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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 have suggested that potassium, like urea, undergoes medullary recycling. The present cortical and papillary micropuncture studies were designed to confirm the existence of medullary potassium recycling and to determine whether acute infusions of aldosterone affected this phenomenon. Thus, nephron segmental analysis of potassium and sodium transport was conducted in adrenalectomized Munich-Wistar rats and similarly prepared rats that received aldosterone acutely to achieve physiological blood levels. The clearance results demonstrated that aldosterone has an acute antinatriuretic and a kaliuretic effect, whereas the micropuncture studies demonstrated that 1) aldosterone increases potassium secretion between early and late distal tubule punctures; 2) aldosterone causes an increase in delivery of potassium to the papillary collecting duct; 3) aldosterone does not increase potassium secretion across the papillary collecting duct; and 4) aldosterone significantly increases medullary potassium recycling as evidenced by increased quantities of potassium present at the bend of the loop of Henle in response to aldosterone infusions. Thus, the studies confirm the existence of potassium recycling and suggest that this phenomenon is a feedback system that, in part, regulates urinary potassium excretion.
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PMID:Effects of aldosterone on potassium recycling in the kidney of adrenalectomized rats. 397 Feb 11

These experiments were designed to evaluate the hypothesis that K+ deficiency may be associated with decreased delivery of urea to the renal papillary collecting duct and/or decreased reabsorption of urea from the papillary collecting duct. Either of these factors would result in diminished capacity for urea recycling and might explain the mechanism of the urinary concentrating defect that is observed in K+ depletion. Munich-Wistar rats were fed 25 ml of water and 12 g of normal (CON) or K+-deficient (KD) diet each day for 21 days. Papillary collecting duct samples were obtained by micropuncture through the intact ureter. Fractional delivery of H2O to the base and tip of the papillary collecting duct was increased in KD as compared to CON rats (1.50 +/- 0.30% in KD vs 0.72 +/- 0.09% in CON at the base, P less than 0.01; and 0.55 +/- 0.08% in KD vs 0.30 +/- 0.05% in CON at the tip, P less than 0.01). However, fractional delivery of urea to the base and tip of the papillary collecting duct was not different between KD and CON rats (26.9 +/- 5.6% in KD vs 21.4 +/- 3.3% in CON at the base, P greater than 0.05; and 12.4 +/- 1.5% in KD vs 10.4 +/- 1.4% in CON at the tip, P greater than 0.05). Furthermore, reabsorption of water or urea between the base and tip of the papillary collecting duct was not decreased in KD as compared to CON rats (water reabsorption was 57.8 +/- 4.4% in KD and 55.9 +/- 5.11% in CON and urea reabsorption was 45.0 +/- 6.5% in KD and 45.9 +/- 5.4% in CON, P greater than 0.05). These results demonstrate that water reabsorption, but not urea reabsorption, is impaired in renal tubules proximal to the accessible papillary collecting duct in hydropenic rats.
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PMID:Urea reabsorption along the papillary collecting duct in potassium-deficient rats. 399 1

The analysis of the central core model of the renal medulla is extended to multisolute systems. It is shown that total solute concentration obeys the same differential equations for core and ascending limb as in a single solute system. Equations are derived for the concentration of individual solutes. Application of these equations to a two solute system shows that a central core system can concentrate with all transport being down a concentration gradient. This analysis applied to the renal medulla shows that mixing of urea from the collecting duct (CD) and salt from the loop of Henle in the central core of the inner medulla contributes to the concentration of urine during antidiuresis. It also sets criteria for completely passive function of the loop in the inner medulla, but whether these are satisfied cannot be determined from present experimental data.
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PMID:Concentrating engines and the kidney. II. Multisolute central core systems. 471 47

1. The changes in urinary and renal tissue composition in conscious rats were determined for up to 2 hr following the cessation of intravenous infusion of lysine vasopressin, LVP (at 60 muu./min. 100 g body wt. for 4(1/2) hr). A constant water load (4% body wt.) was maintained during and after lysine vasopressin infusion, by quantitative replacement of excreted water. In these circumstances, any changes in urinary and renal tissue composition are presumed to represent direct consequences of the rapid plasma and tissue clearance of lysine vasopressin.2. Urinary flow increased and osmolality decreased, rapidly, reaching stable values characteristic of sustained water diuresis after about 60 min.3. The steepness of the corticomedullary solute concentration gradients also decreased rapidly. Papillary Na and urea concentrations fell to values characteristic of sustained water diuresis in about 45 min.4. The changes in medullary composition were compounded of a moderate significant increase in water content, a moderate, significant decrease in Na content, and a profound decrease in urea content.5. In the eventual steady-state water diuresis, urinary outputs of Na and K were significantly lower, and of NH(4) significantly higher, than those observed in control experiments where LVP infusion was continued for the corresponding 2 hr.6. It is concluded that the diuresis following the cessation of LVP infusion is due not merely to reduced nephron permeability to water but also to a rapid reduction in the osmotic force responsible for water reabsorption from the collecting duct.
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PMID:Time course of changes in renal tissue and urinary composition after cessation of constant infusion of lysine vasopressin in the conscious, hydrated rat. 503 24

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.
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PMID:ostnatal development of renal function: micropuncture and clearance studies in the dog. 554 75

1. The time course and extent of changes in the composition of renal tissue slices in osmotic diuresis were determined by sacrificing groups of rats before and during the intravenous infusion of mannitol (15 g/100 ml.) for up to 7(1/2) hr.2. Very rapid changes in tissue water and solute contents occurred within 15 min, preceding the times of maximal diuresis, with little subsequent change even up to 7(1/2) hr.3. The main changes were:(a) an increase in water content in all slices, particularly the papilla; (b) a very profound decrease in papillary and medullary urea content in the first 15 min, with a small, but significant, further decrease, subsequently; (c) a small, but significant, rapid decrease in papillary sodium, and small non-significant increases in the outer medulla and cortex. Subsequent changes in any segment were small and non-significant; (d) apart from small changes in the first 15 min ammonium and potassium contents remained fairly constant.4. The rates of change in papillary and urinary urea concentrations were similar, so that after 30 min, any differences between tip and urinary concentrations were small and non-significant.5. The findings are discussed in terms of factors influencing counter-current mechanisms. It is concluded that altered medullary blood flow is mainly responsible for the rapid changes in medullary composition.6. The relation between papillary and urinary urea concentrations is explicable in terms of passive handling, with equilibration across a freely permeable collecting duct membrane.
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PMID:The time course of changes in renal tissue composition during mannitol diuresis in the rat. 571 51

To study the renal medullary transport and accumulation of urea in dogs independent of water transport, we obliterated the medullary electrolyte gradient by a sustained ethacrynic acid diuresis. Infusions of urea were also given at various rates to vary urinary urea concentration. In the steady state, the kidneys were removed, and slices were analyzed for water, urea, and electrolytes. In every experiment in 15 dogs over a range of urinary urea concentration from 19 to 230 mmoles per L and urine flow from 0.5 to 9.7 ml per minute per kidney, an intrarenal urea gradient persisted, and urinary urea concentration was always lower than papillary water urea concentration. The magnitude of this uphill urinary-papillary gradient (mean +/- SE = - 21 +/- 2.9 mmoles per L) was not affected by hemorrhagic hypotension or a nonprotein diet. In 12 additional experiments begun similarly, inhibitors were infused into one renal artery. Both iodoacetate, an inhibitor of anaerobic glycolysis, and acetamide, an analogue of urea, markedly and significantly reduced both the intrarenal urea gradient and the uphill urinary-papillary gradient. In contrast, cyanide, an inhibitor of oxidative metabolism, had no observable effect on the urea gradients. The data are best explained by postulating an active transport system for urea in the medullary collecting duct deriving its energy from anaerobic glycolysis.
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PMID:Uphill transport of urea in the dog kidney: effects of certain inhibitors. 602 74

Vasopressin affects a variety of cell systems. This review is focused on permeability changes induced by vasopressin in tight epithelia such as the collecting duct of the mammalian kidney and the skin and the bladder of anurans. These vasopressin effects are discussed with reference to current concepts and models of the microstructure of the plasma membrane. The transport of three major chemical species--Na, urea and water--is analyzed. In each instance, the hormone appears to activate selective membrane pathways situated at the rat-limiting barrier of the epithelium, i.e., the apical membrane. Available data suggest that two intra-cellular messengers -- cAMP and calcium -- plan a key role in the coupling between stimulus (receptor occupancy) and biological effect (permeability change). The enhancement of Na transport (natriferic effect) depends on the opening and/or the insertion of Na channels, the biophysical and biochemical characteristics of which have been investigated by fluctuation analysis and by means of several chemical blockers of Na transport, particularly the amiloride molecule and its congeners. Likewise, the finding of inhibitors and activators of urea transport, which do not cause any appreciable change in Na or water permeability, led to the notion of selective urea channels or pores. Finally, the enhancement of water transport (hydrosmotic effect) possibly results from the insertion in the apical membrane of water channels already present in vesicular cytoplasmic structures. The restructuring of the apical membrane underlying the transition from a low to a higher state of water permeability is very likely related to the appearance of intramembrane particle aggregates detectable with the freeze-fracture technique in epithelia exposed to vasopressin. The putative water channels (or pores) appear to be so narrow that trans-apical water movement is constrained to single-file diffusion. Recent data also suggest that, in addition to cAMP, microtubules and microfilaments, the calmodulin-Ca complex is a major element in the hydrosmotic effect of vasopressin.
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PMID:The mode of action of vasopressin: membrane microstructure and biological transport. 626 76

Micropuncture of the rat renal papilla has disclosed an outward transepithelial gradient for NaCl at the bend of Henle's thin loop and an electrical potential difference, lumen positive, in the ascending thin limb. Substantial water extraction and urea secretion occur somewhere proximal to the bend, but direct evidence for transepithelial NaCl movement across the rat descending thin limb is lacking. In the hamster, water is extracted and urea secreted, but no NaCl gradient has been found, and in Psammomys there is indirect evidence for transepithelial entry of NaCl into the descending limb. Fluid is diluted in the ascending thin limb by reabsorption of NaCl. The lack of unequivocal evidence for active NaCl reabsorption has stimulated a search for alternative mechanisms of osmotic work in the inner medulla. The collecting duct plays a crucial role by its differential reabsorption of water (primarily in the cortex) and urea (exclusively in the inner medulla) but has not yet been shown to supply useful energy to the concentrating mechanism by active sodium reabsorption. Exposure of the papillary tip by ureteral excision impairs urinary osmolality. Ureteral peristalsis normally causes intermittent flow of fluid in the collecting duct, but abolition of intermittent flow by paralysis of the ureter does not decrease urinary osmolality. Superperfusion of the exposed papilla by a urea solution prevents the decline in osmolality but the amount of urea used greatly exceeds that available from the urine. Nevertheless, it is the intactness of the ureter that is somehow essential to maximum urinary concentration, perhaps by preventing loss of solute from the papilla rather than by supplying energy.
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PMID:The renal concentrating mechanism: micropuncture studies of the renal medulla. 634 Oct 87

The role of prostaglandins in the regulation of sodium and water excretion has been widely studied, but little is known about the influence of prostaglandins (PGs) on the tubular handling of calcium, magnesium or phosphorus. Recent observations have suggested that PGE2 and vasopressin may interact and influence reabsorption of calcium and phosphorus in the cortical collecting duct. The present study investigated the effect of meclofenamate (2 mg/kg), and inhibitor of PG synthesis, on the excretion of calcium, magnesium and phosphorus. Experiments were performed in antidiuretic and water diuretic rats to examine potential PG-vasopressin interactions on the reabsorption of these ions by renal tubules. In antidiuretic rats given meclofenamate, urine osmolality increased whereas urine flow and the fractional excretion of water, urea, sodium, calcium and magnesium decreased by 30 to 50%. In water diuretic animals, urine osmolality and urea excretion were unaltered after meclofenamate administration. Fractional excretion of sodium, water, calcium and magnesium declined approximately 50% in water diuretic rats given meclofenamate. Urinary excretion of PGE2 was not significantly different in water diuretic and antidiuretic rats averaging 262 +/- 78 vs. 167 +/- 35 pg/min, respectively. Meclofenamate significantly reduced urinary excretion of PGE2 in both groups. The results indicate that renal PGs modulate renal tubular reabsorption of calcium and magnesium, as well as sodium and water.
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PMID:Prostaglandin-vasopressin interactions on the renal handling of calcium and magnesium. 658 91


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