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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnesium homeostasis was determined in 48 healthy premenopausal women and in 54 early postmenopausal women. After an initial examination, the 54 postmenopausal women were randomly allocated to two groups with 33 receiving placebo treatment and 21 receiving estrogen substitutional therapy for 2 years. The 24-hour mean urinary excretion rates of magnesium were increased in the 54 postmenopausal women compared with the premenopausal women, namely: 467 +/- 20 (SEM) versus 355 +/- 13 mmol/mol creatinine (p less than 0.001) or 33.9 +/- 1.2 versus 24.3 +/- 1.0 mumol/l glomerular filtration (p less than 0.001). The same pattern was observed when the excretion rates were determined on fasting 1-hour morning urinary collections. This postmenopausal hypermagnesiuria was reduced to the premenopausal level during 2 years of estrogen substitutional therapy (p less than 0.001). As no evidence of hypomagnesemia was found, postmenopausal hypermagnesiuria probably originates from increased intestinal magnesium absorption, somehow induced by estrogen deficiency.
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PMID:Effect of menopause and estrogen substitutional therapy on magnesium metabolism. 660 48

Saliva was collected from the mandibular glands of anaesthetized common wombats (Vombatus ursinus) to ascertain maximal flow rates, salivary composition and possible adaptations, particularly PO4(3-) secretion, to assist digestion. After temporary catheterization of the main duct through its oral opening, salivary secretion was evoked at flow rates ranging from 0.02 +/- 0.002 (+/- SEM) ml.min-1 (0.7 +/- 0.07 microliter.min-1.kg body weight-1) to 0.4 +/- 0.05 ml.min-1 (14 +/- 1.9 microliters.min-1.kg body weight-1) by ipsilateral intracarotid infusion of acetylcholine. The [Na+] (15 +/- 5.1 to 58 +/- 8.6 mmol.l-1) and [HCO3-] (35 +/- 1.9 to 60 +/- 1.9 mmol.l-1) were positively correlated with salivary flow rate. The [K+] (58 +/- 5.2 to 30 +/- 2.4 mmol.l-1), [Ca2+] (10.4 +/- 1.67 to 4.1 +/- 0.44 mmol.l-1), [Mg2+] (0.94 +/- 0.137 to 0.17 +/- 0.032 mmol.l-1), [Cl-] (71 +/- 9.2 to 45 +/- 6.0 mmol.l-1), [urea] (9.3 +/- 0.79 to 5.1 +/- 0.54 mmol.l-1), H+ activity (29 +/- 1.6 to 17 +/- 1.6 nEq.l-1) and amylase activity (251 +/- 57.4 to 92 +/- 23.3 mu kat.l-1) were negatively correlated with flow. Both concentration and osmolality fell with increasing flow at the lower end of the flow range but osmolality always increased again by maximal flow whereas the relation between protein and flow was not consistent at the higher levels of flow and stimulation. Salivary [PO4(3+)] was not correlated with flow and at 3-14% of the plasma concentration was extremely low.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secretion of electrolytes, protein and urea by the mandibular gland of the common wombat (Vombatus ursinus). 773 31

Na+/Mg2+ antiport and Na(+)-independent Mg2+ efflux were investigated in erythrocytes of 41 patients with cystic fibrosis and 26 controls. Na(+)-independent Mg2+ efflux was unchanged in cystic fibrosis, but a significantly increased activity of Na+/Mg2+ antiport was detected (control: 0.16 +/- 0.02, cystic fibrosis: 0.39 +/- 0.06, Mg2+ efflux, mmol/30 min x 1 cells, mean +/- SEM, p < 0.01). An increased activity of Na+/Mg2+ antiport was only found in patients with severe clinical symptoms. There was no correlation of the increased Na+/Mg2+ antiport to the dF508 genotype. In a patient with increased Na+/Mg2+ antiport, the capacity of this transport system was unchanged 14 weeks after double lung transplantation but reached control values after 53 weeks. The sweat of cystic fibrosis patients with severe clinical symptoms showed a significantly increased Mg2+ concentration (control (n = 12): 0.053 +/- 0.08, cystic fibrosis (n = 9): 0.123 +/- 0.016 mmol/l, mean +/- SEM, p < 0.001).
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PMID:Increased Na+/Mg2+ antiport in erythrocytes of patients with cystic fibrosis. 788 79

The aim of this study was to determine whether the final enzymes in the two biosynthetic pathways for platelet-activating factor (PAF) (the 'de novo' and the 'membrane remodelling' pathways) are present in mouse embryos, zygotes and oocytes. The enzymes are dithiothreitol-insensitive cytidinediphosphocholine: 1-O-alkyl-2-acetyl-sn-glycerol cholinephosphotransferase (cholinephosphotransferase) in the de novo pathway and acetyl-coenzyme A:1-O-alkyl-2-lyso-sn-glycero-3-phosphocholine acetyltransferase (acetyltransferase) in the membrane remodelling pathway. Activity of both enzymes was detected in the unfertilized oocyte, the zygote and also in the preimplantation embryo (48, 72 and 96 h after the ovulatory injection of hCG). In both cases the activity was destroyed by boiling and increased linearly with incubation time and the concentration of embryo homogenate present, indicating that the reactions were catalysed by enzymes. The product of the reactions was confirmed as PAF using HPLC and structural analyses by enzymatic digestion. Cholinephosphotransferase required Mg2+ and was inhibited by Ca2+, while acetyltransferase required the presence of NaF (a phosphatase inhibitor). The activity of cholinephosphotransferase was similar in unfertilized oocytes and zygotes, and did not change significantly with advancing developmental stage in preimplantation embryos. Acetyltransferase had a significantly lower specific activity (0.078 +/- 0.044 fmol PAF per oocyte per min, mean +/- SEM) in unfertilized oocytes than in zygotes of corresponding age (0.358 +/- 0.097 fmol PAF per zygote per min) (P < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detection and preliminary characterization of two enzymes involved in biosynthesis of platelet-activating factor in mouse oocytes, zygotes and preimplantation embryos: dithiothreitol-insensitive cytidinediphosphocholine: 1-O-alkyl-2-acetyl-sn-glycerol cholinephosphotransferase and acetyl-coenzyme A:1-O-alkyl-2-lyso-sn-glycero-3-phosphocholine acetyltransferase. 793 73

We have previously demonstrated (M. Stubbs, Z. M. Bhujwalla, G. M. Tozer, L. M. Rodrigues, R. J. Maxwell, R. Morgan, F. A. Howe, and J. R. Griffiths, NMR Biomed., 5: 351, 1992) that the intracellular pH (pHi) of several rat tumors is higher (> pH 7.0) than that of the tumor extracellular fluid (pHe), in contrast to normal tissues (e.g., liver) in which pHi is lower than pHe. In this paper we confirm a pHe of 6.8 +/- 0.07 (SEM) in Morris hepatoma 9618a by an independent method and report the tissue content of other ions by both 31P magnetic resonance spectroscopy and by conventional analysis in hepatomas and livers in rats. Compared with liver, tissue Na+ was 2-fold higher and tissue K+ was lower. Tissue Ca2+ was 8-fold higher (7.4 +/- 4.3 mumol/g wet weight) and tissue Pi was 2-fold higher (8.5 +/- 1.3 mumol/g wet weight) suggesting the presence of insoluble calcium phosphate. Cl- was unchanged (approximately 40 mumol/g wet weight), whereas HCO3- was lower in the hepatoma (12.4 +/- 0.83 compared to 15.5 +/- 0.76 mumol/g wet weight). Total tissue Mg2+ was similar in both tissues, but free [Mg2+] (calculated by two different methods) was approximately 5-fold lower in the hepatoma. The ATP values were 3.5-fold and [NAD]/[NADH] 9-fold lower in the hepatoma. The results are compatible with the hypothesis that the chronic partial hypoxia of tumor tissue involves changes in the linked equilibria of many ions and metabolites and may help explain such pathologies as calcification.
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PMID:Metabolic consequences of a reversed pH gradient in rat tumors. 803 32

The effects of high intracellular concentrations of various calcium buffers on the myoplasmic calcium transient and on the rate of release of calcium (Rrel) from the sarcoplasmic reticulum (SR) were studied in voltage-clamped frog skeletal muscle fibers. The changes in intracellular calcium concentration (delta[Ca2+]) for 200-ms pulses to 0-20 mV were recorded before and after the injection of the calcium buffer and the underlying Rrel was calculated. If the buffer concentration after the injection was high, the initial rate of rise of the calcium transient was slower after injection than before and was followed by a slow increase of [Ca2+] that resembled a ramp. The increase in myoplasmic [Mg2+] that accompanies the calcium transient in control was suppressed after the injection and a slight decrease was observed instead. After the injection the buffer concentration in the voltage-clamped segment of the fiber decreased as the buffer diffused away toward the open ends. The calculated apparent diffusion coefficient for fura-2 (Dapp = 0.40 +/- 0.03 x 10(-6) cm2/s, mean +/- SEM, n = 6) suggests that approximately 65-70% of the indicator was bound to relatively immobile intracellular constituents. As the concentration of the injected buffer decreased, the above effects were reversed. The changes in delta[Ca2+] were underlined by characteristic modification of Rrel. The early peak component was suppressed or completely eliminated; thus, Rrel rose monotonically to a maintained steady level if corrected for depletion. If Rrel was expressed as percentage of SR calcium content, the steady level after injection did not differ significantly from that before. Control injections of anisidine, to the concentration that eliminated the peak of Rrel when high affinity buffers were used, had only a minor effect on Rrel, the peak was suppressed by 26 +/- 5% (mean +/- SE, n = 6), and the steady level remained unchanged. Thus, the peak component of Rrel is dependent on a rise in myoplasmic [Ca2+], consistent with calcium-induced calcium release, whereas the steady component of Rrel is independent of myoplasmic [Ca2+].
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PMID:Microinjection of strong calcium buffers suppresses the peak of calcium release during depolarization in frog skeletal muscle fibers. 838 43

We used the whole cell patch clamp technique to investigate the characteristics of modification of cardiac Na+ channel gating by the sea anemone polypeptide toxin anthopleurin-A (AP-A). Guinea pig ventricular myocytes were isolated enzymatically using a retrograde perfusion apparatus. Holding potential was -140 mV and test potentials ranged from -100 to +40 mV (pulse duration 100 or 1000 ms). AP-A (50-100 nM) markedly slowed the rate of decay of Na+ current (INa) and increased peak INa conductance (gNa) by 38 +/- 5.5% (mean +/- SEM, P < 0.001, n = 12) with little change in slope factor (n = 12) or voltage midpoint of the gNa/V relationship after correction for spontaneous shifts. The voltage dependence of steady-state INa availability (h infinity) demonstrated an increase in slope factor from 5.9 +/- 0.8 mV in control to 8.0 +/- 0.7 mV after modification by AP-A (P < 0.01, n = 14) whereas any shift in the voltage midpoint of this relationship could be accounted for by a spontaneous time-dependent shift. AP-A-modified INa showed a use-dependent decrease in peak current amplitude (interpulse interval 500 ms) when pulse duration was 100 ms (-15 +/- 2%, P < 0.01, n = 17) but showed no decline when pulse duration was 100 ms (-3 +/- 1%). This use-dependent effect was probably the result of a decrease in the recovery from inactivation caused by AP-A which had a small effect on the fast time constant of recovery (from 4.1 +/- 0.3 ms in control to 6.0 +/- 1.1 ms after AP-A, P < 0.05) but increased the slow time constant from 66.2 +/- 6.5 ms in control to 188.9 +/- 36.4 ms (P < 0.002, n = 19) after exposure to AP-A. Increasing external divalent cation concentration (either Ca2+ or Mg2+) to 10 mM abolished the effects of AP-A on the rate of INa decay. These results demonstrate that modification of cardiac Na+ channels by AP-A markedly slowed INa inactivation and altered the voltage dependence of activation; these alterations in gating characteristics, in turn, caused an increase in gNa presumably by increasing the number of channels open at peak INa. AP-A slows the rate of recovery of INa from inactivation which is probably the basis for a use-dependent decrease in peak amplitude. Finally, AP-A binding is sensitive to external divalent cation concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Modification of cardiac Na+ channels by anthopleurin-A: effects on gating and kinetics. 839 71

Intracellular calcium ion ([Ca2+]i) transients were measured in single rat ventricular myocytes with the fluorescent indicator furaptra. Cells were voltage clamped with a single patch electrode containing the K+ salt of furaptra and fluorescence at 500 nm was measured during illumination with 350 and 370 nm light. Depolarizing voltage-clamp pulses elicited [Ca2+]-dependent fluorescent transients in 30 of 33 cells tested. The peak change in [Ca2+]i elicited by 50-ms depolarizations from -70 to +10 mV was 1.52 +/- 0.25 microM (mean +/- SEM, n = 7). The size of the [Ca2+]i transient increased in response to 10 microM isoproterenol, prolongation of the depolarization, and increasing pipette [Na+]. Because furaptra is sensitive to Ca2+ and Mg2+, changes in [Mg2+]i during the [Ca2+]i transient could not be measured. Instead, a single-compartment model was developed to simulate changes in [Mg2+] during [Ca2+] transients. The simulations predicted that a 2 microM [Ca2+] transient was accompanied by a slow increase in [Mg2+] (14-29 microM), which became larger as basal [Mg2+] increased (0.5-2.0 mM). The [Mg2+] transient reached a peak approximately 1 s after the peak of the [Ca2+] transient with the slow changes in [Mg2+] dominated by competition at the Ca2+/Mg2+ sites of Troponin. These changes in [Mg2+], however, were so small and slow that they were unlikely to affect the furaptra fluorescence signal at the peak of the [Ca2+]i transient. The [Ca2+]i transient reported by furaptra appears to be larger than that reported by other Ca2+ indicators; however, we conclude this larger transient is at least as accurate as [Ca2+]i transients reported by the other indicators.
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PMID:Ca transients in cardiac myocytes measured with a low affinity fluorescent indicator, furaptra. 849 88

Modulatory actions of Zn2+ (0.05-2 mM) on spontaneous, stimulus evoked excitatory postsynaptic potentials (EPSPs) or currents (EPSCs) and GABA, L-glutamate induced depolarizations were examined in current- and voltage-clamp conditions. Identified and unidentified Helix pomatia L. neurons were used in the experiments. Zn2+ increased the frequency of the spontaneous EPSPs or EPSCs in a dose-dependent manner but the excitation slowly declined with time. Two phasic effects of Zn2+ on stimulus evoked EPSPs or EPSCs were characteristic in both normal and low Ca(2+)-high Mg2+ salines. Zn2+ in a low dose (0.05-0.4 mM) increased, but in a higher dose decreased the amplitude of the evoked EPSP or EPSCs. Higher than 1 mM Zn2+ sustained the voltage dependence of the stimulus evoked EPSPs or EPSCs. Sodium-potassium dependent depolarizations of GABA and glutamate responses were attenuated by zinc ions. The zinc ion sensitivity of neurons derived from active animals was higher then of hibernating species (IC50 = 0.73 +/- 0.006; 1.33 +/- 0.12, respectively, mean +/- SEM, n = 12). We conclude that zinc ions have both pre- and post-synaptic effects. Zinc induced actions on Helix neuronal synapses based on the modulation of a complex phenomenon appear to be more than one mechanism.
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PMID:Actions of Zn2+ on spontaneous, stimulus and transmitter evoked events in Helix neurons. 885 14

To establish the role of pituitary adenylate cyclase activating polypeptide (PACAP), a member of vasoactive intestinal polypeptide (VIP) family, as a neurotransmitter/neuromodulator in the central nervous system, the effects of PACAP38, PACAP27 and VIP on the single neuron activity in the magnocellular portion of the hypothalamic paraventricular nucleus (mg.PVN) were examined in rat brain slice preparations. Extracellular recordings were made from 111 neurons in the mg.PVN, which fired spontaneously at an average rate of 1.85 +/- 0.2 spikes/s (mean +/- SEM). PACAP38 and PACAP27 were applied to 78 and 33 of the 111 neurons, respectively. Perfusion with PACAP38 in doses between 10 nM and 1 microM increased the firing rate of 56 (71.8%) of the 78 neurons in a dose-dependent manner. The threshold dose of PACAP38 to excite the neurons seemed to lie below 10 nM. The application of PACAP27 (1 microM) also increased the firing rate of 19 (57.6%) of the 33 neurons tested. Eleven (52.4%) of 21 neurons which were excited by PACAP38 also showed excitation following perfusion with VIP (1 microM). The responses to PACAP38 in 12 of 20 neurons and those to VIP in 6 of 9 neurons tested were still observed in a low Ca2+ and high Mg2+ medium. Although there was no difference in the mean latency between the responses to PACAP38 (1 microM) and VIP (1 microM) (2.1 +/- 0.1 min and 2.4 +/- 0.4 min, respectively), the duration of the PACAP38-induced excitation (59.0 +/- 5.0 min) was much longer than that of the VIP-induced one (18.8 +/- 3.1 min). The PACAP38 (30 nM)-induced excitation was reversibly blocked by a concurrent application of PACAP5-38 (300 nM), a PACAP receptor antagonist. While a selective VIP receptor antagonist, [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP (1 microM), did not affect the excitatory responses to PACAP38 (300 nM), it completely blocked the VIP (1 microM)-induced excitation. These findings suggest that PACAP may therefore modulate the secretion of the pituitary hormones at least partly by its action on the neurons in the mg.PVN through the activation of specific receptors for PACAP.
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PMID:Facilitatory effects of pituitary adenylate cyclase activating polypeptide (PACAP) on neurons in the magnocellular portion of the rat hypothalamic paraventricular nucleus (PVN) in vitro. 886 61


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