Conformation and packing properties of membrane lipids: the crystal structure of sodium dimyristoylphosphatidylglycerol

The conformation and molecular packing of sodium 1,2-dimyristoyl-sn-glycero-phospho-rac-glycerol (DMPG) have been determined by single crystal analysis (R = 0.098). The lipid crystallizes in the monoclinic spacegroup P2(1) with the unit cell dimensions a = 10.4, b = 8.5, c = 45.5 A and beta = 95.2 degrees. There are two independent molecules (A and B) in the asymmetric unit which with respect to configuration and conformation of their glycerol headgroup are mirror images. The molecules pack tail to tail in a bilayer structure. The phosphoglycerol headgroups have a layer-parallel orientation giving the molecules an L-shape. At the bilayer surface the (-) phosphoglycerol groups are arranged in rows which are separated by rows of (+) sodium ions. Laterally the polar groups interact by an extensive network of hydrogen, ionic and coordination bonds. The packing cross-section per molecule is 44.0 A2. The hydrocarbon chains are tilted (29 degrees) and have opposite inclination in the two bilayer halves. In the chain matrix the chain planes are arranged according to a so far unknown hybride packing mode which combines the features of T parallel and O perpendicular subcells. The two fatty acid substituted glycerol oxygens have mutually a - synclinal rather than the more common + synclinal conformation. The conformation of the diacylglycerol part of molecule A and B is distinguished by an axial displacement of the two hydrocarbon chains by four methylene units. This results in a reorientation of the glycerol back bone and a change in the conformation and stacking of the hydrocarbon chains. In molecule A the beta-chain is straight and the gamma-chain is bent while in molecule B the chain conformation is reversed.     

Essential sulfhydryl groups of rat liver monoamine oxidase.

The inhibition by some thiol reagents of partly purified mitochondrial monoamine oxidase (MAO) (EC 1.4.3.4) from rat liver was studied, and the molar content of sulfhydryl groups in the enzyme determined. Sodium nitroprusside and 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) inhibited the enzyme, apparently reversibly, while sodium arsenite was not inhibitory. Concentrations of the respective inhibitors causing 50% inhibition after 15 min of preincubation with the enzyme at pH 7.0 and 37 degrees C are 5.80 times 10(-4) M and 4.35 times 10(-5) M. The thiol compounds cysteine, dithiothreitol, and 2-mercaptoethanol did not inhibit MAO. The average number of sulfhydryl groups per mole of enzyme, determined by reaction with DTNB, increased from 3.6 +/- 0.2 freely reacting sulfhydryl groups (n = 4) to 18.4 to total sulfhydryl groups (n = 2) on denaturation with 8 M urea.     

Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis.

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium x kg body wt-1 x day-1) or high-sodium (HS = 7.5 mmol sodium x kg body wt-1 x day-1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial PO2 34.4 +/- 2.1 Torr), plasma pH increased from 7.37 +/- 0.01 to 7.48 +/- 0.01 (P < 0.05) because of hyperventilation (arterial PCO2 25.6 +/- 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.     

Sodium dependence of acetate formation by the acetogenic bacterium Acetobacterium woodii.

Growth of Acetobacterium woodii on fructose was stimulated by Na+; this stimulation was paralleled by a shift of the acetate-fructose ratio from 2.1 to 2.7. Growth on H2-CO2 or on methanol plus CO2 was strictly dependent on the presence of sodium ions in the medium. Acetate formation from formaldehyde plus H2-CO by resting cells required Na+, but from methanol plus H2-CO did not. This is analogous to H2-CO2 reduction to methane by Methanosarcina barkeri, which involves a sodium pump (V. Müller, C. Winner, and G. Gottschalk, Eur. J. Biochem. 178:519-525, 1988). This suggests that the reduction of methylenetetrahydrofolate to methyltetrahydrofolate is the Na+-requiring reaction. A sodium gradient (Na+ out/Na+ in = 32, delta pNa = -91 mV) was built up when resting cells of A. woodii were incubated under H2-CO2. Acetogenesis was inhibited when the delta pNa was dissipated by monensin.     

Preliminary crystallographic study of glucose-6-phosphate dehydrogenase from rat liver

Crystals of D-glucose-6-phosphate: NADP+ oxidoreductase were obtained with the hanging drop, vapor diffusion and batch methods from ammonium sulfate-containing solutions. X-ray diffraction photographs indicate that the crystals belong to the orthorhombic space groups I222 or I2(1)2(1)2(1) with unit cell dimensions of a = 66.0 A, b = 140.8 A and c = 177.8 A. These data, together with results from sodium dodecyl sulfate/polyacrylamide gel electrophoresis and crystal density experiments, indicate that there is one 116,000 Mr dimer per asymmetric unit. The crystals diffract to at least 2.2 A and are suitable for X-ray crystallographic structure determination.     

Aldosterone-stimulated sodium uptake by apical membrane vesicles from A6 cells

Sodium fluxes in plasma membrane vesicles prepared from the cultured toad kidney epithelial cell line A6 are studied. The vesicles are enriched 7-10 times in apical membrane markers. Sodium uptake is osmotically sensitive and inhibited by low concentrations of amiloride (K0.5 = 7 X 10(-8) M at 1 mM NaCl). Vesicles prepared from aldosterone-treated cells (4.5 h at 10(-7) M aldosterone) show a 2-fold enhancement of amiloride-sensitive sodium flux relative to appropriate controls. The above observations are in good agreement with studies of sodium transport across the apical membrane of intact A6 epithelia. Thus, the amiloride-sensitive sodium transporter in the apical membrane of these cells is preserved in the vesicle preparation, making it possible to study the effects of aldosterone in the absence of nonmembrane-related phenomena.     

Role of the renin-angiotensin system during alterations of sodium intake in conscious mice

The present studies were performed to quantify circulating components of the renin-angiotensin-aldosterone axis and to determine the functional importance of this system during alterations in sodium intake in conscious mice. Increasing sodium intake from approximately 200 to 1,000 microeq/day significantly decreased plasma renin concentration from 472 +/- 96 to 304 +/- 83 ng ANG I. ml(-1). h(-1) (n = 5) but did not alter plasma renin activity from the low-sodium level of 7.7 +/- 1.1 ng ANG I. ml(-1). h(-1). Despite the elevated plasma renin concentration, plasma ANG II in mice on low-sodium level averaged 14 +/- 3 pg/ml and was significantly suppressed to 6 +/- 1 pg/ml by high-sodium intake (n = 7). Consistent with the modulation of ANG II, plasma aldosterone significantly decreased from 41 +/- 8 to 8 +/- 3 ng/dl when sodium intake was elevated (n = 6). In a final set of experiments, the continuous infusion of ANG II (20 ng. kg(-1). min(-1)) led to a mild salt-sensitive increase in mean arterial pressure from 108 +/- 2 to 131 +/- 2 mmHg as sodium intake was varied from low to high (n = 7). In vehicle-infused mice, mean arterial pressure was unaltered from 109 +/- 2 mmHg when sodium intake was increased (n = 6). These studies indicate that the physiological suppression of circulating ANG II may be required to maintain a constancy of arterial pressure during alterations in sodium intake in normal mice.     

Crystallization and preliminary X-ray analysis of L-2-haloacid dehalogenase from Xanthobacter autotrophicus GJ10.

Haloacid dehalogenases are enzymes that cleave carbon-chlorine or carbon-bromine bonds of 2-haloalkanoates. X-ray-quality crystals of L-2-haloacid dehalogenase from the 1,2-dichloroethane-degrading bacterium Xanthobacter autotrophicus GJ10 have been grown at room temperature from 20% PEG 8000, 200 mM sodium formate at pH 6.8-7.0, using macroseeding techniques. The crystals, which diffract in the X-ray beam up to 2.0 A resolution, belong to the spacegroup C2221. Cell parameters are a = 58.8 A, b = 93.1 A, c = 84.2 A. A native data set to 2.3 A has been collected, with a completeness of 97% and an Rsym of 6.0%.     

Localization of receptor sites for insect-selective toxins on sodium channels by site-directed antibodies.

Site-directed antibodies corresponding to conserved putative extracellular segments of sodium channels, coupled with binding studies of radiolabeled insect-selective scorpion neurotoxins, were employed to clarify the relationship between the toxins' receptor sites and the insect sodium channel. (1) The depressant insect toxin LqhIT2 was shown to possess two noninteracting binding sites in locust neuronal membranes: a high-affinity (KD1 = 0.9 +/- 0.6 nM) and low-capacity (Bmax1 = 0.1 +/- 0.07 pmol/mg) binding site as well as a low-affinity (KD2 = 185 +/- 13 nM) and high-capacity (Bmax2 = 10.0 +/- 0.6 pmol/mg) binding site. (2) The high-affinity site serves as a target for binding competition by the excitatory insect toxin AaIT. (3) The binding of LqhIT2 was significantly inhibited in a dose-dependent manner by each of four site-directed antibodies. The binding inhibition resulted from reduction in the number of binding sites. (4) The antibody-mediated inhibition of [125I]AaIT binding differs from that of LqhIT2: three out of the four antibodies which inhibited LqhIT2 binding only partially affected AaIT binding. Two antibodies, one corresponding to extracellular and one to intracellular segments of the channel, did not affect the binding of either toxin. These data suggest that the receptors to the depressant and excitatory insect toxins (a) comprise an integral part of the insect sodium channel, (b) are formed by segments of external loops in domains I, III, and IV of the sodium channel, and (c) are localized in close proximity but are not identical in spite of the competitive interaction between these toxins.     

Sodium-free fluid ingestion decreases plasma sodium during exercise in the heat.

This study assessed whether replacing sweat losses with sodium-free fluid can lower the plasma sodium concentration and thereby precipitate the development of hyponatremia. Ten male endurance athletes participated in one 1-h exercise pretrial to estimate fluid needs and two 3-h experimental trials on a cycle ergometer at 55% of maximum O2 consumption at 34 degrees C and 65% relative humidity. In the experimental trials, fluid loss was replaced by distilled water (W) or a sodium-containing (18 mmol/l) sports drink, Gatorade (G). Six subjects did not complete 3 h in trial W, and four did not complete 3 h in trial G. The rate of change in plasma sodium concentration in all subjects, regardless of exercise time completed, was greater with W than with G (-2.48 +/- 2.25 vs. -0.86 +/- 1.61 mmol. l-1. h-1, P = 0.0198). One subject developed hyponatremia (plasma sodium 128 mmol/l) at exhaustion (2.5 h) in the W trial. A decrease in sodium concentration was correlated with decreased exercise time (R = 0.674; P = 0.022). A lower rate of urine production correlated with a greater rate of sodium decrease (R = -0. 478; P = 0.0447). Sweat production was not significantly correlated with plasma sodium reduction. The results show that decreased plasma sodium concentration can result from replacement of sweat losses with plain W, when sweat losses are large, and can precipitate the development of hyponatremia, particularly in individuals who have a decreased urine production during exercise. Exercise performance is also reduced with a decrease in plasma sodium concentration. We, therefore, recommend consumption of a sodium-containing beverage to compensate for large sweat losses incurred during exercise.     

Renal function in experimental potassium depletion. II. Indomethacin and effects of lysine-8-vasopressin in hypotonic polyuria

Renal function has been studied by the clearance (cl.) method during hypotonic polyuria--four 15-min cl. periods--and successive antidiuresis--two 60-min cl. periods (A1, A2)--induced by lysine-8-vasopressin (LVP), 5 mU in bolus followed by infusion at a rate of 0.04 mU/min. The endogenous creatinine cl. (Cc) and the osmotic cls. (Cosm, CH2O) were determined by the usual methods as well as the absolute and fractional urinary excretions of water, sodium, chloride and potassium. The urinary concentrations of PGE2, 6-keto-PGF1 alpha and TxB2 were determined by the RIA method. This study protocol has been applied to 20 healthy women submitted to paired functional explorations in both the absence and presence of indomethacin (100 mg i.m.); the drug effects have been evaluated in both normal potassium balance (N2, n = 6) and in two groups of potassium depletion (KD) with potassium cumulative deficit of 160 +/- 43 (D2, n = 8) and 198 +/- 22 meq (D3, n = 6), respectively. As regards the early % effects of LVP, i.e. (A1-P)% of P (mean polyuria), the inhibition of prostanoid synthesis with indomethacin produced significant changes: 1) an enhanced reduction in renal chloride excretion in all experimental groups; 2) a reduction in renal sodium and chloride fractional excretions in both KD groups; 3) an enhanced antidiuretic effect in D3 only, i.e. in the experimental condition with inhibition of prostanoid renal synthesis present during the control study.     

Aggregation patterns of bile salts: crystal structure of calcium cholate chloride heptahydrate

Crystals of calcium cholate chloride heptahydrate, CaC24H39O7Cl . 7H2O, are monoclinic, space group P2(1), with a = 11.918(2), b = 8.636(1), c = 15.302(3) A, beta = 97.93(3) degrees, V = 1559.9(8) A3, and Z = 2. A trial structure was obtained by Patterson and Fourier techniques and was refined by full-matrix least-squares calculations using absorption corrected CuK-alpha diffractometer data. The final R index is 0.047. The crystal structure contains bilayer-type arrangements, with hydrophobic portions of cholate rings sandwiched between layers of polar groups that are interacting with calcium ions and water molecules. The calcium ion is coordinated to five water molecules and to the two carboxylate oxygen atoms of the cholate residue. Two additional water molecules are involved only in crystal packing through the formation of hydrogen bonds. Cholate-cholate hydrophobic interactions involve contacts between the hydrocarbon portions of the carboxylate sidechains and the A and B rings. This results in a staggered packing pattern that is nearly identical to that found in crystals of sodium cholate and rubidium deoxycholate. Similar bilayer aggregation patterns may also be involved in the formation of bile salt micelles in aqueous media. The characteristic bilayer packing arrangement can accommodate a variety of cation-binding patterns, as evidenced by the finding that calcium, sodium, and rubidium ions interact with the polar faces of the bilayers in different ways. The carboxylate sidechain displays two different conformations in the crystal structure of calcium cholate chloride heptahydrate. Variation in sidechain conformation may be of importance in the adjustment required to accommodate different cation coordination schemes.     

Renal function in experimental potassium depletion. I. Effects of lysine-8-vasopressin in hypotonic polyuria

Renal function has been studied by the clearance (cl.) method during hypotonic polyuria--four 15-min cl. periods--and successive antidiuresis--two 60-min cl. periods (A1, A2)--induced by lysine-8-vasopressin (LVP), 5 mU in bolus followed by infusion at a rate of 0.04 mU/min. The endogenous creatinine cl. (Cc) and the osmotic cls. (Cosm, CH2O) were determined by the usual methods as well as the absolute and fractional urinary excretions of water, sodium, chloride and potassium. The urinary concentrations of PGE2, 6-keto-PGF1 alpha and TxB2 were determined by the RIA method. This study protocol has been applied to 28 healthy women either in normal potassium balance (N, n = 14) or after potassium depletion (KD) induced by low potassium dietary intake (less than or equal to 10 meq/d) plus natriuretic treatment according to two different time patterns: two KD groups were obtained with potassium cumulative deficit of 160 +/- 43 (D2, n = 8) and 198 +/- 22 meq (D3, n = 6). The early % effects of LVP, i.e. (A1-P)% of P (mean polyuria), were significantly different only in D3 as compared to N. Precisely, the LVP-effect to reduce Cc was blunted; moreover a LVP-effect to reduce renal sodium and chloride fractional excretions and a tendentiously enhanced LVP-effect to reduce water fractional excretion were observed. These tubular effects are likely related to the inhibited renal synthesis of prostanoids in the D3 group.     

Effect of calcitonin on fractional delivery of sodium and solutes to the juxtamedullary end-descending limb of the rat

The purpose of the present studies was to examine, by micropuncture, the effect of salmon calcitonin on fractional sodium and solutes deliveries to the juxtamedullary end-descending limb of the rat. All animals were postprandial and thyroparathyroidectomized Munich-Wistar rats. Group 1 (N = 8) consisted of time control water-diuretic rats; group 2 (N = 8) received synthetic salmon calcitonin (10 mU/min) intravenously while undergoing water diuresis; group 3 (N = 8) was treated as group 2 but also received calcium intravenously to prevent the calcitonin-induced fall in plasma calcium. Calcitonin, alone and with calcium, produced a marked fall in urine flow rate and a marked increase in urinary osmolality. Concomitant fractional water delivery to the end-descending limb fell significantly (28 +/- 0.8 to 21 +/- 1.0%, p less than 0.05), while fractional solute and sodium deliveries increased significantly (36 +/- 1.3 to 55 +/- 2.6%, p less than 0.05; 34 +/- 2.0 to 48 +/- 3.5%, p less than 0.05, respectively). The three groups did not significantly differ in fractional water and sodium deliveries to the superficial end-accessible proximal tubule. We conclude that salmon calcitonin is antidiuretic in the rat and that it also produces an increase in fractional sodium and total solute deliveries to the end-descending limb, which we suggest is due to transepithelial sodium addition. The physiological significance of these observations to water homeostasis in vivo remains to be determined.     

Preparation of (25R)- and (25S)-26-functionalized steroids as tools for biosynthetic studies of cholic acids

A new synthesis of both epimeric forms of 26-cholestanoic acids and 26-alcohols containing a 3beta-hydroxy-Delta(5)- or a Delta(4)-3-keto-functionality in ring A is described starting from stigmasterol or (20S)-3beta-acetoxy-pregn-5-en-20-carboxylic acid. The obtained compounds are useful as standards for studies of cholic acids. Construction of the side chain was achieved by linkage of steroidal 23-iodides to sulfones prepared from (2R)- and (2S)-3-hydroxy-2-methylpropanoates. Oxidation of intermediate 26-alcohols into the corresponding carboxylic acids ensuring preservation of stereochemistry at C-25 and functional groups in the cyclic part was achieved with sodium chlorite catalyzed by TEMPO and bleach.     

Association of calcium and sodium handling in the rabbit nephron. A micropuncture study.

Two-phase recollection micropuncture experiments were performed on female New Zealand rabbits to investigate the effect of flow rate (volume-expansion) compared to reabsorptive rate (furosemide) on calcium and sodium handling along the nephron. Group 1 (n = 6) rabbits represented nonvolume-expanded animals. Each experiment was conducted with a control phase followed by a second phase of furosemide administration (1 mg/kg/min). Group 2 rabbits (n = 6) were initially volume-expanded to 3% body weight with modified Ringers. The fractional excretion of sodium and calcium in the control phase of group I and II was 3 +/- 1 and 22 +/- 6% and 4 +/- 1 and 26 +/- 2%, respectively. Fractional excretion of sodium, calcium and magnesium rose after furosemide administration. The effect of volume expansion on sodium, calcium and magnesium remaining in the proximal tubule was relatively modest and not affected by furosemide. Our distal micropuncture data reveal that volume expansion has a greater inhibitory effect on fluid reabsorption at a site beyond the proximal micropuncture site (group 1, 9 +/- 2%, group 2,22 +/- 2%). After furosemide infusion, the amount of electrolytes remaining rose similarly in both groups; however, additional sodium and calcium reabsorption did not occur in the volume-expanded group in the final segment of the nephron. These results indicate that calcium reabsorption by the cortical terminal segment of the rabbits is passive similar to that suggested by the in vitro perfused study since no additional calcium reabsorption is seen in the volume-expanded rabbit.     

Sugar interaction with metal ions. Crystal structure and FT-IR spectroscopic study of strontium galactarate mono-hydrate

The crystal structure of strontium galactarate mono-hydrate, Sr2+ x C6H8O8(2-) x H2O, Mr = 313.76, monoclinic, P2(1)/c, a = 10.268(2), b = 10.333(2), c = 10.194(2) A, beta = 117.87(3) degrees, lambda(Mo K alpha) = 0.71073 A, Z = 4, Dx = 2.180 Mg m(-3), V = 956.1(3) A3, mu = 5.676 mm(-1), F(000) = 624, T = 293(2) K, R = 0.0260 for 1690 observed reflections and 145 parameters refined, has been determined. The galactarate ion is centro-symmetrical in the crystal structure, although it contains independent half-ions. The Sr2+ ion is nine-coordinated (tricapped trigonal prism) with five Sr-O bonds from carboxylic groups, and four from hydroxyl groups. The water molecule does not take part in the coordination. Six hydrogen bonds are formed, three of them related to the water molecule. The spectroscopic evidence shows that the carboxylic acid dimers of the free acid dissociate. The asymmetric stretching vibrations of the anionic COO groups in the salt are observed at 1609 and 1548, and 1581 cm(-1), assigned to a mono-dentate and a tetra-dentate coordination, respectively. The symmetric stretching vibration is located at 1397 cm(-1). The hydroxyl groups of the galactarate skeleton take part in the metal-oxygen interaction, and the hydrogen-bonding network is rearranged upon sugar metalation.     

Effect of increased surface tension and assisted ventilation on 99mTc-DTPA clearance

Experiments were performed to determine the effects of conventional mechanical ventilation (CMV) and high-frequency oscillation (HFO) on the clearance of technetium-99m-labeled diethylenetriamine pentaacetate (99mTc-DTPA) from lungs with altered surface tension properties. A submicronic aerosol of 99mTc-DTPA was insufflated into the lungs of anesthetized, tracheotomized rabbits before and 1 h after the administration of the aerosolized detergent dioctyl sodium sulfosuccinate (OT). Rabbits were ventilated by one of four methods: 1) spontaneous breathing; 2) CMV at 12 cmH2O mean airway pressure (MAP); 3) HFO at 12 cmH2O MAP; 4) HFO at 16 cmH2O MAP. Administration of OT resulted in decreased arterial PO2 (PaO2), increased lung wet-to-dry weight ratios, and abnormal lung pressure-volume relationships, compatible with increased surface tension. 99mTc-DTPA clearance was accelerated after OT in all groups. The post-OT rate of clearance (k) was significantly faster (P less than 0.05) in the CMV at 12 cmH2O MAP [k = 7.57 +/- 0.71%/min (SE)] and HFO at 16 cmH2O MAP (k = 6.92 +/- 0.61%/min) groups than in the spontaneously breathing (k = 4.32 +/- 0.55%/min) and HFO at 12 cmH2O MAP (4.68 +/- 0.63%/min) groups. The clearance curves were biexponential in the former two groups. We conclude that pulmonary clearance of 99mTc-DTPA is accelerated in high surface tension pulmonary edema, and this effect is enhanced by both conventional ventilation and HFO at high mean airway pressure.     

AVP-Induced Increase in AQP2 and p-AQP2 Is Blunted in Heart Failure during Cardiac Remodeling and Is Associated with Decreased AT1R Abundance in Rat Kidney

AimThe objective was to examine the renal effects of long-term increased angiotensin II and vasopressin plasma levels in early-stage heart failure (HF). We investigated the regulations of the V2 vasopressin receptor, the type 1A angiotensin II receptor, the (pro)renin receptor, and the water channels AQP2, AQP1, AQP3, and AQP4 in the inner medulla of rat kidney.MethodsHF was induced by coronary artery ligation. Sixty-eight rats were allocated to six groups: Sham (N = 11), HF (N = 11), sodium restricted sham (N = 11), sodium restricted HF (N = 11), sodium restricted sham + DDAVP (N = 12), and sodium restricted HF + DDAVP (N = 12). 1-desamino-8-D-arginine vasopressin (0.5 ng h-1 for 7 days) or vehicle was administered. Pre- and post-treatment echocardiographic evaluation was performed. The rats were sacrificed at day 17 after surgery, before cardiac remodeling in rat is known to be completed.ResultsHF rats on standard sodium diet and sodium restriction displayed biochemical markers of HF. These rats developed hyponatremia, hypo-osmolality, and decreased fractional excretion of sodium. Increase of AQP2 and p(Ser256)-AQP2 abundance in all HF groups was blunted compared with control groups even when infused with DDAVP and despite increased vasopressin V2 receptor and Gsα abundance. This was associated with decreased protein abundance of the AT1A receptor in HF groups vs. controls.ConclusionEarly-stage HF is associated with blunted increase in AQP2 and p(Ser256)-AQP2 despite of hyponatremia, hypo-osmolality, and increased inner medullary vasopressin V2 receptor expression. Decreased type 1A angiotensin II receptor abundance likely plays a role in the transduction of these effects.     

Preliminary X-ray analysis of crystals of fasciculin 1, a potent acetylcholinesterase inhibitor from green mamba venom

Fasciculin 1 from Dendroaspis angusticeps has been crystallized by vapour diffusion, in sodium acetate using sodium thiocyanate as precipitant. Tetragonal crystals (space group P4(1)2(1)2 or P4(3)2(1)2) diffract to 1.8 A resolution. The unit cell parameters are a = 40.4 A and c = 81.1 A. We estimated the presence of one molecule in the asymmetric unit.