Functional identification of protein phosphatase 1-binding consensus residues in NBCe1-B

Protein phosphatase 1 (PP1) is involved in various signal transduction mechanisms as an extensive regulator. The PP1 catalytic subunit (PP1c) recognizes and binds to PP1-binding consensus residues (FxxR/KxR/K) in NBCe1-B. Consequently, we focused on identifying the function of the PP1-binding consensus residue, ⁹²²FMDRLK⁹²⁷ , in NBCe1-B. Using site-directed mutagenesis and co-immunoprecipitation assays, we revealed that in cases where the residues were substituted (F922A, R925A, and K927A) or deleted (deletion of amino acids 922–927), NBCe1-B mutants inhibited PP1 binding to NBCe1-B. Additionally, by recording the intracellular pH, we found that PP1-binding consensus residues in NBCe1-B were not only critical for NBCe1-B activity, but also relevant to its surface expression level. Therefore, we reported that NBCe1-B, as a substrate of PP1, contains these residues in the C-terminal region and that the direct interaction between NBCe1-B and PP1 is functionally critical in controlling the regulation of the HCO₃⁻ transport. These results suggested that like IRBIT, PP1 was another novel regulator of HCO₃⁻ secretion in several types of epithelia.

Renal intercalated cells and blood pressure regulation

Type B and non-A, non-B intercalated cells are found within the connecting tubule and the cortical collecting duct. Of these cell types, type B intercalated cells are known to mediate Cl⁻ absorption and HCO₃⁻ secretion largely through pendrin-dependent Cl⁻/HCO₃⁻ exchange. This exchange is stimulated by angiotensin II administration and is also stimulated in models of metabolic alkalosis, for instance after aldosterone or NaHCO₃ administration. In some rodent models, pendrin-mediated HCO₃⁻ secretion modulates acid-base balance. However, the role of pendrin in blood pressure regulation is likely of more physiological or clinical significance. Pendrin regulates blood pressure not only by mediating aldosterone-sensitive Cl⁻ absorption, but also by modulating the aldosterone response for epithelial Na⁺ channel (ENaC)-mediated Na⁺ absorption. Pendrin regulates ENaC through changes in open channel of probability, channel surface density, and channels subunit total protein abundance. Thus, aldosterone stimulates ENaC activity through both direct and indirect effects, the latter occurring through its stimulation of pendrin expression and function. Therefore, pendrin contributes to the aldosterone pressor response. Pendrin may also modulate blood pressure in part through its action in the adrenal medulla, where it modulates the release of catecholamines, or through an indirect effect on vascular contractile force. This review describes how aldosterone and angiotensin II-induced signaling regulate pendrin and the contributory role of pendrin in distal nephron function and blood pressure.

Renal intercalated cells and blood pressure regulation

Type B and non-A, non-B intercalated cells are found within the connecting tubule and the cortical collecting duct. Of these cell types, type B intercalated cells are known to mediate Cl⁻ absorption and HCO₃⁻ secretion largely through pendrin-dependent Cl⁻/HCO₃⁻ exchange. This exchange is stimulated by angiotensin II administration and is also stimulated in models of metabolic alkalosis, for instance after aldosterone or NaHCO₃ administration. In some rodent models, pendrin-mediated HCO₃⁻ secretion modulates acid-base balance. However, the role of pendrin in blood pressure regulation is likely of more physiological or clinical significance. Pendrin regulates blood pressure not only by mediating aldosterone-sensitive Cl⁻ absorption, but also by modulating the aldosterone response for epithelial Na⁺ channel (ENaC)-mediated Na⁺ absorption. Pendrin regulates ENaC through changes in open channel of probability, channel surface density, and channels subunit total protein abundance. Thus, aldosterone stimulates ENaC activity through both direct and indirect effects, the latter occurring through its stimulation of pendrin expression and function. Therefore, pendrin contributes to the aldosterone pressor response. Pendrin may also modulate blood pressure in part through its action in the adrenal medulla, where it modulates the release of catecholamines, or through an indirect effect on vascular contractile force. This review describes how aldosterone and angiotensin II-induced signaling regulate pendrin and the contributory role of pendrin in distal nephron function and blood pressure.

Mechanisms underlying contraction of rat isolated coronary artery induced by acidosis / 中国病理生理杂志

AIM:To explore the mechanisms underlying contraction induced by extracelluar acidosis (pHex6.8) in rat isolated coronary artery (RCA).METHODS:Using the microvessel tension recorder system, the effects of acid-base transporters on RCA contraction induced by pHex6.8 were explored by applying the selective pharmacological inhibitors of Na+-H+ exchanger 1 (NHE-1) and Na+-HCO-3 cotransporter (NBC), HOE-642 and S0859, respectively.The effects of chloride channel on RCA contraction induced by pHex6.8 were explored by applying the inhibitors of chloride channel (NPPB and NFA), and by replacing the extracellular NaCl with equimolar NaBr.RESULTS:pHex6.8 augmented the resting tension of RCA, and the maximum contraction was (3.90±0.95) mN.HOE-642 at 30 μmol/L and S0859 at 100 μmol/L both inhibited the contraction of RCA induced by pHex6.8 (P<0.01).NPPB and NFA both inhibited the contraction of RCA induced by pHex6.8 or KCl (60 mmol/L) in a concentration-dependent manner.NPPB and NFA (100 μmol/L) both inhibited the contraction of RCA induced by U46619 (1 μmol/L).Replacing the extracellular NaCl with equimolar NaBr almost completely inhibited RCA contraction induced by pHex6.8 (P<0.01), but had no obvious effect on the contraction induced by KCl (60 mmol/L) or U46619 (1 μmol/L).CONCLUSION:Extracellular acidosis-induced contraction in RCA may be related to the activated NHE-1 and NBC, and it may be also related to the enhanced chloride transport across the membrane.

Ahcyl2 upregulates NBCe1-B via multiple serine residues of the PEST domain-mediated association

Inositol-1,4,5-triphosphate [IP3] receptors binding protein released with IP3 (IRBIT) was previously reported as an activator of NBCe1-B. Recent studies have characterized IRBIT homologue S-Adenosylhomocysteine hydrolase-like 2 (AHCYL2). AHCYL2 is highly homologous to IRBIT (88%) and heteromerizes with IRBIT. The two important domains in the N-terminus of AHCYL2 are a PEST domain and a coiled-coil domain which are highly comparable to those in IRBIT. Therefore, in this study, we tried to identify the role of those domains in mouse AHCYL2 (Ahcyl2), and we succeeded in identifying PEST domain of Ahcyl2 as a regulation region for NBCe1-B activity. Site directed mutagenesis and coimmunoprecipitation assay showed that NBCe1-B binds to the N-terminal Ahcyl2-PEST domain, and its binding is determined by the phosphorylation of 4 critical serine residues (Ser151, Ser154, Ser157, and Ser160) in Ahcyl2 PEST domain. Also we revealed that 4 critical serine residues in Ahcyl2 PEST domain are indispensable for the activation of NBCe1-B using measurement of intracellular pH experiment. Thus, these results suggested that the NBCe1-B is interacted with 4 critical serine residues in Ahcyl2 PEST domain, which play an important role in intracellular pH regulation through NBCe1-B.

Unexpected results from direct measurement, with a torsion microbalance in a closed system, of calcification rates of the coral Agaricia agaricites (Scleractinia:Agariicidae) and concomitant changes in seawater pH / Resultados inesperados de medición directa, con una microbalanza de torsión en un sistema cerrado, de las tasas de calcificación de los corales Agaricia agaricites (Scleractinia:Agariicidae) y concomitantes cambios de pH en el medio del mar

Ocean acidification is impacting the calcification of corals, but the mechanisms of calcification are still unclear. To explore the relationship between calcification and pH, small pieces of coral were suspended from a torsion microbalance in gently stirred, temperature controlled, seawater in a closed chamber. Net calcification rate and pH were continuously monitored while light, temperature or pH could be manipulated. The coral pieces were from the edges of thin plates of Agaricia agaricites and were studied alive and freshly collected. Unexpectedly, when calcification was taking place (n=9, 0.082 mg.hr-1.cm-2), as determined by weight increase, the pH of the surrounding seawater medium changed little (n=10, -0.0047 pH units.hr-1.cm-2). When calcification was not taking place the decrease of seawater pH was an order of magnitude higher, -0.013 pH units.hr-1.cm-2. This is the opposite of what is expected when calcium carbonate (CaCO3) forms. Similarly, fresh skeleton initially showed no change of pH in the seawater medium although the rates of weight gain were high (upto 1.0 mg hr-1.cm-2). After 10 hours, as the rate of deposition decreased following a generalized Michaelis-Menten growth curve, the pH began to decrease dramatically indicating an increase of CO2 in the seawater. These unexpected results can be explained if unstable calcium bicarbonate (Ca(HCO³)2) is formed in the organic matrix/carbonic anhydrase surface and slowly transforms later to CaCO3. Pieces of living coral monitored in the chamber for 30 hours gained weight during the day and loss it at night. The loss would be consistent with the transformation of Ca(HCO³)2 to CaCO3 with the release of CO2. The mean calcification rate of live coral was greater (n=8, p=0.0027) in high light (120 μmol.s-1.m-2) at 0.098 mg.hr-1.cm-2, compared to 0.063 mg.hr-1.cm-2 in low light (12 μmol.s-1.m-2). However, at the same time the mean rate of pH change was -0.0076 under low light compared to -0.0030 under high light (n=8, p=0.0001). The difference can be explained by CO2 being used for photosynthesis by zooxanthellae. The deposition rate of live coral was not affected by the addition of phosphate but the rate of weight gain by the freshly collected skeleton was strongly enhanced by phosphate. These results indicate that care should be applied in the application of the alkalinity anomaly technique for the measurement of calcification in corals.

La acidificación del océano está impactando la calcificación de los corales, pero los mecanismos de la calcificación son aún inciertos. Para explorar la relación entre la calcificación y pH, pequeños trozos de coral fueron suspendidos en una microbalanza de torsión en agitado suave, temperatura controlada, y agua de mar en una cámara cerrada. La tasa de calcificación neta y el pH se monitorearon continuamente mientras que la luz, temperatura o pH podían ser manipulados. Las piezas de coral eran de los bordes de placas finas de Agaricia agaricites y se estudiaron vivos y recién colectados. Inesperadamente, cuando la calcificación (n= 9, 0.082 mg.hr-1.cm-2) se estaba dando, según lo determinado por el aumento de peso, el pH del agua de mar circundante cambió poco (n = 10,-0.0047 pH units.hr-1.cm-2). Durante los períodos cuando la calcificación no se estaba dando la disminución del pH del agua de mar era un orden de magnitud mayor, -0.013 pH units.hr-1.cm-2. Esto es exactamente lo contrario de lo que se espera cuando se forma carbonato de calcio (CaCO3). Del mismo modo un esqueleto recién colectado al inicio no mostró cambios de pH en el agua de mar aunque eran muy altas las tasas de ganancia de peso (hasta 1.0 mg hr-1.cm-2). Después de 10 horas, la tasa de deposición disminuyó hasta seguir una curva de crecimiento generalizada de Michaelis-Menten, el pH comenzó a disminuir drásticamente, lo que indica un aumento de CO2 en el agua de mar. Estos resultados inesperados pueden explicarse si el bicarbonato de calcio inestable (Ca(HCO³)2) se forma en la superficie de la anhidrasa carbónica/matriz orgánica y lentamente se transforma más tarde a CaCO3. Piezas de coral vivo vigiladas en la cámara durante 30 horas demostraron un patrón de ganancia de peso durante el día y de pérdida en la noche. La pérdida sería coherente con la transformación de la Ca (HCO3)2 a CaCO3 con el lanzamiento de CO2. La tasa de calcificación media de coral vivo fue mayor (n= 8, p= 0.0027) en luz alta (120 μmol.s-1.m-2) a 0.098 mg.hr-1.cm-2, en comparación con 0.063 mg.hr-1.cm-2 en condiciones de poca luz (12 μmol.s-1.m-2). Sin embargo, al mismo tiempo la tasa media de cambio de pH fue de -0.0076 bajo luz baja en comparación con -0.0030 bajo luz alta (n= 8, p= 0,0001). La diferencia puede explicarse porque el CO2 está siendo utilizado para la fotosíntesis por zooxantelas. La tasa de deposición de coral vivo no fue afectada por la adición de fosfato pero la tasa de ganancia de peso de los esqueletos recién colectados era fuertemente reforzada por fosfato. Estos resultados indican que la atención debe aplicarse en la aplicación de la técnica de alcalinidad anormal para la medición de la calcificación de los corales.

The incidence and types of acid-base disorder of critically ill patients in emergency / 中华急诊医学杂志

Objective To reveal the incidence and types of acid-base disorder (ABD) of critically ill patients in emergency.Methods The clinical data of critically ill patients in the resuscitation room were collected prospectively from December 1,2008 to March 31,2009.Both arterial and venous blood samples were collected to detect arterial blood gas analysis and serum electrolytes simultaneously and their ABD were analyzed.Results Of totally 766 cases,the incidence of ABD was 97.3％ (745 cases).Among ABD the simple acid-base disorder ( SA BD) was 149 cases ( 20.0％ ),dual acid-base disorder (DABD) 525 (70.5％ ) and triple acid-base disorder (TABD) 71 (9.5％ ).After calculating anion gap (AG),the incidence of TABD increased from 12 to 71 cases and the missed diagnosis rate were 83.1％ (59 cases) and after calculating potential HCO3-,the incidence of TABD increased from 8 to 71 cases and the missed diagnosis rate were 88.7％ (63 cases).The age of patients with TABD (77.9 ± 10.7 years old) was older ( P ＜ 0.01 ) than that of other two groups of SABD and DABD as well as APACHEⅡ score (25.9 ± 7.1 ) and incidence (22.5％ ) of MODS in TABD were higher (P ＜0.01 ).The mortality of patients with TABD on the first,second,third and seven day were 14.1％,23.9％,26.8％ and 38.0％ respectively and significantly higher than those in SABD and DABD (P ＜0.05 or P ＜0.01 ).Conclusions The incidence of ABD was 97.3％.Calculation of AG and potential HCO3- would help find metabolic acidosis and TABD.The age and APACHEⅡ score were key factors to poor prognosis of patients with TABD.

Roles of ERK and cPLA2α in biphasic regulation of renal proximal Na+-HCO3-transport by angiotensin Ⅱ / 中华肾脏病杂志

Objective To clarify the signaling mechanisms underlying angiotensin Ⅱ biphasic regulation of renal proximal Na+-HCO3- transport. Methods Different concentration Ang Ⅱ to the responses of Na+-HCO3- cotransporter (NBC) activity in isolated proximal tubules, with or without ATR, MAPK, cPLA2α, P450 blockade was compared in wild-type and Ang Ⅱ type 1a receptor (AT1aR)-deficient mice. The phospholipase of ERK was examined by Western blotting. AT1aR mRNA was examined by RT-PCR from kidney proximal tubules. Results (1)In isolated wild-type mouse, renal proximal tubules showed biphasic effects of Ang Ⅱ on NBC activity. Low concentration Ang Ⅱ (10-10 mol/L) increased NBC activity, but high concentration Ang Ⅱ (10-6 mol/L) decreased NBC activity. Olmcsartan (AT1 antagonist) blocked both stimnlatory and inhibitory effects of Ang Ⅱ on NBC activity, but PD98059 (mitogen-activated protein kinase inhibitor) blocked only the stimulatory effect of low concentration Ang Ⅱ ( 10-10 mol/L). (2)In AT1aR-deficient mice, only the stimulatory effect by high concentration of Ang Ⅱ (10-6 mol/L) was observed, which was blocked by olmesartan and PD98059. (3)In wild-type mice, pharmacological blockade of cPLA2 or P450 converted the inhibition effect by high concentration Ang Ⅱ (10-6 mol/L) to the stimulation, which was blocked by olmesanan and PD98059. These results indicated that the extracellular sigual-regulated kinase (ERK) activation via AT1 mediated only the stimulatory effect of Ang Ⅱ, while the cPLA2α/P450 activation via AT1 mediated the inhibitory effect of Ang Ⅱ independently of ERK. The analysis of ERK phosphorylation by Ang Ⅱ also supported a view that the cPLA2α/P450 pathway worked to suppress the ERK activation. Conclusions Ang Ⅱ activates ERK and cPLA2α with different concentration dependency via AT1. The balance between ERK and cPLA2α activities determines the final responses to Ang Ⅱ in intact proximal tubules.

Altered Regulation of type 3 Na+/H+ exchanger, type 1 Na+/HCO3- cotransporter, and Na+,K+-ATPase in the Kidney of Rats with Experimental Rhabdomyolysis

Metabolic acidosis was shown to correlate with deterioration of renal function in patients with rhabdomyolysis. The present study was aimed to investigate whether the changes of type 3 Na+/H+ exchanger (NHE3), type 1 Na+/HCO3- cotransporter (NBC1), and Na+,K+-ATPase alpha1 subunit may play a role in the pathogenesis of metabolic acidosis in glycerol-induced experimental rhabdomyolysis. Male Sprague-Dawley rats were deprived of fluid intake for 24 hours, and then were injected with 50% glycerol in normal saline (10 mL/kg, intramuscularly). At 24 hours after the glycerol injection, rats were sacrificed by decapitation. Control rats were injected with normal saline. The protein expression of NHE3, NBC1 and Na+,K+-ATPase alpha1 subunit was determined in the cortex of the kidney by immunoblotting and immunohistochemistry. Following the treatment of glycerol, creatinine clearance was significantly decreased, and high anion gap metabolic acidosis developed. In the experimental group, the expression of Na+,K+-ATPase alpha1 subunit was significantly decreased in the cortex of the kidney. On the contrary, the expression of NHE3 and NBC1 was significantly increased. Immunohistochemical analyses confirmed the immunoblotting data. In conclusion, the coordinate up-regulation of NHE3 and NBC1 may play an adaptive role against the metabolic acidosis in glycerol-induced rhabdomyolysis.

An Application of SIG and Other Diadynamic Criteria of Acid-Base Derangements in Trauma / 医学研究杂志

Objective To Investigate the application value of strong ion gap(SIG),anion gap(AG)and other four indicators in the trauma disease.Methods Blood was taken from trauma patients admitted to hospital immediately,with the heparin anticoagulation,misce bene.Blood gas was measured.Creatinine(Cr),phosphorus and albumin(ALB)was measured simultaneously.Results Betwean traumatic group and control group,there was signifrcant difference in SIG,AG,potential HCO3-,and other 5 item(P4mmol/L.

Regulations of Bicarbonate Ions in Pregnant Rat Kidney / 대한해부학회지

The marked hemodynamic and hormonal changes of normal pregnancy are associated with striking alterations in renal physiology involving structure, dynamics, tubular function, and volume homeostasis. A number of acid-base or electrolyte disorders are associated with decreased or increased HCO3-reabsorption in the renal tubules. The present study was to examine the alterations of expression and distribution of Na+/HCO3-cotransporter (NBC), Na+/H+ exchanger-3 (NHE-3), and carbonic anhydrase I and II (CA I, II) proteins in the kidneys of non-pregnant (NP) and pregnant rats using Western blot analysis and immunohistochemistry. Sprague-Dawley female rats were studied on days 10 (P 10), 12 (P 12), 14 (P 14), 17 (P 17), and 19 (P 19) of pregnancy. Western blot analysis demonstrated that the expression of NBC, ~110 kDa at molecular mass, was increased in pregnant rats, particularly P 12, compared with NP rat. The expression of NHE-3, ~83 kDa at molecular mass, was increased in pregnant rats, particularly P 12 and P 14. The expression of CA I, ~30 kDa at molecular mass, was decreased in pregnant rats, particularly P 14, but, CA II protein, ~30 kDa at molecular mass, was similar NP rat. In immunohistochemistry, strong immunoreactivity of NBC of NP rat was exclusively detected in the basolateral membranes of S1 and S2 segment of proximal tubules whereas not in S3 segment. In pregnant rats, the pattern of cellular labeling of NBC was identical to that of NP rat, but signal intensity was increased, particularly P 12. In NHE-3, strong immunoreactivity was detected in apical membranes and brush borders of S3 segments and moderate in S1 and S2 segments. In pregnant rats, the pattern of cellular labeling was identical to that of NP rat, but the signal intensity was increased, particularly P 12 and P 14. Expression of CA I and II proteins was detected in entire collecting duct. Signal intensity was prominent in type A intercalated cells and moderate in type B intercalated cells. In pregnant rats, the pattern of cellular labeling of CA I and II proteins was identical to that of non-pregnant rat, but the signal intensity of CA I was decreased in cortical collecting duct, particularly P 14 and CA II was identical to that of NP rat. These results suggest that the regulation of NBC and NHE-3 expressions in the proximal tubules and CA I expression in cortical collecting duct may maintain HCO3-concentration during the pregnancy.

Electrolyte and Gas Analysis from Dorsal Vein of Hand during General Inhalational Anesthesia / 대한구급학회지

BACKGROUND: To assess the acid-base status and to measure PO2 and PCO2, arterial blood gases (ABG) has been checked usually. We compared the venous blood gases (VBG) from dorsal vein of hand to ABG from radial artery, and tried to determine whether venous blood gas analysis (VBGA) could be the alternative of ABGA. METHODS: Thirty patients who needed continuous arterial pressure monitoring were chosen. At the completion of stability of HR and BP after induction of general inhalational anesthesia, the ABG from radial artery and VBG from dorsal vein of hand were compared. RESULTS: Laboratory findings were as follows (mean+/-SD): arterial pH, 7.44+/-0.04; venous pH, 7.43+/-0.04; arterial HCO3-, 25.56+/-2.39 mmol/L; venous HCO3-, 25.51+/-2.09 mmol/L. The mean values of arterial and venous PO2 were significantly different (247.8+/-48.9 mmHg versus 187.8+/-41.6 mmHg), but the arterial and venous PO2 values were significantly correlated (r=0.706). The PCO2 (r= 0.883), pH (r=0.912), and HCO3- (r=0.901) values, and base excesses of arterial and venous blood (r=0.926) were highly correlated. Also, arterial and venous serum electrolyte (sodium, potassium, and calcium) were highly correlated. CONCLUSIONS: Venous blood gas analysis from dorsal vein of hand can be effectively used as the alternative method to evaluate the acid-base status, PO2, and PCO2, instead of ABGA during general inhalational anesthesia.

Regulations of Bicarbonate Ions in Hypokalemic Rat Kidney / 대한해부학회지

A number of acid-base or electrolyte disorders are associated with decreased or increased HCO3- reabsorption in the renal tubules. There has been a general agreement that potassium depletion induces and maintains metabolic alkalosis in rats. However, many researchers have approached such issue only from functional studies to investigate Na+/H+ exchanger (NHE-3) and Na+/HCO(3-) cotransporter (NBC) activity which closely relates to potassium depletion. In addition the results obtained vary according to their researchers. Thus the present study was employed Western blot analysis and immunohistochemistry together, to examine the alterations of expression and distribution of NHE-3 and NBC-1 with reference to HCO3- reabsorption in the kidneys of rats fed potassium free diets according to the periods. Western blot analysis demonstrated that NHE-3 protein, ~83 kDa at molecular mass, was abundantly expressed in normal group. All potassium-depleted groups showed significantly increased NHE-3 protein compared to normal group. NBC-1 protein, ~110 kDa at molecular mass, was moderately expressed in normal group. All potassium-depleted groups had much higher amounts of the protein than normal group. There was a highly increased amount of NBC-1 protein especially in K-depleted 1 week group. Immunohistochemistry showed positive immunoreactivity of NHE-3 in the apical membranes and brush borders of proximal renal tubule cells. Its reactivity was most prominent in the S3.S1 and S2 had moderate immunoreactivity. Potassium-depleted groups had an identical pattern of cellular labeling of NHE-3 protein compared with that of normal group. However the signal intensity of NHE-3 protein in potassium-depleted groups was much higher than that of normal group. Immunoreactivity of NBC-1 was observed exclusively in the basolateral plasma membranes of proximal tubule cells. There was a strong reactivity in the S1 and S2, whereas S3 did not show any reactivity. Potassium-deprived rats exhibited an identical pattern of cellular labeling of NBC-1 protein compared with that of normal rats. However, the signal intensity of NBC-1 protein was markedly increased in potassium-deprived rats. These results suggest that increased NHE-3 and NBC-1 expression resulted from potassium depletion in the renal proximal tubules, enhances HCO3-reabsorption and consequently maintains metabolic alkalosis.

Water Diuresis Promotes Urine Acidification with Decreases in HCO3- Concentration / 日本農村医学会雑誌

It is known that the reabsorption of filtered HCO<SUB>3</SUB><SUP>-</SUP>depends on the tubular flowrate in the proximal uniferous tubule. In animal experiments, studies have demonstratedthat, when diuresis was induced, the pH of the collecting duct urine decreased, resulting from the decrease in HCO<SUB>3</SUB><SUP>-</SUP>concentration with no change in the pCO<SUB>2</SUB> level.The present study was designed to examine changes in urine acidification in humansunder a water diuretic state. Urine pH, pCO<SUB>2</SUB> levels, and HCO<SUB>3</SUB><SUP>-</SUP>concentration weremeasured before and after the drinking of water. In 120 minutes after hydration, theurine pH level fell about 0.5 pH unit from that before the intake of water. The urine HCO<SUB>3</SUB><SUP>-</SUP>concentration coincidentally decreased significantly. However, pCO<SUB>2</SUB> values remainedunchanged. These results indicated that also in humans, water diuresis promotesurine acidification, resulting from a decrease in HCO<SUB>3</SUB><SUP>-</SUP>concentration with nochange in the pCO<SUB>2</SUB> level, which may contribute to the prevention of the loss of plasmaHCO<SUB>3</SUB><SUP>-</SUP>into the urine when the urine flow rate increases.

Effect of furosemide on Cl -/HCO_3~- exchange in IMCD cell in rabbit kidney / 解放军医学杂志

Objective To evaluate the effect of furosemide on Cl -/HCO- 3 exchange of inner medullary collecting duct(IMCD) in rabbit kidney. Methods The effect of furosemide in different concentrations on the changes in Cl -/HCO- 3 exchange in mono-layer of IMCD cell in rabbit kidney was determined by fluorescent probe technique. Results Cl -/HCO- 3 exchange in IMCD cell could be inhibited by 4.3% by 15?mol/L furo semide solution, and 480?mol/L furosemide solution could inhibit the exchange by 97.4%. The Cl -/HCO- 3 exchange rates of the groups, in which the final concentrations of furosemide were equal to or higher than 30?mol/L, were significantly lower than that of the control group(P

Cl- channel expression in choroid plexus epithelial cells

No abstract available.

Bicarbonate transport in microperfused pancreatic ducts

No abstract available.

A Case of Congenital Chloridorrhea / 대한주산의학회잡지

Congenital chloridorrhea is a rare autosomal recessive disease and results from impairment of active transport of chloride in the ileum and colon. Absence of the Cl-/HCO3-, exchange pump causes polyhydramnios, distended bowel loop and absence of meconium before birth. Prenatal ultrasound examination shows a great number of circular anechoic area in the fetal abdomen, as well as polyhydramnios. Massive watery diarrhea is apparent from the first days of life. This fluid loss, with its attendant impairment of electrolyte homeostasis, is life threatening. Exact replacement of water, NaCl and KCl can prevent the growth and psychomotor retardation and the development of progressive renal damage. We experienced one case of congenital chloridorrhea and present it with brief review of literatures.

Acid-Base and Blood-Gas Status of Newborn Umbilical Blood according to Induction-Delivery and Uterine Incision-Delivery Intervals under General Anesthesia for Cesaeran Section / 대한마취과학회지

In cesarean section under general anesthesia, inhalation anesthetics may compound fetal acidosis brought by maternal hypoxia or uteroplacental insufficiency. The chance af fetal distress may be increased with prolonged induction-delivery (ID) and uterine incision-delivery (UD) intervals in such cases. These studies were undertaken to evaluate the changes of fetal acid-base and blood-gas status according to these intervals in 58 parturients given cesarean section under general anesthesia. 58 neonates were divided into three groups according to their ID interval [group 1 (N=26): less than 6 minutes, group 2 (N=25): 6 to 10 minutes, group 3 (N=7): 10 to 15 minutes] and four groups according to their UD interval[group A (N=25): less than 60 seconds, group B (N=22): 60 to 90 seconds, group C (N=9): 90 to 120 seconds, group D (N=2): 120 to 180 seconds]. The pH, PCO2, PO2 and HCO3 values of the umbilical vein blood at delivery in the groups 1, 2, 3 divided according to ID intervals were 7.37+/-0.03, 7.36+/-0.04, 7.36+/-0.03; 39.75+/-4.83, 41.76+/- 4.03, 38.81+/-2.31; 34.35+/-745, 32.65+/-9.63, 30.89+/-11.28 (in mmHg); and 23.21+/-0.33, 23.30+/-0.26, 22.15+/-0.52 (in mEq/L), respectively, and in groups A, B, C, D divided according to UD intervals, they were 7.37+/-0.02, 7.37+/-0.02, 7.37+/-0.03, 7.36+/-0.06; 40.30+/-5.20, 40,63+/-3.11, 39.96+/-4.42, 40.03 +/-5.09; 32.35+/-8.23, 31.82+/-0.17, 35.67+/-8.35, 33.53+/-10.53 (in mmHg); and 23.14+0.26, 23.60+/-0.36, 22.88+/-0.67, 23.35+/-0.35 (in mEq/L), respectively. No significant differences in these values were present between these ID- or UD- based groups.

The Effect of CSF Changes on the Action of Local Anesthetics in Pregnant Woman / 대한마취과학회지

Spinal fluid(CSF) was analyzed in ten pregnant women at term undergoing C-section with spinal anesthesia and in ten non-pregnant women undergoing gynecological operation with spinal anesthesia. The acid-base status, protein and sugar levels in the CSF of the CSF are summarized in Table-2 and Table-3. The pH was slightly higher in the pregnant group compared to that of the non-pregnant controls. The bicarbonate level and the total CO2 content were significantly lower in the pregnant group compared to non-pregnant controls. The protein and sugar level were lower in the pregnant group compared to non-pregnant controls. Acid base changes can markedly affect dissociation of the local anesthetics. More free base will be available for transfer across lipid barriers in a relatively more alkalotic medium which was found in spinal fluid of pregnant women. In addition, lower bicarbonate levels may also affect dissociation of local anesthetic and activity by changing the buffering capacity. In conclusion, our results show that pregnancy induces significant changes in the acid base balance of the spinal fluid. These changes may contribute to the facilitated spread of local anesthetics in both the epidural and subarachnoid spaces.