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)

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

Previous studies have suggested the presence of an H(+)-K(+)-ATPase in rat cortical and medullary intercalated cells with similar properties to the gastric proton pump. The purpose of this study was to determine the functional contribution of an H(+)-K(+)-adenosinetriphosphatase(ATPase) to total CO2 (tCO2) transport along the rat collecting duct. After baseline determination of tCO2 transport in isolated perfused collecting duct segments, Sch 28080 (10 microM) was added to either the perfusate or bath. When Sch 28080 was added to the perfusate, there was no effect in the cortical collecting duct (CCD, 20.8 +/- 6.7 vs. 25.3 + 3.0 pmol.mm-1.min-1), but a marked decrease in tCO2 absorption was effected in both the outer medullary (OMCD, 37.6 + 6.2 vs. 10.7 +/- 4.1 pmol.mm-1.min-1) and initial inner medullary collecting duct (IMCD1, 34.4 +/- 8.1 vs. 16.2 +/- 5.6 pmol.mm-1.min-1). In the CCD from rats with acute alkalosis in vivo, Sch 28080 added to the bath inhibited tCO2 secretion in the CCD (-17.1 +/- 4.4 vs 3.5 + 3.3 pmol.mm-1.min-1). These findings suggest that 1) H(+)-K(+)-ATPase is important in tCO2 absorption in the OMCD and IMCD1 and in tCO2 secretion in the CCD, 2) HCO3(-)-absorbing intercalated cells differ functionally in the cortex and medulla, 3) HCO3- secretion is not the reverse process of HCO3- absorption in the CCD, and 4) H(+)-K(+)-ATPase is important in distal acidification under normal and altered acid-base conditions.
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PMID:H(+)-K(+)-ATPase activity in rat collecting duct segments. 131 8

To examine the mechanism by which mineralocorticoids regulate HCO3- absorption in the rabbit inner stripe of the outer medullary collecting duct, we microfluorometrically measured intracellular pH (pHi) in in vitro perfused tubules using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) assaying the apical and basolateral membrane H+/OH-/HCO3- transport processes in three groups of animals: those receiving chronic in vivo DOCA treatment (5 mg/kg per d x 2 wk); those with surgical adrenalectomy (ADX, [chronic x 2 wk]) on glucocorticoid replacement; and controls. Baseline pHi was not different in the three groups. Cellular volume (vol/mm) was increased 38% in DOCA tubules versus controls, but unchanged in ADX tubules versus controls. Buffer capacities (BT) were not different in the three groups. Apical membrane H+ pump activity, assayed as the Na(+)-independent pHi recovery from an acid load (NH3/NH4+ prepulse) and expressed as JH (dpHi/dt.vol/mm.BT) was increased 76% in DOCA tubules versus controls, and decreased 56% in ADX tubules versus controls. Basolateral membrane Cl-/HCO3- exchange activity assayed as the pHi response to basolateral Cl- addition was increased 73% in DOCA tubules versus controls, and decreased 44% in ADX tubules versus controls. When examined as a function of varying [Cl-], the Vmax of Cl-/HCO3- exchange activity was significantly increased in DOCA tubules (control, 72.7 +/- 15.7 pmol.mm-1.min-1 vs DOCA, 132.3 +/- 22.5 pmol.mm-1.min-1, P less than 0.02), while the K1/2 for Cl- was unchanged. Basolateral membrane Na+/H+ antiporter activity assayed as the Na(+)-dependent pHi recovery from an acid load was not changed in chronic DOCA tubules versus controls. In conclusion, the apical membrane H+ pump and basolateral membrane Cl-/HCO3- exchanger of the rabbit OMCDi are regulated in parallel without chronic alterations in pHi under the conditions of mineralocorticoid excess and deficiency. The parallel changes in these transporters accounts for the alterations in OMCDi HCO3- absorption seen under these conditions.
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PMID:Mineralocorticoid modulation of apical and basolateral membrane H+/OH-/HCO3- transport processes in the rabbit inner stripe of outer medullary collecting duct. 132 41

Resistance to the hydrosmotic effects of vasopressin has been described in K depletion. It is not clear whether other effects of vasopressin, notably its effects on the Na-K pump in the collecting duct, are similarly affected. Adrenalectomized male Sprague-Dawley rats were allocated to either a normal K (NK) or low-K (LK) diet. Na-K pump activity (pmol.mm-1.h-1) in cortical collecting duct (CCD) and medullary collecting duct (MCD) was determined at 21 days after allocation to the dietary groups before and after exogenous vasopressin (0.1 U twice daily for 3 days). In animals on NK diet, vasopressin (AVP) led to a doubling of Na-K pump activity in the CCD from 502 +/- 47 to 1,144 +/- 41 pmol.mm-1.h-1 (P < 0.01). In K-depleted animals, which had a higher baseline Na-K pump activity, an increase was also observed from 1,056 +/- 97 to 1,239 +/- 65 pmol.mm-1.h-1 (P < 0.05), but this increase was quantitatively less, with the change being 183 vs. 642 pmol.mm-1.h-1 in K-replete rats. The findings in the MCD were similar; in rats on a NK diet, AVP led to a significant increase in Na-K pump activity from 498 +/- 29 to 830 +/- 28 pmol.mm-1.h-1 (P < 0.01). With K depletion, this directional change was preserved, increasing from 1,380 +/- 49 to 1,556 +/- 45 pmol.mm-1.h-1 (P < 0.05), but was quantitatively less than in K-replete rats, the change being 176 vs. 332 pmol.mm-1.h-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin resistance in potassium depletion: role of Na-K pump. 132 58

We measured fluoride flux (JF; pmol.min-1.mm-1) in the isolated rabbit cortical collecting duct (CCD) to investigate the determining factors of JF. The perfusate contained 100 microM fluoride and the bath was fluoride-free. Osmotically-induced lumen-to-bath water flux did not affect JF. When perfusate pH was reduced from 7.4 to 6.1 and from 6.1 to 5.0, JF increased from 0.008 +/- 0.002 to 0.027 +/- 0.007 (P less than 0.01) and from 0.018 +/- 0.003 to 0.040 +/- 0.005 (P less than 0.01), respectively. Acetazolamide at 10(-4) M in the bath reduced JF slightly though not statistically. The anion-transport inhibitor, 4,4'-diisothiocyanato-stilbene-2,2'-disulfonic acid (DIDS), at 10(-4) M in the perfusate did not affect JF. Substitution of luminal chloride with gluconate failed to affect JF in tubules from normal rabbits or from rabbits treated with deoxycorticosterone which stimulates chloride-bicarbonate exchange in the CCD. JF showed no correlation with transepithelial voltage which ranged from +4 to -104 mV. We conclude that the luminal pH represents the primary determining factor influencing JF in the rabbit CCD, and fluoride does not use a chloride-mediated or a DIDS-inhibitory transport pathway.
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PMID:Fluoride flux in the rabbit CCD: a pH-dependent event. 155 7

The mechanism by which prostaglandin E2 (PGE2) inhibits sodium absorption (JNa) in the rabbit cortical collecting duct (CCD) was explored. PGE2 activates at least three signaling mechanisms in the CCD: (a) by itself PGE2 increases cAMP generation (b) PGE2 also inhibits vasopressin-stimulated cAMP accumulation, and (c) PGE2 raises intracellular calcium([Ca++]i). We tested the contribution of these signaling pathways to PGE2's effect on Na+ absorption, measuring 22Na flux (JNa) and [Ca++]i (using fura-2) in microperfused rabbit CCDs. In control studies PGE2 reduced JNa from 28.2 +/- 3.4 to 15.6 +/- 2.6 pmol.mm-1.min-1. Lowering bath calcium from 2.4 to 45 nM did not by itself alter JNa but in this setting PGE2 failed to inhibit JNa (28.6 +/- 5.4 to 38.5 +/- 4.0). In separate tubules, PGE2 raised [Ca++]i in a spike-like fashion followed by a sustained elevation. However, in 45 nM bath Ca++, PGE2 failed to produce a sustained [Ca++]i elevation. While pretreatment of CCDs with pertussis toxin blocked PGE2 inhibition of vasopressin-stimulated water permeability, it did not block the effect of PGE2 on JNa. To see if cAMP generation contributes to the effect of PGE2 on JNa, we tested the effect of exogenous cAMP, (8-chlorophenylthio(CPT)cAMP) on JNa. 0.1 mM 8-CPTcAMP reduced JNa from 35.75 +/- 2.3 to 21.6 +/- 2.2. However, the addition of PGE2 further blunted JNa to 15.9 +/- 1.3. In CCDs pretreated with indomethacin, 8-CPTcAMP did not significantly decrease JNa 33.6 +/- 2.8 vs. 28.4 +/- 2. However, superimposed PGE2 reduced JNa to 19.0 +/- 3.0. We conclude that PGE2 inhibits sodium transport predominantly by increasing intracellular calcium. This action is not mediated by a pertussis toxin-sensitive G protein. Finally, cAMP, through a cyclooxygenase-dependent mechanism, also inhibits CCD JNa and may contribute to the effects of PGE2 on JNa in the rabbit CCD.
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PMID:Prostaglandin E2 inhibits sodium transport in rabbit cortical collecting duct by increasing intracellular calcium. 164 47

Distal nephron segments are heterogenous with respect to adenylate cyclase responses to stimulation with parathyroid hormone (PTH) or calcitonin (CT). We examined effects of these hormones and of 8-(p-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate (CPTcAMP) on net Ca absorption (Jnet Ca2+, pmol.min-1.mm-1) in rabbit distal nephron segments by in vitro microperfusion technique. We studied three segments, including distal convoluted tubule (DCT), connecting tubule (CNT), and cortical collecting duct (CCD). PTH (1 nM) in bath significantly increased Jnet Ca2+ from 2.28 +/- 0.35 to 9.44 +/- 1.13 in CNT, but did not affect Jnet Ca2+ in DCT or CCD. CT (1 nM) in bath significantly increased Jnet Ca2+ from 1.58 +/- 0.29 to 4.45 +/- 1.01 in DCT, whereas it did not affect Jnet Ca2+ either in CNT or in CCD. CPTcAMP (30 microM) in bath significantly increased Jnet Ca2+ from 2.29 +/- 0.42 to 3.97 +/- 0.43 in DCT and from 2.43 +/- 0.18 to 5.83 +/- 0.37 in CNT, but it did not affect Jnet Ca2+ in CCD. When Na+ was removed from bathing fluid or when 0.1 mM ouabain was added to bath, Jnet Ca2+ in both DCT and CNT significantly decreased. Furthermore, stimulatory effects of PTH and CT on Ca2+ absorption in the respective segments were abolished under these conditions. These results suggest that PTH and CT increase Ca2+ absorption in CNT and DCT, respectively, through cAMP-mediated mechanisms. Presence of a basolateral Na(+)-Ca2+ exchange process seems to be a prerequisite for effects of these hormones. However, exact intracellular mechanisms remain uncertain.
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PMID:Effects of PTH, calcitonin, and cAMP on calcium transport in rabbit distal nephron segments. 169 36

Insulin is known to play an important role in the regulation of extrarenal K homeostasis. Previous clearance studies have shown that insulin decreases urinary K excretion, but the responsible nephron segments have not been identified. In this microperfusion study, in vitro, the effect of insulin on K transport in the cortical collecting duct (CCD), which is thought to be an important segment for regulation of the final urinary K excretion, was investigated. Basolateral insulin (10(-6) M) significantly inhibited net K secretion by 20% (mean JK = -26.2 +/- 4.2 peq.mm-1.min-1 for controls compared with -21.1 +/- 3.4 with insulin, P less than 0.001) and depolarized the transepithelial voltage (VT, from -14.6 +/- 3.5 to -10.8 +/- 3.5 mV, P less than 0.005), recovery did not occur over 60 min. Insulin (10(-11)-10(-5) M) depressed K secretion and depolarized the VT in a concentration-dependent manner. The half-maximal concentration was 5 x 10(-10) M, which is within the physiological range of plasma insulin concentration. In tubules of deoxycorticosterone acetate-treated rabbits, insulin also produced a significant fall in K secretion (from -43.4 +/- 7.5 to -36.1 +/- 5.7 peq.mm-1.min-1, P less than 0.05). Although luminal Ba (2 mM) decreased K secretion (from -14.4 +/- 2.9 to -7.0 +/- 1.7 peq.mm-1.min-1), basolateral insulin (10(-6) M) inhibited K secretion further (to -4.7 +/- 1.3 peq.mm-1.min-1, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of insulin on potassium secretion in rabbit cortical collecting ducts. 173 94

The mechanism of compensatory adaptation and hypertrophy of the cortical collecting duct (CCD) was studied by in vitro microperfusion technique after surgical loss of functioning nephrons in the rabbit. Sodium transport was increased at 1 wk (lumen-to-bath sodium transport of 127 +2- 9 vs. 61 +/- 11 pmol.mm-1.min-1 in sham-operated animals, P less than 0.01) and 3 wk (111 +/- 19 vs. 54 +/- 7 pmol.mm-1.min-1, P less than 0.05) but not 16 h (81 +/- 13 vs. 78 +/- 8 pmol.mm-1.min-1) after loss of renal mass. The functional adaptation was accompanied by an increase in the size of the CCD. A rise in plasma aldosterone levels preceded and accompanied the increased sodium transport rate. Adrenalectomy at the time of reduction of renal mass totally prevented the development of both hypertrophy and sodium transport adaptation (sodium transport 15 +/- 8 pmol.mm-1.min-1). When adrenalectomy was combined with clamping the plasma aldosterone level in the nonstressed physiological range, compensatory hypertrophy and adaptation also failed to develop (sodium transport, 66 +/- 10 pmol.mm-1.min-1), but with high-dose aldosterone replacement both the hypertrophy and adaptation of sodium transport (130 +/- 23 pmol.mm-1.min-1) were restored. The results document the importance of increased mineralocorticoid activity in the development of compensatory hypertrophy and adaptation of sodium transport in rabbit CCD after loss of renal mass.
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PMID:Role of mineralocorticoids in adaptation of rabbit cortical collecting duct after loss of renal mass. 205 2

Previous studies in chloride-depletion metabolic alkalosis (CDA) generated by intraperitoneal dialysis have suggested major alterations in chloride and bicarbonate transport beyond the distal convoluted tubule. To investigate the possible role of the cortical collecting duct (CCD) in the pathophysiology of CDA, isolated CCD segments were perfused in vitro from either control (CON) rats dialyzed against Ringer-bicarbonate or those made alkalotic by peritoneal dialysis with 0.15 M NaHCO3. Tubules from CDA animals secreted CO2 for greater than or equal to 3 h after dissection (-22.4 +/- 7.2 pmol.mm-1.min-1) compared with CON tubules that absorbed CO2 (18.3 +/- 4.2 pmol.mm-1.min-1). Replacement of luminal chloride with gluconate in the perfusate abolished net total CO2 (tCO2) secretion in tubules from CDA animals (from -21.5 +/- 4.5 to -2.7 +/- 2.3 pmol.mm-1.min-1) but did not alter net tCO2 absorption in tubules from CON animals. In contrast, removal of bath chloride increased net tCO2 secretion (-12.1 +/- 2.9 to -26.1 +/- 3.6 pmol.mm-1.min-1) in CDA tubules, whereas net tCO2 flux was altered from absorption to secretion in CON tubules (15.5 +/- 4.0 to -13.6 +/- 9.2 pmol.mm-1.min-1). These results demonstrate that 1) CDA generated in vivo within 45 min results in stable net tCO2 secretion in vitro up to 240 min in the CCD; 2) luminal chloride is necessary for tCO2 secretion; 3) the shift of net tCO2 flux from absorption to secretion in CON tubules in vitro was not sustained in contrast to CDA tubules.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Total CO2 transport in rat cortical collecting duct in chloride-depletion alkalosis. 210 36


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