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Sodium Transport (sodium + transport)
Selected AbstractsIntracellular pH, intrauterine growth and the insulin resistance syndromeCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2001Jonathan H. Pinkney Defects of both sodium,hydrogen exchange (NHE) and sodium,lithium countertransport (SLC) have been described in subjects at increased risk of coronary heart disease (CHD). Sodium transport is linked to the regulation of cell volume, intracellular pH and cell growth, which may explain aspects of this association. However, impaired growth in early life is also linked to adult CHD, and ,programmed' alterations of cell behaviour are postulated to be responsible for this. In this study, therefore, we examined whether NHE or SLC in adults are predicted by anthropometric measures at birth, as well as being associated with insulin resistance syndrome (IRS) variables in adulthood. Red cell SLC was measured in 26 adults, and NHE in dermal fibroblasts from another 15 subjects characterized anthropometrically at birth. SLC activity correlated with LDL cholesterol, triglycerides and urate (r=0·42 , 0·49; 0·05 > P>0·01), but not birth anthropometry. NHE Vmax correlated with plasma insulin (r=0·80; P<0·001), but birth weight was unrelated to Vmax, Km or Hill coefficient for H+i. However, pHi correlated with birth weight (r=0·74; P=0·002), insulin sensitivity (r=0·52; P<0·05), fasting glucose (r=,0·52; P<0·05) 2 h insulin (r=0·51; P<0·05) 2 h glucose (r=,0·54; P<0·05). In conclusion, red cell SLC is related to IRS variables, but not with birth weight measures. In contrast, low intracellular pHi is related to both low birth weight and adult insulin resistance, suggesting it might be a ,programmed' cell phenotype, although this is not apparently explained by altered NHE kinetics. [source] Elevated sweat sodium associated with pulmonary oedema in meningococcal sepsisEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2004M. Eisenhut Abstract Background, We observed a temporary positive sweat test with sodium and chloride levels greater than 60 mmol L,1 following meningococcal septicaemia. Objective was to investigate whether this finding is reproducible and whether this disturbance in epithelial sodium transport is related to sepsis-induced pulmonary oedema. Materials and methods, Twenty-four children with a diagnosis of meningococcal septicaemia and 10 controls with noninfectious critical illness admitted to the Royal Liverpool Children's Hospital were included. Sweat collection was by pilocarpine iontophoresis in the acute phase of the illness (days 1,5) and on follow up. Sodium and chloride concentrations were determined by flame photometry. Results, In patients with meningococcal septicaemia, sweat sodium and chloride concentrations were significantly higher in the acute compared with the recovery phase, with a mean (SD) of 31·0 (14·6) mmol L,1 in the acute vs. 19·6 (10·2) mmol L,1 on recovery for sodium and 21·0 (12·1) mmol L,1 in the acute vs. 11·8 (4·9) mmol L,1 on recovery for chloride (P < 0·01, t -test, for sodium and chloride). Sweat sodium and chloride were significantly higher in patients with meningococcal disease compared with controls and in the acute phase in patients with septicaemia-related pulmonary oedema [mean (SD) sodium: 41·0 (15·4) mmol L,1 and chloride: 28·8 (14·3) mmol L,1] compared with septic patients without [mean (SD) sodium: 24·5 (10·1) mmol L,1 and chloride: 15·3 (7·9) mmol L,1] (P < 0·01 for sodium and chloride). Conclusions, This is the first study to provide in vivo evidence of reduced epithelial sodium transport in children with septicaemia and of its association with pulmonary oedema. [source] Standardized procedure for measurement of nasal potential difference: An outcome measure in multicenter cystic fibrosis clinical trials,PEDIATRIC PULMONOLOGY, Issue 5 2004Thomas A. Standaert PhD Abstract Patients with cystic fibrosis (CF) can be discriminated from healthy subjects by measurement of the nasal potential difference, which has become a useful outcome measure for therapies directed toward correcting defective electrolyte transport in CF. A standard operating procedure was developed by a CF Foundation clinical trials network, to be followed by all sites performing collaborative studies. Key variables in the measurement included type of voltmeter, exploring probe, reference electrodes, and solutions used to assess both sodium transport and chloride conductance. Eight sites submitted data on 3,8 normal and 4,5 CF subjects. Baseline voltage, an index of sodium transport, was ,18.2,±,8.3 mV (mean,±,SD) for normals, and ,45.3,±,11.4 mV for CF patients. There was no CFTR-mediated chloride secretion in CF subjects, as evidenced by the lack of response to perfusion with zero chloride,+,beta agonist solutions (+3.2,±,3.5 mV) vs. that in normals (,23.7,±,10.2 mV). The standardized nasal potential difference measurement minimizes variability between operators and study sites. Valid and consistent results can be attained with trained operators and attention to technical details. These data demonstrate the procedure to be sufficient for multicenter studies in the CF Foundation network. Pediatr Pulmonol. 2004; 37:385,392. © 2004 Wiely-Liss, Inc. [source] MECHANISMS MEDIATING PRESSURE NATRIURESIS: WHAT WE KNOW and WHAT WE NEED TO FIND OUTCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2005Roger G Evans SUMMARY 1.,It is well established that pressure natriuresis plays a key role in long-term blood pressure regulation, but our understanding of the mechanisms underlying this process is incomplete. 2.,Pressure natriuresis is chiefly mediated by inhibition of tubular sodium reabsorption, because both total renal blood flow and glomerular filtration rate are efficiently autoregulated. Inhibition of active sodium transport within both the proximal and distal tubules likely makes a contribution. Increased renal interstitial hydrostatic pressure (RIHP) likely inhibits sodium reabsorption by altering passive diffusion through paracellular pathways in ,leaky' tubular elements. 3.,Nitric oxide and products of cytochrome P450-dependent arachidonic acid metabolism are key signalling mechanisms in pressure natriuresis, although their precise roles remain to be determined. 4.,The key unresolved question is, how is increased renal artery pressure ,sensed' by the kidney? One proposal rests on the notion that blood flow in the renal medulla is poorly autoregulated, so that increased renal artery pressure leads to increased renal medullary blood flow (MBF), which, in turn, leads to increased RIHP. An alternative proposal is that the process of autoregulation of renal blood flow leads to increased shear stress in the preglomerular vasculature and, so, release of nitric oxide and perhaps products of cytochrome P450-dependent arachidonic acid metabolism, which, in turn, drive the cascade of events that inhibit sodium reabsorption. 5.,Central to the arguments underlying these opposing hypotheses is the extent to which MBF is autoregulated. This remains highly controversial, largely because of the limitations of presently available methods for measurement of MBF. [source] Renal And Cardiovascular Actions Of 20-Hydroxyeicosatetraenoic Acid And Epoxyeicosatrienoic AcidsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2000Richard J Roman SUMMARY 1. Arachidonic acid (AA) is metabolized by cytochrome P450 (CYP)-dependent pathways to epoxyeicosatrienoic acids (EET) and 20-hydroxyeicosatetraenoic acid (20-HETE) in the kidney and the peripheral vasculature. 2. The present short review summarizes the renal and cardiovascular actions of these important mediators. 3. Epoxyeicosatrienoic acids are vasodilators produced by the endothelium that hyperpolarize vascular smooth muscle (VSM) cells by opening Ca2+ -activated K+ (KCa) channels. 20-Hydroxyeicosatetraenoic acid is a vasoconstrictor that inhibits the opening of KCa channels in VSM cells. Cytochrome P450 4A inhibitors block the myogenic response of small arterioles to elevations in transmural pressure and autoregulation of renal and cerebral blood flow in vivo. Cytochrome P450 4A blockers also attenuate the vasoconstrictor response to elevations in tissue PO2, suggesting that this system may serve as a vascular oxygen sensor. Nitric oxide and carbon monoxide inhibit the formation of 20-HETE and a fall in 20-HETE levels contributes to the activation of KCa channels in VSM cells and the vasodilator response to these gaseous mediators. 20-Hydroxyeicosatetraenoic acid also mediates the inhibitory actions of peptide hormones on sodium transport in the kidney and the mitogenic effects of growth factors in VSM and mesangial cells. A deficiency in the renal production of 20-HETE is associated with the development of hypertension in Dahl salt-sensitive rats. 4. In summary, the available evidence indicates that CYP metabolites of AA play a central role in the regulation of renal, pulmonary and vascular function and that abnormalities in this system may contribute to the pathogenesis of cardiovascular diseases. [source] Delayed clearance of fetal lung liquid and sodium transport,genetic predisposition not evident yetACTA PAEDIATRICA, Issue 3 2005Mikko HALLMANArticle first published online: 2 JAN 200 Abstract The epithelial Na+ channel (ENaC) contributes to the clearance of fetal lung liquid. In premature infants, low ENaC activity and low expression level of ,-ENaC have been associated with respiratory failure. The polymorphism in the ,-ENaC gene remains to be studied as a factor explaining the variation in the incidence of transient tachypnoea or respiratory distress syndrome in the newborn. Conclusion : The study of genetic predisposition to common multifactorial diseases requires analyses of large, well-defined cohorts for representative variants of relevant candidate genes. [source] | ||||||||||