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)

Vasopressin is known to increase the permeability of the toad bladder, an analogue of the mammalian collecting duct, to water and hydrophilic solutes such as urea. In the present study, the effect of vasopressin on the permeability of a series of lipophilic compounds, including many commonly used drugs, has been determined. In all cases, permeability increased from 50 to 100%. The response to vasopressin was mediated by cyclic adenosine monophosphate (cAMP), and was generally not altered by phloretin, an agent that inhibits amide movement through the amide transport pathway. Evidence that these compounds move directly through the lipid phase of the membrane was provided in studies of phenobarbital permeability at low and high luminal pH. We would conclude from these studies that the effect of vasopressin on the luminal cell membrane is a widespread one, modifying both lipid components and components involved in amide, sodium and water transport. This may be of importance in the renal tubular reabsorption of many drugs, including barbiturates, glutethimide and antibiotics.
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PMID:Vasopressin-stimulated movement of drugs and uric acid across the toad urinary bladder. 0 5

A) The proximal nephron and perinatal regulation of extracellular volume. 1. The glomerular capillary permeability coefficient (Kf) changes mainly because of an increasing capillary hydraulic conductance (Lp) within the autoregulatory range of renal perfusion pressure. 2. Proximal tubule hydrostatic hydraulic conductance and response to transmural protein concentration gradients is high during perinatal adaptation. 3. Proximal tubule paracellular shunt pathways are more important for absorption during differentiation than at maturity. 4. Basolateral membrane area of the single epithelial segment (10(-6) micron2 mm-1) increases and the typical basal labyrinth architecture develops. 5. The activity of the transport enzyme Na-K-ATPase increases in parallel to the basolateral membrane area to result in a constant number of enzyme sites during normal ontogeny. B) The distal nephron and perinatal regulation of extracellular osmotic activity. 6. Inner medullary urea content increases at osmotic equilibrium between interstitium and collecting duct. 7. The loop of Henle gradually dilutes the isotonic luminal fluid in the course of perinatal differentiation. 8. The thick ascending segment of the loop of Henle differentiates its anisotonic transport by increasing the Na-Chloride transport at constant hydraulic conductivity. 9. Ultrastructure and N-A-K-ATPase activity of the diluting segment (TAL) change greatly during ontogeny. 10. The centrifugal pattern of renal maturation from the juxtamedullary towards the superficial cortical layers leads to an intracortical profile of structure and function.
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PMID:Nephron function and perinatal homeostasis. 15 Feb 48

Vasopressin increases the permeability of the total urinary bladder, an analogue of the mammalian renal collecting duct, to water and small solutes, especially the amide urea. We have observed that three general anesthetic agents of clinical importance, the gases methoxyflurane and halothane and the ultrashortacting barbiturate methohexital, reversibly inhibit vasopressin-stimulated water flow, but do not depress permeability to urea, or the the lipophilic solute diphenylhydantoin. In contrast to their effects in vasopressin-treated bladders, the anesthetics do not inhibit cyclic AMP-stimulated water flow, consistent with an effect on vasopressin-responsive adenylate cyclase. The selectivity of the anesthetic-induced depression of water flow suggests that separate adenylate cyclases and cyclic AMP pools may exist for control of water and urea permeabilities in to toad bladder. Furthermore, theophylline's usual stimulatory effect on water flow, but not its effect on urea permeability, was entirely abolished in methoxyflurane-treated bladders, suggesting that separate phosphodiesterases that control water and urea permeabilities are present as well. We conclude that the majority of water and urea transport takes place via separate pathways across the rate-limiting luminal membrane of the bladder cell, and that separate vasopressin-responsive cellular pools of cyclic AMP appear to control permeability to water and to urea.
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PMID:Selective inhibition of osmotic water flow by general anesthetics to toad urinary bladder. 18 13

A mathematical model of the nephron was developed by writing a set of material balance equations for the flow of urea, salt and water along the foregoing study and are taken here as a basis, in particular the model configuration of the collecting duct system. The stimulation of the model equatentration profiles which at the ends of the several tubular sections were consistent with the values observed in experimental investigations.e medullary interstitial solute concentration profiles are taken to increase linearly in outer and inner zone. The several transeptithelial fluxes are driven by diffusion, osmosis, solvent drag and active transport. The development of osmotic gradient in the inner medulla is taken here to be caused by active secretion of salt into the descending LImb of Henle's loop. The parameters in the flux equations for all parts of the nephron and the concentration values at the end of each tubular section are determined by collecting and averaging the values given in literature and by extrapolating the measurement data. The simulation of the model equations with these averaged parameters resulted in concentration profiles which at the ends of the several tubular sections were consistent with the values observed in experimental investigations.
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PMID:A functional model of the rat kidney. 42 7

After a short review of the functional anatomy of the kidney, we express the usual hypotheses about the phenomena of reabsorption and filtration in the loop of Henle and the collecting duct. Starting from these hypotheses and the laws of biophysics, we formulate the equations of the model. This model accounts for the great increase in concentration of electrolyte and urea in the loop of Henle, the collecting duct and the interstitium, as we "go down" from the outer medullary area towards the inner areas, the active transportation of sodium in the loop of Henle being limited to the thick ascending limb.
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PMID:[Model of the function of the nephron]. 51 80

The renal reabsorption of water independent of solute is the result of the coordinated function of the collecting duct and the ascending limb of the loop of Henle. The unique juxtaposition of the ascending and descending portions of the loop of Henle and of the vasa recta permits the function of a counter-current multiplier system in which water is removed from the tubular lumen and reabsorbed into the circulation. The driving force for reabsorption is the osmotic gradient in the renal medulla which is dependent, in part, on chloride (followed by sodium) pumping from the thick ascending loop of Henle. Urea trapping is also thought to play an important role in the generation of a hypertonic medullary interstitium. Arginine vasopressin (AVP) acts by binding to receptors on the cell membrane and activating adenylate cyclase. This, inturn, results in the intracellular accumulation of cyclic adenosine monophosphate (AMP) which in some fashion abruptly increases the water permeability of the luminal membrane of cells in the collecting duct. As a consequence, water flows along an osmotic gradient out of the tubular lumen into the medullary interstitium. Diabetes insipidus is the clinical condition associated with either a deficiency of or a resistance to AVP. Central diabetes insipidus is due to diminished release of AVP following damage to either the neurosecretory nuclei or the pituitary stalk. Possible causes include idiopathic, familial, trauma, tumor, infection or vascular lesions. Patients present with polyuria, usually beginning over a period of a few days. The diagnosis is made by showing that urinary concentration is impaired after water restriction but that there is a good response to exogenous vasopressin therapy. Nephrogenic diabetes insipidus can be identified by a patient's lack of response to AVP. Nephrogenic diabetes insipidus is caused by a familial defect, although milder forms can be acquired as a result of various forms of renal disease. Central diabetes insipidus is eminently responsive to replacement therapy, particularly with dDAVP, a long lasting analogue of AVP. Nephrogenic diabetes insipidus is best treated with a combination of thiazide diuretics as well as a diet low in sodium and protein.
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PMID:The clinical physiology of water metabolism. Part II: Renal mechanisms for urinary concentration; diabetes insipidus. 54 67

1. The diffusional permeabilities of collecting duct membranes to THO, 14C-urea and 22Na+ have been measured at different concentrations of urea, NaCl and mannitol. 2. In the absence of urea in perfusate and bath or in its presence in low concentrations, the diffusional permeability to urea was 2.0 (s.e.m. = 0.15, n = 58) micrometer s-1, compared with 0.87 (s.e.m. = 0.06, n = 29) microgram s-1 when 200 mmol/l urea was present. The permeability of the collecting ducts to THO or Na+ was not affected by the different urea concentrations. 3. High concentrations of sodium chloride increased the diffusional permeability of collecting ducts to water and urea but did not affect the diffusional permeability of the collecting duct to Na+. 4. Mannitol had effects similar to those of sodium chloride. 5. In all media tested there was an increase in THO and urea permeability when supramaximal amounts of antidiuretic hormone were added. The increases in the various media for each substance were similar, despite widely different starting permeabilities. 6. The results suggest that solutes and water move across collecting duct epithelium by several pathways that respond differently to various stimuli.
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PMID:The effects of sodium chloride, urea and mannitol on the permeability in vitro fo rat papillary collecting ducts to THO, 14C-urea and 22Na. 58 72

The effect of tubular obstruction on renal function has been understood poorly at the tubular level and from the clinical standpoint. In our review the evidence for a direct influence of hydrostatic pressure on tubular transport and glomerular filtration is examined. The data generated to date indicate a direct influence of hydrostatic pressure on tubular transport only at the level of the distal convoluted tubule and collecting duct. With respect to glomerular filtration increased tubular pressure reduces the net driving force for filtration and reduces glomerular filtration rate in the absence of a compensatory increase in glomerular hydrostatic pressure. We next review physiological data concerning the mechanism of post-obstructive diuresis. Available information suggests 4 factors that play a significant role in the clinical syndrome of post-obstructive diuresis: 1) medullo-papillary washout, 2) decreased fractional and absolute salt and water reabsorption in the collecting duct, presumably secondary to direct influence of hydrostatic pressure on transport mechanisms, 3) osmotic diuresis secondary to retention of urea and other osmotic solutes during the period of obstruction and 4) prior salt and water administration in the absence of excretion, resulting in extracellular fluid volume expansion.
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PMID:The influence of increased tubular hydrostatic pressure on renal function. 77 39

Thirty minutes after indomethacin (10 mg/kg, iv), a prostaglandin synthesis inhibitor, had been given to 10 rats, the Na concentration in renal papilla averaged 349 mEq/kg H2O, whereas it averaged only 181 in 14 "non-indomethacin" control rats (P less than 0.0001). Papillary plasma flow was closely similar in both groups. In a subsequent study, eight "indomethacin" rats had the same papillary flow as seven non-indomethacin rats but had a papillary Na concentration of 358 vs. 185 in the non-indomethacin controls (P less than 0.0001). In nine more rats, indomethacin increased Cl concentration in papillas by 66% (P less than 0.0001), while Na concentration increased 60% (P less than 0.0001). In eight other rats, micropuncture indicated that indomethacin does not greatly alter delivery of fluid out of late proximal tubule. Meclofenamate, another inhibitor, increased papillary Na just as much as indomethacin. Papillary urea is not changed with indomethacin. Thus, papillary Na concentration was almost twice as high in indomethacin rats, despite similar papillary plasma flow and late proximal flow. Apparently, inhibiting prostaglandin synthesis is associated with either a great increase in Na or Cl "pumping" or a great decrease in Na or Cl "leak" in either collecting duct or ascending limb, or in both. The collecting duct and papillary interstitial cells both synthesize prostaglandins, which seem to have a profound effect on medullary net Na transport.
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PMID:Evidence that prostaglandin synthesis inhibitors increase the concentration of sodium and chloride in rat renal medulla. 87 Feb 22

1. Antidiuretic hormone (ADH) was infused into normal male rats at a rate of 60 muu./min. 100 g body wt., to maintain an effectively constant maximal circulating level. Four groups of rats were used; they were water-loaded by receiving together with the ADH, I.V. infusions of hypotonic dextrose (2.5 g/100 ml.) at different rates (1.0, 4.5, 9.0 and 12 ml./hr, respectively), over an infusion period of 4 hr.2. Urine flow rate increased in all groups, the rate and extent of the increase being related to the volume rate of infusion. The differences in urine flow rates between the four groups were due almost entirely to increases in free water clearance, with no consistent differences in osmolal clearance between the groups. At the end of the 4 hr infusion period, osmolal clearances were closely similar in the four groups.3. Papillary and medullary tissue solute concentrations were progressively reduced at the higher rates of infusion. The changes were due to small increases in the water content, together with a profound decrease in urea concentration and a smaller decrease in sodium concentration. However, papillary osmolality was consistently higher than urine osmolality at the three highest rates of dextrose infusion.4. As urine flow rate increased, there was a progressive reduction in the degree of osmotic equilibration between the final urine and the papillary tip. For urea, however, the degree of equilibration remained high.5. It is concluded that, in the rat, the rate of flow per se, along the collecting duct, is an important determinant of final urine concentration; even if there is an osmotic driving force for water re-absorption in the renal medulla, and the collecting duct walls are permeable to water, osmotic equilibration is restricted by tubular flow rate.
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PMID:Collecting duct dlow rate as a determinant of equilibration between urine and renal papilla in the rat in the presence of a maximal antidiuretic hormone concentration. 90 5


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