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R Quigley

Publications and source records attributed to R Quigley.

At least 37 records · Page 2Linked to original sources

Extubation failure due to post-extubation stridor is better correlated with neurologic impairment than with upper airway lesions in critically ill pediatric patients.

The incidence of post-extubation stridor (PES) in a pediatric intensive care unit (PICU) and the need for reintubation is not known. Predictors of success on a subsequent extubation attempt and the efficacy of dexamethasone treatment prior to a subsequent extubation attempt are not established. In a prospective randomized double blind-controlled study in two PICU's in a university children's hospital setting, of 5,566 admissions over 35-months, we identified 32 patients who failed primary extubation and were reintubated for PES. Twenty-six patients were enrolled in the study and three subsequently excluded. Twelve were randomized to receive dexamethasone and 11 received sodium chloride placebo. Fifteen patients succeeded study extubation and eight failed. Of those receiving dexamethasone, nine patients succeeded and three failed. Of those receiving placebo, six patients succeeded and five failed. There was a poor correlation between anatomical abnormalities of the airway and failure of study extubation. Extubation failure was better correlated with neurologic impairment in the patients. We present a stridor score and demonstrate that it is an excellent predictor of success versus failure for the study extubation. Dexamethasone pre-treatment did not reduce stridor score. We are unable to conclude if dexamethasone pre-treatment reduces extubation failure. We speculate that neurologic impairment leads to extubation failure in critically ill pediatric patients.

Adrenal Cortex Hormones↗

Maturational changes in rabbit renal cortical phospholipase A2 activity.

Several studies have demonstrated that the neonatal kidney has a markedly attenuated response to parathyroid hormone (PTH); however, the cause for this blunted response is unknown. PTH stimulated cAMP production by 215 +/- 18% in neonatal proximal tubule suspensions compared to a 35 +/- 7% increase in adult proximal tubules. Thus, neonatal proximal tubules have functioning PTH receptors and a greater adenylate cyclase response than the adult segment. In adult proximal tubules, PTH stimulates phospholipase A2 (PLA2) activity and the inhibition of Na,K-ATPase activity by PTH is blocked by inhibitors of PLA2. We examined whether maturational changes in renal cortical activity could play a role in the attenuated response to PTH in the neonatal proximal tubule. Compared to adults, neonates had a lower renal cortical cytosolic PLA2 (cPLA2) activity, assessed as the release of 14C-arachidonic acid (AA) from labeled phosphatidyl choline (0.44 +/- 0.10 vs. 0.74 +/- 0.06% 14C-AA released/min/mg protein, P < 0.05) and microsomal PLA2 activity (0.32 +/- 0.03 vs. 1.20 +/- 0.13% 14C-AA released/min/mg protein, P < 0.001). The protein abundance of cPLA2 was not different between the neonatal and adult renal cortex as assessed by immunoblot assay. Thus, the difference in activities must be due to a difference in regulation of cPLA2. Annexin 1 (lipocortin 1) has been shown to inhibit PLA2 activity by binding to phospholipid substrate. Annexin 1 protein abundance was higher in neonatal than in adult renal cortex (P < 0.001). Thus, the lower activity of PLA2 in the neonatal tubules may be due in part to higher expression of annexin 1. PLA2 activation by PTH, -8-bromo-cAMP and PMA was assessed as 3H-AA release from prelabeled suspensions of neonatal and adult proximal tubules. PTH (10(-7) M), 8-bromo-cAMP (10(-4) M) and PMA (5 x 10(-8) M) significantly increased 3H-AA release from adult tubules (P < 0.05) but had no effect on neonatal tubules (P = NS). Thus, PTH, 8-bromo-cAMP and PMA stimulated PLA2 in adult but not neonatal proximal tubules. In conclusion, the maturational changes in renal cortical PLA2 activity may be a factor in the blunted response of neonatal proximal tubules to PTH.

8-Bromo Cyclic Adenosine Monophosphate↗

Effect of luminal angiotensin II on rabbit proximal convoluted tubule bicarbonate absorption.

The present in vitro microperfusion study examined the effect of luminal angiotensin II on proximal convoluted tubule (PCT) volume absorption and bicarbonate transport. Neither 10(-11) M, 10(-10) M, nor 2 x 10(-8) M luminal angiotensin II significantly affected PCT transport. When tubules were first perfused with enalaprilat to inhibit endogenous angiotensin II production, addition of 10(-10) M luminal angiotensin II increased volume absorption (0.72 +/- 0.08 vs. 0.86 +/- 0.07 nl x mm(-1) xmin(-1), P < 0.01) and bicarbonate transport (52.3 +/- 3.7 vs. 67.9 +/- 4.2 pmol x mm(-1) min(-1), P < 0.01). Addition of 10(-6) M losartan, an AT1 inhibitor, to the luminal perfusate inhibited volume absorption (0.95 +/- 0.14 vs. 0.72 +/- 0.11 nl x mm(-1) x min(-1), P < 0.05) and bicarbonate transport (65.0 +/- 7.3 vs. 54.7 +/- 9.2 pmol x mm(-1) x min(-1), P < 0.05). Addition of 10(-4) M luminal PD-123319, an AT2 inhibitor, was without effect. In tubules perfused with 10(-4) M luminal enalaprilat and 10(-4) M luminal PD-123319, addition of 10(-10) M luminal angiotensin II in the experimental period resulted in a stimulation in volume absorption (0.61 +/- 0.08 vs. 0.81 +/- 0.10 nl x mm(-1) x min(-1), P < 0.01) and bicarbonate transport (49.9 +/- 6.3 vs. 77.4 +/- 14.3 pmol x mm(-1) x min(-1), P < 0.01). In tubules perfused with 10(-6) M losartan and 10(-4) M enalaprilat, addition of luminal 10(-10) M angiotensin II resulted in no change in transport. These data are consistent with endogenous angiotensin II affecting PCT bicarbonate transport in vitro via luminal AT1 receptors.

Absorption↗

Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent.

Cystic fibrosis (CF) is an exocrine disease affecting multiple organ systems. Patients with CF usually present with respiratory or gastrointestinal abnormalities. This study presents a case of a previously healthy 17-yr-old man who was diagnosed with CF after presenting with metabolic alkalosis and hypokalemia. The defect associated with CF is in the cystic fibrosis transmembrane regulator (CFTR), which acts primarily as a chloride channel. Partially functional CFTR may be associated with less severe pulmonary and gastrointestinal manifestations, as in the case presented. Dysfunctional CFTR in the sweat ducts of CF patients are responsible for excessive chloride and sodium losses, especially in warm weather. Hypokalemia seen with heat stress is secondary to sweat as well as renal potassium wasting. Metabolic alkalosis is maintained by the excessive sweat sodium chloride losses which leads to extracellular fluid (ECF) volume contraction and chloride depletion. Generation of alkalosis may be related to dysfunctional CFTR in the kidney, but is most likely secondary to hypokalemia with ECF volume contraction. Finally, one must consider CF when confronted with hypokalemia and alkalosis in a previously healthy patient.

Acidosis↗

Developmental changes in rabbit juxtamedullary proximal convoluted tubule water permeability.

The mammalian proximal tubule reabsorbs the bulk of the glomerular filtrate in a nearly isosmotic fashion due to the high osmotic water permeability (Pf) of this segment. Although the characteristics of proximal tubule water transport have been studied in the adult proximal tubule, little is known about the neonatal segment. The present study directly measured the Pf and diffusional water permeability (PDW) of neonatal (10 +/- 2 day old) and adult rabbit juxtamedullary proximal convoluted tubules (PCT) using in vitro microperfusion. The Pf of neonatal juxtamedullary PCT was greater than the Pf of adult juxtamedullary PCT. In contrast, the PDW was not different between the two groups. The Pf and PDW values of both neonatal and adult tubules were inhibited to the same degree by p-chloromercuribenzene sulfonate and had identical activation energies. The transepithelial reflection coefficients of NaCl and NaHCO3 were also found to be similar in both the neonatal and adult proximal tubules. Thus neonatal and adult juxtamedullary PCT have many characteristics of water transport that are identical; however, neonatal Pf is three to five times that of the adult value. This difference in Pf with identical PDW values may give an insight into the transepithelial pathway for water movement in the neonatal tubule.

Aging↗

Maturation of rabbit proximal convoluted tubule chloride permeability.

Chloride transport in the rabbit proximal convoluted tubule (PCT) has components of active, transcellular, and passive, paracellular transport. The preferential reabsorption of bicarbonate and organic solutes by the early proximal tubule leaves the luminal fluid with a higher chloride concentration than that in the peritubular capillaries. Previous studies have suggested that solute permeability of the paracellular pathway may be higher in the neonatal PCT and that the neonatal proximal tubule reabsorbs solutes by passive mechanisms to a greater extent than the adult segment. A higher chloride permeability would provide a mechanism for the greater rate of passive NaCl transport by the neonatal proximal tubule. The purpose of the present in vitro microperfusion study was to directly examine the chloride permeability of neonatal and adult PCT. Superficial and juxtamedullary, neonatal and adult PCT were perfused with a high chloride perfusate without organic solutes, simulating late proximal tubular fluid, at 20 degrees C, and bathed in a serum-like albumin solution. Chloride concentrations in the perfusate and the collected fluid were measured by electrometric titration. Neonatal juxtamedullary PCT chloride permeability (PCl) was significantly lower than adult juxtamedullary PCT PCl (0.15 +/- 0.25 x 10(-5) cm/s versus 5.23 +/- 0.57 x 10(-5) cm/s, p < 0.001). The PCl of neonatal superficial PCT was not different from that of adult superficial PCT (0.81 +/- 0.48 x 10(-5) cm/s versus 0.05 +/- 0.62 x 10(-5) cm/s). Thus, there is a maturational increase in juxtamedullary PCT PCl, whereas superficial PCT PCl remains very low. The passive diffusion of chloride in neonatal PCT is extremely low and is not a mechanism to explain a higher rate of passive NaCl transport in this segment.

Animals↗

Heterogeneity of chloride/base exchange in rabbit superficial and juxtamedullary proximal convoluted tubules.

Active transcellular NaCl transport in the proximal convoluted tubule (PCT) is via apical parallel Na/H and Cl/base exchange. The mechanism of Cl/base exchange remains unclear. The present in vitro microperfusion study examined the mechanism of Cl/base exchange in superficial and juxtamedullary PCT by examining the rate of change in intracellular pH in response to luminal Cl removal. In superficial PCT the rate of Cl/base exchange was 24.0 +/- 2.3 without formate, 36.4 +/- 6.6 with 10 microM formate (P < 0.05), and 43.6 +/- 2.8 pmol.mm-1.min-1 (P < 0.001) with 1 mM luminal formate. Cl/base exchange was inhibited by luminal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) in the presence and absence of formate. In juxtamedullary PCT, Cl/base exchange was 22.2 +/- 3.8 without formate and 25.0 +/- 5.4 pmol.mm-1.min-1 in the presence of 1 mM luminal formate [P = not significant (NS)]. Cl/base exchange was inhibited by luminal DIDS in juxtamedullary PCT. The rates of Cl/base exchange in both superficial and juxtamedullary PCT were not affected by 0.1 mM acetazolamide and 2 mM cyanide and were the same in the presence and absence of HCO3/CO2, consistent with Cl/OH rather than Cl/HCO3 exchange. To examine the effect of formate on PCT transport, tubules were perfused with a high-Cl solution without organics simulating late proximal tubular fluid. In superficial PCT net volume absorption (JV) was 0.00 +/- 0.05 in the absence of formate and 0.14 +/- 0.06 nl.mm-1.min-1 in the presence of 1 mM formate (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Stimulation of proximal convoluted tubule phosphate transport by epidermal growth factor: signal transduction.

The present study investigated the signal-transduction pathway responsible for the epidermal growth factor (EGF) stimulation of phosphate transport (JPhos) in the rabbit proximal convoluted tubule (PCT). Genistein, 10(-4) M, bath and lumen, an inhibitor of EGF receptor tyrosine kinase activity, blocked the EGF effect on JPhos, consistent with a role for tyrosine kinase in the signal-transduction pathway. Both staurosporine (5 x 10(-8) M) and calphostin C (10(-8) M), inhibitors of protein kinase C, blocked the EGF stimulation of JPhos, indicating that protein kinase C is involved in EGF signaling. Intracellular calcium (Ca2+i) concentrations were measured in perfused tubules using fura PE3 to determine whether changes in Ca2+i were also part of the signaling pathway. After addition of 3 nM EGF, there was no change in Ca2+i, suggesting that stimulation of protein kinase C is not from phosphatidylinositol hydrolysis by phospholipase C-gamma. To determine whether phospholipase A2 (PLA2) is involved, the inhibitor mepacrine was used. Mepacrine (5 x 10(-5) M) had no direct effect on PCT transport but blocked the stimulatory effect of EGF on JPhos. PLA2 activity, assessed as free arachidonic acid release from proximal tubules in suspension, increased by 18.8% with 3 nM EGF. Thus the stimulation of JPhos by EGF is mediated via a signal-transduction pathway involving tyrosine kinase, protein kinase C, and PLA2.

Animals↗

Hyperphosphatemia in tumor lysis syndrome: the role of hemodialysis and continuous veno-venous hemofiltration.

We report a 4-year-old boy who developed tumor lysis syndrome complicated by severe hyperphosphatemia and acute renal failure, following chemotherapy for T-cell acute lymphoblastic leukemia. Despite successful treatment of hyperphosphatemia with hemodialysis, there was an immediate rebound in the high serum phosphorus level. The patient underwent a second treatment with hemodialysis which was then followed by continuous veno-venous hemofiltration (CVVH). CVVH maintained his serum phosphorus at a stable level until his renal function improved. CVVH can be used in conjunction with hemodialysis to successfully treat the hyperphosphatemia associated with tumor lysis syndrome.

Acute Kidney Injury↗

Effects of epidermal growth factor and transforming growth factor-alpha on rabbit proximal tubule solute transport.

The present in vitro microperfusion study examined the direct effects of epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha) on rabbit proximal convoluted tubule (PCT) solute transport. Tubules were perfused with an ultrafiltrate-like solution and bathed in an ultrafiltrate-like solution containing albumin. Albumin binding studies showed that both growth factors were highly protein bound with a free fraction of EGF of 0.31 +/- 0.04% and TGF-alpha of 1.08 +/- 0.15%. EGF at concentrations from 3 x 10(-11) M to 3 x 10(-8) M stimulated phosphate transport (JPhos) in a dose-dependent fashion but did not affect volume absorption (Jv) or bicarbonate transport (JtCO2). At 3 x 10(-7) M, EGF stimulated PCT Jv and JtCO2 in addition to the stimulation in JPhos. TGF-alpha stimulated Jv, JtCO2, and JPhos, but its effects were seen at a concentration that was 100-fold lower than that where EGF affected PCT transport. At 3 x 10(-13) M, TGF-alpha stimulated JtCO2, and at 3 x 10(-12) M, TGF-alpha also stimulated Jv and JPhos. EGF receptor downregulation with 3 x 10(-8) M EGF was able to block the effect of 3 x 10(-10) M TGF-alpha on Jv and JtCO2. Neither luminal EGF nor TGF-alpha had an effect on PCT transport. PCT bicarbonate and mannitol permeabilities were also not affected by either growth factor. These results demonstrate that EGF and TGF-alpha have direct effects on PCT solute transport.

Animals↗

Maturation of proximal tubular acidification.

Neonatal juxtamedullary proximal convoluted tubules (PCTs) transport bicarbonate at one-third the rate of adult rabbit PCTs. The lower rate of bicarbonate transport could be due to a greater permeability of the neonatal PCT to bicarbonate or to a lower rate of active bicarbonate transport. This review discusses potential factors which could result in a lower rate of bicarbonate transport by the neonatal PCT. In isolated perfused PCT, bicarbonate permeability is lower in neonatal than adult PCT, and thus it does not account for the lower rate of bicarbonate transport in neonatal PCT. In the adult PCT, apical proton secretion occurs via the Na+/H+ antiporter and H(+)-ATPase; basolateral bicarbonate exit occurs via the Na(HCO3)3 symporter. The activity of transporters can be ascertained by measuring intracellular pH with the fluorescent dye BCECF. Apical Na+/H+ antiporter, apical H(+)-ATPase and basolateral Na(HCO3)3 symporter activity are all significantly lower in neonatal PCT. The factors which stimulate PCT maturation are unknown, however glucocorticoids have been postulated to play an important role in this process. Administration of dexamethasone to pregnant does results in higher rates of PCT volume absorption, bicarbonate transport, Na+/H+ antiporter and Na(HCO3)3 symporter activities than in PCT from vehicle-treated controls. Thus, the lower rate of neonatal PCT bicarbonate transport is due to lower activities of the apical Na+/H+ antiporter, apical H(+)-ATPase and basolateral Na(HCO3)3 symporter. Glucocorticoids may be an important factor in the maturation of PCT acidification.

Animals↗

Glucocorticoids stimulate rabbit proximal convoluted tubule acidification.

Glucocorticoids have an important role in renal acidification; however, a direct effect of glucocorticoids on proximal convoluted tubule (PCT) acidification has not been directly demonstrated. In the present in vitro microperfusion study PCT from animals receiving dexamethasone (600 micrograms/kg twice daily for 2 d and 2 h before killing) had a significantly higher rate of bicarbonate absorption than did controls (92.0 +/- 13.3 vs 59.9 +/- 3.2 pmol/mm.min, P < 0.01). To examine if glucocorticoids had a direct epithelial action, dexamethasone was added to the bath of PCT perfused in vitro. After 3 h of incubation in paired experiments 10(-6) M and 10(-5) M dexamethasone resulted in an approximately 30% stimulation in the rate of bicarbonate absorption. 10(-7) M dexamethasone and 10(-6) M aldosterone had no effect on bicarbonate absorption. The stimulation of acidification by 10(-5) M dexamethasone was blocked by actinomycin D and cycloheximide. These data are consistent with a direct effect of glucocorticoids on PCT acidification, and this effect is dependent upon protein synthesis.

Aldosterone↗

Prenatal glucocorticoids stimulate neonatal juxtamedullary proximal convoluted tubule acidification.

The rate of neonatal proximal convoluted tubule (PCT) HCO3 absorption is lower than that of adult animals. The present in vitro microperfusion study examined whether prenatal dexamethasone (60 micrograms/kg daily to the doe for 3 days before delivery) would accelerate the maturation of neonatal juxtamedullary PCT acidification. Control neonates studied within 48 h of birth had a urine pH of 7.06 +/- 0.15 and a urine HCO3 concentration of 34.3 +/- 7.0 meq/l. Animals receiving dexamethasone had a urine pH of 6.47 +/- 0.11 and a urine HCO3 concentration of 10.1 +/- 4.0 meq/l, both of which were significantly lower than control (P less than 0.01). In juxtamedullary PCTs perfused in vitro, volume absorption was 0.27 +/- 0.03 nl.mm-1.min-1 in controls and 0.39 +/- 0.02 nl.mm-1.min-1 in dexamethasone-treated animals (P less than 0.05). HCO3 absorption was stimulated in the dexamethasone group (52.6 +/- 4.6 vs. 34.1 +/- 6.3 pmol.mm-1.min-1, P less than 0.05); however, glucose transport was not significantly affected (24.8 +/- 1.3 in dexamethasone vs. 21.5 +/- 3.5 pmol.mm-1.min-1 in controls). Intracellular pH was measured using 2',7'-bis(carboxyethyl)-5(6)-carboxyflourescin to examine whether prenatal dexamethasone stimulated the apical Na(+)-H+ antiporter and the basolateral Na(HCO3)3 symporter. Apical Na(+)-H+ antiporter proton flux was 108.5 +/- 14.2 pmol.mm-1.min-1 in the control group and 250.7 +/- 31.3 pmol.mm-1.min-1 in the dexamethasone group (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Role of adenosine triphosphate (ATP) and NaK ATPase in the inhibition of proximal tubule transport with intracellular cystine loading.

Cellular cystine loading with cystine dimethyl ester inhibits volume absorption, transepithelial potential difference, glucose transport, and bicarbonate transport in proximal convoluted tubules perfused in vitro. This study examined the roles of ATP and NaK ATPase in this in vitro model of the Fanconi syndrome of cystinosis. Intracellular ATP was measured using the luciferin-luciferase assay. Intracellular ATP was reduced by 60% in proximal convoluted tubules incubated with 0.5 mM cystine dimethyl ester for 15 min at 37 degrees C (P less than 0.001). Incubation of cystine loaded tubules with 1 mM exogenous ATP increased intracellular ATP to levels not significantly different than that of controls. On the other hand, Vmax NaK ATPase activity was unchanged even though the incubation times and the concentration of cystine dimethyl ester were doubled to 30 min and 1 mM, respectively. In proximal convoluted tubules perfused in vitro, 0.5 mM cystine dimethyl ester resulted in an 89% inhibition in volume absorption (0.81 +/- 0.14 to 0.09 +/- 0.09 nl/mm.min), while there was only a 45% inhibition in volume absorption (P less than 0.01) due to cellular cystine loading in the presence of 1 mM lumen and bath ATP (0.94 +/- 0.05 to 0.52 +/- 0.11 nl/mm.min). These data demonstrate that proximal tubule cellular cystine loading decreases cellular ATP concentration, but does not directly inhibit NaK ATPase activity. The inhibition in transport and decrease in intracellular ATP due to cellular cystine loading was ameliorated by exogenous ATP. These data are consistent with cellular ATP depletion playing a major role in the inhibition of proximal tubule transport due to intracellular cystine loading.

Adenosine Triphosphate↗

Effects of growth hormone and insulin-like growth factor I on rabbit proximal convoluted tubule transport.

This in vitro microperfusion study examined the effects of growth hormone and insulin-like growth factor I (IGF-I) on proximal convoluted tubule (PCT) transport. Tubules were perfused with an ultrafiltrate-like solution and bathed in a serum-like albumin solution. Neither a physiologic (5 x 10(-10) M), nor a pharmacologic (5 x 10(-8) M) dose of growth hormone had an effect on PCT phosphate or bicarbonate transport, or volume absorption. Addition of 5 x 10(-9) M and 5 x 10(-8) M IGF-I, but not 5 x 10(-10) M IGF-I, to the bathing solution resulted in an increase (12-15%) in phosphate transport, but no change in volume absorption or bicarbonate transport. Addition of IGF-I to the luminal perfusate also stimulated phosphate transport. The effect was noted at a concentration of 5 x 10(-11) M IGF-I (27% stimulation) and was maximal at a concentration of 5 x 10(-10) M IGF-I (46% stimulation). There was no effect of luminal IGF-I on volume absorption or bicarbonate transport. These data indicate that growth hormone has no direct effect on PCT transport. In the PCT, IGF-I stimulates phosphate transport specifically and acts via both basolateral and apical membranes. However, the magnitude of the maximal response to the luminal addition of IGF-I was threefold greater than that measured upon addition of the hormone to the bath, and the stimulation occurred at a 100-fold lower concentration. These data are consistent with IGF-I mediating the in vivo stimulation of phosphate transport by growth hormone.

Animals↗

The attitude of parents to the use of computer-assisted interviewing in a child psychiatry service.

Before undergoing interview, parents reported that a computer-assisted interview would lack the friendly and personal approach of one conducted by a clinician but, after completing the interview, parents showed more acceptance of the procedure. Computer-assisted interviewing has the potential to play an important role in the collection of clinically relevant information from both parents and children referred to child psychiatry services.

Attitude to Computers↗

Developmental changes in rabbit juxtamedullary proximal convoluted tubule bicarbonate permeability.

The bicarbonate transport rate in neonatal rabbit juxtamedullary proximal convoluted tubules (JMPCT) is lower than that in adults. The reduced rate of transport could be due to a decrease in active bicarbonate transport or an increase in the passive permeability of the tubule to bicarbonate. The present in vitro microperfusion study directly measured the bicarbonate permeability of neonatal and adult JMPCT. Bicarbonate permeability was measured at both slow and fast perfusion rates to simulate the neonatal and adult proximal tubule flow rates, respectively. At 38 degrees C in tubules perfused at 3 nL/min, bicarbonate permeability was 0.29 +/- 0.11 x 10(-5) cm/s in neonates and 1.70 +/- 0.49 x 10(-5) cm/s in adult PCT (p less than 0.05). At a perfusion rate of 10 nL/min, bicarbonate permeability was 0.11 +/- 0.27 x 10(-5) cm/s in neonatal PCT and 2.31 +/- 0.15 x 10(-5) cm/s in adult PCT (p less than 0.05). These results demonstrate that bicarbonate permeability in neonatal JMPCT is significantly lower than that in adult JMPCT. Thus, the lower rate of bicarbonate transport in neonatal PCT is entirely due to a lower rate of active bicarbonate transport.

Animals↗