Interactions between sodium balance, intrarenal dopamine synthesis, and sympathetic activity in HLA-identical kidney donors and recipients

Intrarenal dopamine (DA) synthesis, sympathetic activity andsodium homeostasis were studied in eight HLA-identical kidneyrecipient and donor pairs at 50, 150, and 300 mmol sodium intake.Trimethaphan was given intravenously (i.v.), to mimic acutedenervation, tyramine i.v. to induce noradrenaline (NE) release,and the DA precursor DOPA i.v. to study DOPA to DA conversion.Blood pressure was higher in the recipients (P<0.05) andwas not influenced by sodium intake. Cumulative sodium balanceswere not different between the groups. Sodium intake did notaffect DA excretion in either group. The recipients had higherDA (P<0.05) and DOPA (P<0.01) excretions and lower urinaryDA over DOPA ratio (U_DA/DOPA, P<0.01) and lower NE excretion(P<0.05) during the whole study. High sodium intake suppressedthe U_DA/DOPA in both groups (P<0.05). Trimetaphan decreasedrenal vascular resistance (RVR) and increased sodium excretiononly in the donors (P<0.05), while GFR increased in bothgroups. During HiSo tyramine increased RVR in the recipients(P<0.01) and U_DA/DOPA in the donors (P<0.05). DOPA infusionincreased DA excretion four to fivefold but did not change sodiumexcretion in either group. It is concluded that the recipientsmaintained sodium homeostasis well but seem to have an impairedfunctional innervation of the transplanted kidney. NE releaseseem to stimulate intrarenal DOPA to DA conversion. In bothgroups a direct relation between DA and sodium excretion waslacking.     

Increased human erythrocyte sodium-Iithium countertransport in hyperlipidaemic patients may indicate increased membrane lipid fluidity

Abstract. Erythrocyte sodium-lithium countertransport (SLC) activity, membrane fluidity, plasma trigly-ceride and cholesterol were measured in hyperlipidaemic patients and normal subjects. Fluidity was assessed by the fluorescence anisotropy (inversely related to fluidity) of the probes 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1,4-trimethylammonium-3,5-hexatriene (TMA-DPH). In a second group of patients the maximum velocity (Vmax) and external sodium affinity constant (k_m) of SLC was also measured.
In the first group of patients, SLC activity was increased compared with the controls (0.279 ± 0.019 vs. 0.213 ± 0.013, P = 0.006) as was membrane fluidity in the deep hydrophobic regions (DPH anisotropy 0.211 ± 0.0007 vs. 0.215 ± 0.0011, P = 0.007). There was a strong correlation between SLC and DPH anisotropy (Rs= -0.72, P= < 0.001) which was due to the correlation between Vmax and DPH anisotropy (Rs=-0.90, P= < 0.001).
Increases in Vmax of SLC in hyperlipidaemic patients may be due to differences in lipid organisation in the deep hydrophobic regions of the membrane which may affect the turnover rate of the transporter.     

ANTEROVENTRAL WALL OF THE THIRD VENTRICLE AND DORSAL LAMINA TERMINALIS: HEADQUARTERS FOR CONTROL OF BODY FLUID HOMEOSTASIS?

1. The subfornical organ, median preoptic nucleus and the organum vasculosum of the lamina terminalis (OVLT) are a series of structures situated in the anterior wall of the third ventricle and form the lamina terminalis. The OVLT and ventral part of the median preoptic nucleus are part of a region known as the anteroventral third ventricle region.
2. Data from many laboratories, using techniques ranging from lesions, electrophysiology, neuropharmacology, Fos expression, immunohistochemistry and receptor localization, indicate that the tissue in the lamina terminalis plays a major role in many aspects of body fluid and electrolyte balance.
3. The subfornical organ and OVLT lack the blood-brain barrier and detect alterations in plasma tonicity and the concentrations of circulating hormones such as angiotensin II and possibly atrial natriuretic peptide and relaxin.
4. This information is then integrated within the lamina terminalis (probably in the median preoptic nucleus) with neural signals from other brain regions. The neural output from the lamina terminalis is distributed to a number of effector sites including the paraventricular (both parvo- and magno-cellular parts) and supraoptic nuclei and influences vasopressin secretion, water drinking, salt intake, renin secretion, renal sodium excretion and cardiovascular regulation.     

Effects of tetrodotoxin monoclonal antibody on the blocking action of tetrodotoxin on sodium channels

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DL-酒石酸的诱导拆分

将(±)-酒石酸制成其钠铵盐,在27℃以下进行诱导拆分,得(+)-和(-)-酒石酸钠铵,经转化为钙盐,再处理精制可得合格的(+)-和(-)-酒石酸。总收率为91%以上。     

瓜蒌皮抗缺氧作用的研究

实验结果显示，瓜蒌皮提取液（ＥＰＴ）腹腔注射４０ ｇ·ｋｇ－１能明显延长常压缺氧、组织缺氧、特异性心肌缺氧小鼠的存活时间，延长率分别为 １４５％， ２．７９％， １１０．７％，使减压缺氧小鼠的存活率达８５％．表明瓜蒌皮确能增强整体动物的抗缺氧能力．     

Glucose and Cation Transport in Rat Jejunum,Ileum and Colon in vivo: Effects of Anionic and Nonionic Surfactants,and of Desoxycholate

Abstract Osmotically balanced solutions of glucose (0.5–300 mM) and sodium chloride, containing surfactants, were instilled into the small or large intestine of anaesthetized rats. Net absorption or secretion of glucose, sodium and potassium was studied. The surfactants tested were dodecylsulphate (3.4–17 mM), dioctyl-sulphosuccinate (1.8–11 m/M), Lubrol WX (0.1–0.5%), Triton × 100 (0.25%) and desoxycholate (2.5 mM). Qualitatively, the results were similar to those obtained previously with cationic compounds, suggesting a common mode of action for all surfactants studied. 17 mM dodecylsulphate seemed to abolish completely physiological glucose transport in the jejunum and ileum. At a lower concentration, and with the other surfactants, normal glucose transport was affected to an intermediate extent.     

Acute and chronic effects of dextropropoxyphene on behaviour and central inhibitory neurotransmission in the rat

There was no overt evidence of the development of physical dependence, as shown by a decrease in the body weight of rats following the abrupt withdrawal of dextropropoxyphene after two weeks administration. The ambulation and rearing scores in the 'open field' apparatus were increased after chronic, but not acute drug administration and returned to control values two days following drug withdrawal. GABA turnover, determined from the rise in GABA concentrations following GABA-transaminase inhibition, was reduced in the frontal and amygdaloid cortex after acute and chronic drug administration; a compensatory rise in GABA turnover in the amygdaloid cortex occurred two days after drug withdrawal. Na+, K+, ATP'ase activity, determined in a synaptosomal fraction from the mid-brain and hippocampus, was decreased in the latter region only during drug administration; a compensatory increase in the activity of this enzyme was found two days after drug withdrawal. These results support the view that chronically administered dextropropoxyphene may cause changes in inhibitory transmission and central neurotransmitter transport.