle, the distal tubule and the collecting duct. It is concluded that prolactin activates medullary adenylate cyclase, and may do so by occupying ADH receptors.
 ...
PMID:Prolactin-induced stimulation of rat renal adenylate cyclase and autoradiographic localization to the distal nephron. 86 55

Differential interference contrast microscopic images were used to assess the cell volume regulatory increase (VRI) response of rat IMCD segments isolated from the mid-inner medullary region of pathogen-free Sprague-Dawley rats and perfused in vitro at 37 degrees C. In the absence of ADH. IMCD cells behaved in an osmometric fashion over the range of extracellular osmolalities 290 to 386 mOsm/kg H2O and had an osmotic space equal to 54.2% of total geometric volume. After initial shrinkage in hypertonic perfusing and bathing solutions (340 mOsm/kg H2O using sucrose), cell volume increased rapidly to the isotonic value only in tubules preincubated in ADH (100 microU/ml). The rates of VIR were: (-ADH) 0.0142 +/- 0.0046 nl.min-1.cm-1 or 0.30 +/- 0.10%/min and (+ADH) 0.7225 +/- 0.1278 nl.min-1.cm-1 or 15.42 +/- 2.31%/min (N = 4; P less than 0.01). An overshoot in cell volume was observed on return to isotonic media only in the ADH exposed tubules showing a hypertonic VRI response, indicating that IMCD cells accumulated solute during hypertonic VRI. In the absence of ADH, one mM dibutyryl cyclic AMP mimicked the effect of hormone on hypertonic VRI. This ADH-dependent VRI process required Na+ and (CO2 + HCO3-) in external media and was reduced or abolished by 0.1 mM amiloride, 0.1 mM 4,4'-diisothiocyanatostilbene-2,2-'-disulfonic acid (DIDS) in peritubular solutions. These data suggest that ADH-dependent, rapid hypertonic cell volume regulation in rat inner medullary collecting duct depends on NA+ uptake, which may be mediated by parallel Na+-H+ and an HCO3(-)-dependent. DIDS-sensitive pathway (such as, Cl+-HCO3- exchanger) in basolateral cell membrane. In addition, a luminal amiloride-sensitive pathway (most likely the cation-selective channel) may contribute to cell volume regulation in the rat IMCD.
 ...
PMID:Rapid hypertonic cell volume regulation in the perfused inner medullary collecting duct. 255 37

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

The water permeability of collecting ducts is greatly increased by the antidiuretic hormone, vasopressin (VP). Freeze-fracture studies were carried out to test if this permeability increase is associated with the appearance of intramembrane particle (IMP) aggregates and whether increased doses of VP lead to an increase in the number and size of particle aggregates in the luminal membrane of principal cells in the isolated cortical collecting duct. Unstimulated cells expressed 17 +/- 6.5 particle aggregates per 100 microns 2. Stimulation with VP at concentrations of 20 or 200 microU/ml increased the number of particle aggregates significantly to 129 +/- 15.8 and 324 +/- 45.8, respectively. The size of the particle aggregates increased from 0.0012 microns 2 under control conditions to 0.025 microns 2 at 20 microU/ml VP and to 0.063 microns 2 at 200 microU/ml VP. In addition, the total area occupied by the IMP increased from 0.02 microns 2/100 microns 2 (controls) to 3.17% and 20.38% (after 20 and 200 microU ADH/ml, respectively). Particle aggregates were also observed in the luminal plasma membrane of isolated collecting ducts fixed immediately after dissection, resembling the in vivo status. These results demonstrate that a dose-dependent relationship exists between the concentration of the applied VP and the number of particle aggregates, as well as the size of the aggregates. Cytoplasmic tubular vesicles in fusion with the apical membrane were observed.
 ...
PMID:Vasopressin-induced intramembrane particle aggregates. A dose-response relationship in the isolated cortical collecting duct of the rabbit kidney. 280 60

Antidiuretic hormone increases the water permeability of the cortical collecting tubule and causes the appearance of intramembrane particle aggregates in the apical plasma membrane of principal cells. Particle aggregates are located in apical membrane coated pits during stimulation of collecting ducts with ADH in situ. Removal of ADH causes a rapid decline in water permeability. We evaluated apical membrane retrieval associated with removal of ADH by studying the endocytosis of horseradish peroxidase (HRP) from an isotonic solution in the lumen. HRP uptake was quantified enzymatically and its intracellular distribution examined by electron microscopy. When tubules were perfused with HRP for 20 min in the absence of ADH, HRP uptake was 0.5 +/- 0.3 pg/min/micron tubule length (n = 6). The uptake of HRP in tubules exposed continuously to ADH during the 20-min HRP perfusion period was 1.3 +/- 0.8 pg/min/micron (n = 8). HRP uptake increased markedly to 3.2 +/- 1.1 pg/min/micron (n = 14), when the 20-min period of perfusion with HRP began immediately after removal of ADH from the peritubular bath. Endocytosis of HRP occurred in both principal and intercalated cells via apical membrane coated pits. We suggest that the rapid decline in cortical collecting duct water permeability which occurs following removal of ADH is mediated by retrieval of water permeable membrane via coated pits.
 ...
PMID:Apical membrane endocytosis via coated pits is stimulated by removal of antidiuretic hormone from isolated, perfused rabbit cortical collecting tubule. 290 50

Free water diuresis in vasopressin-deficient Brattleboro rats does not influence body conservation of chromium (Cr+3), suggesting a proximal tubular site for renal Cr reabsorption. Other data suggest that Cr conservation is accomplished primarily by lack of glomerular filtration or by tissue binding to a specific Cr-binding substance. To provide further data, radiochromium (51Cr) retention and tissue distribution were studied in SHR and WKY rats undergoing saline diuresis. Despite high urine flows, body retention and urinary excretion of 51Cr were unchanged. Tissue content of 51Cr was minimally and not consistently influenced by saline diuresis in either rat strain. Compared to WKY rats, the SHR rats had a trend to lower serum and tissue 51Cr content but higher tissue/serum 51Cr ratios. These data fail to incriminate collecting duct reabsorption in Cr conservation but are compatible with proximal Cr reabsorption or either of the two hypotheses mentioned above. The decreased serum 51Cr content of SHR rats may be due to the mechanical effect of increased plasma and extracellular volumes. One possible explanation for the increased tissue/serum 51Cr ratios may be the presence of a factor in SHR rats promoting cellular Cr transport. However, there is no present evidence to suggest that any of the hormones believed capable of increasing Cr transport (insulin, growth hormone, thyroxine, ADH) are increased in the SHR rat.
 ...
PMID:Radiochromium distribution during saline diuresis. 373 75

The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
 ...
PMID:The aging kidney. 391

Postnatal renal development was studied in dogs between 2 and 77 days. Single, superficial nephrons were evaluated by micropuncture, concurrently with measurements of total renal function and morphometric analyses in the same animals. Glomerular filtration rate for the entire kidney increased linearly from 0.13 ml/min per g kidney weight at 2 days to 0.91 at 77 days. Extraction of p-aminohippurate increased from about 20 to 80%, and renal plasma flow per g kidney weight, measured as Cpah/Epah, increased threefold during the same period. Filtration fraction increased to the mature value during the first half of the postnatal period studied. The clearance of urea per unit of renal mass increased with age, whereas the fraction of filtered urea reabsorbed declined during the early part of the postnatal period. The pattern of fractional urea reabsorption may be due mainly to increased medullary recycling of urea and to a rise in the reabsorption of water from the medullary collecting duct. Urine osmolality was higher than plasma from birth onward and rose with age. Osmolal equality of collecting duct fluid and medullary interstitium reflected mature vasopressin (ADH)-induced water permeability. The rise in urinary concentration was predominantly due to increasing medullary sequestration of urea. Glomerular filtration rate of the superficial nephron increased from 3.2 nl/min at 21 days, when subcapsular nephrons were uniformly patent, to 23.1 at 77 days. Despite this rise in filtered load, fractional reabsorption of sodium and water in superficial proximal tubules was constant and at the mature level from the onset of intratubular perfusion. Changes in arterial plasma protein concentration, in filtration fraction, and in the hydrostatic pressure gradient between proximal tubule and peritubular capillary may interact to maintain glomerulotubular balance. The data, together with results of an accompanying morphological study, demonstrate a sequence of coordinated changes during postnatal renal maturation.
 ...
PMID:ostnatal development of renal function: micropuncture and clearance studies in the dog. 554 75


1 2 3 Next >>