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At least 955 records · Page 53Linked to original sources
PubMed2005

Implications for repetitive application of acetylcholine in the determination of the mechanisms of endothelium-dependent relaxation.

The influence of repetitive vasodilator concentration response curve determination was investigated in rat mesenteric and femoral small arteries. Arteries were precontracted with noradrenaline and relaxed with acetylcholine (ACh) or K+. Mesenteric arteries exhibited attenuation of ACh-stimulated relaxations during repetitive precontraction/relaxation cycles that was not prevented by SQ29548. Apamin, but not charybdotoxin, prevented the attenuation of this relaxation response. Borderline (p=0.064) statistical differences in the relaxations of mesenteric arteries in response to ACh remained in the presence of the nitric oxide synthase inhibitor L-NNA. In contrast, femoral arterial relaxations increased with repeated acetylcholine challenges. The enhanced responsiveness was prevented with L-NNA or Ba2+. In one experimental series, Ba2+ appeared to be without influence upon K+-stimulated relaxation of femoral arteries but a significant inhibitory effect was revealed when appropriate time control experiments were considered. These experiments reveal that impairment of SK(Ca) function and, to a lesser extent, an impaired NO signalling account for the attenuation of the relaxation responses of rat mesenteric arteries. In contrast, alterations of nitric oxide signalling and inward rectifier K channel activity contribute to enhanced relaxation responses in rat femoral arteries. These experiments highlight the importance of appropriate time control experiments for the proper interpretation of results derived from pharmacological experiments directed toward the elucidation of mechanisms of arterial vasorelaxation.

Acetylcholine↗
PubMed2001

Synthesis of 3-hexuloses from 1,2:5,6-di-O-isopropylidenehexitols.

A simple, but low-yielding method for the synthesis of 3-hexuloses has been elaborated. Oxidation of 1,2:5,6-di-O-isopropylidenehexitols with bromine in the presence of barium carbonate, followed by mild-acid hydrolysis of the oxidation products gave the free hexuloses. Oxidation occurred at only one of the carbon atoms bearing free hydroxyl groups. From the D-mannitol derivative, D-arabino-3-hexulose was obtained via the di-O-isopropylidene derivative, whereas the D-glucitol derivative gave a mixture of the 1,2:5,6-di-O-isoprpylidene derivatives of L-xylo- and D-ribo-3-hexulose, separable by column chromatography. Mild-acid hydrolysis of the oxidation products afforded the free hexuloses.

Barium↗
PubMed2000

Effect of leachability on environmental risk assessment for naturally occurring radioactive materials in petroleum oil fields.

Elevated concentrations of naturally occurring radioactive material (NORM), including 238U, 232Th, and their progeny found in underground geologic deposits, are often encountered during crude oil recovery. Radium, the predominant radionuclide brought to the surface with the crude oil and produced water, co-precipitates with barium in the form of complex compounds of sulfates, carbonates, and silicates found in sludge and scale. These NORM deposits are highly stable and very insoluble under ambient conditions at the earth's surface. However, the co-precipitated radium matrix is not thermodynamically stable at reducing conditions which may enable a fraction of the radium to eventually be released to the environment. Although the fate of radium in uranium mill tailings has been studied extensively, the leachability of radium from crude oil NORM deposits exposed to acid-rain and other aging processes is generally unknown. The leachability of radium from NORM contaminated soil collected at a contaminated oil field in eastern Kentucky was determined using extraction fluids having wide range of pH reflecting different extreme environmental conditions. The average 226Ra concentration in the samples of soil subjected to leachability testing was 32.56 Bq g(-1) +/- 0.34 Bq g(-1). The average leaching potential of 226Ra observed in these NORM contaminated soil samples was 1.3% +/- 0.46% and was independent of the extraction fluid. Risk assessment calculations using the family farm scenario show that the annual dose to a person living and working on this NORM contaminated soil is mainly due to external gamma exposure and radon inhalation. However, waterborne pathways make a non-negligible contribution to the dose for the actual resident families living on farmland with the type of residual NORM contamination due to crude oil recovery operations.

Animal Feed↗
PubMed1998

Metabotropic glutamate group II receptors activate a G protein-coupled inwardly rectifying K+ current in neurones of the rat cerebellum.

1. The effects of the group II metabotropic glutamate receptor (mGluR) agonists DCG-IV and LY354740 were examined in neurones freshly dissociated from the rat cerebellum and olfactory bulb, using the whole-cell configuration of the patch-clamp technique. 2. Under experimental conditions in which K+ currents would be inward, rapid application of DCG-IV and LY354740 to interneurones expressing the group II mGluRs induced an inward current in a subpopulation of interneurones of the cerebellum, the unipolar brush cells. 3. The currents induced by DCG-IV and LY354740 had the major characteristics of a G protein-coupled inwardly rectifying K+ channel (GIRK) current; namely, rapid activation and deactivation upon agonist application and removal, G protein dependence, strong inward rectification, Cs+ and Ba2+ sensitivity, and K+ selectivity. 4. In Golgi cells of the cerebellum and interneurones of the accessory olfactory bulb, which also express group II mGluRs, LY354740 did not induce GIRK activation but inhibited voltage-gated Ca2+ channel currents. 5. These results demonstrate that, in unipolar brush cells, native group II mGluRs can functionally couple to activation of GIRKs. Thus, the absence of coupling in the majority of CNS neurones examined to date may be due to restricted cellular co-localization or co-expression of the appropriate proteins.

Animals↗
PubMed1986

Characteristics of phasic and tonic sympathetic ganglion cells of the guinea-pig.

Intracellular recording techniques have been used to determine the electrophysiological properties of sympathetic neurones in ganglia of the caudal lumbar sympathetic chain (l.s.c.) and in the distal lobes of inferior mesenteric ganglia (i.m.g.) isolated from guinea-pigs. Passage of suprathreshold depolarizing current initiated transient bursts of action potentials in 97% of l.s.c. neurones, but only 13% of i.m.g. cells ('phasic' neurones). Most i.m.g. neurones fired continuously during prolonged depolarizing pulses ('tonic' neurones). Passive membrane properties varied; mean cell input resistance was similar between groups, but phasic neurones had smaller major input time constants on average than had tonic cells. Current-voltage relations determined under both current clamp and voltage clamp were linear around resting membrane potential (approximately 60 mV), where membrane conductance was lowest. Instantaneous and time-dependent rectification varied in the different neurone types. The current underlying the after-hyperpolarization following the action potential was significantly larger on average in tonic i.m.g. cells than in phasic neurones, although its time course (tau = 100 ms) was similar. Phasic neurones fired tonically when depolarized after adding the muscarinic agonist, bethanechol (10(-5) M to 10(-4) M), to the bathing solution. Bethanechol blocked a proportion of the maintained outward current (presumably the M-current, IM, Adams, Brown & Constanti, 1982) in phasic neurones; this current was small or absent in tonic neurones. Transient outward currents resembling the A-current (IA, Connor & Stevens, 1971 a) were evoked in tonic but not in phasic neurones by depolarization from resting membrane potential. IA could only be demonstrated in phasic neurones after a period of conditioning hyperpolarization. After a step depolarization to approximately --50 mV, IA reached peak amplitude at about 7 ms and then decayed with a time constant of about 25 ms in both neurone types. Activation characteristics of IA were similar for phasic and tonic neurones, but inactivation curves, although having the same shape, were shifted to more depolarized voltages in tonic neurones. That is, IA was largely inactivated at resting membrane potential in phasic, but not tonic neurones. It is concluded that the discharge patterns of the two populations of sympathetic neurones result from differences in the voltage-dependent potassium channels present in their membranes. The anatomical occurrence of the different cell types suggests that phasic neurones are vasoconstrictor and tonic neurones are involved with visceral motility.

4-Aminopyridine↗
PubMed2003

Five ADNFLE mutations reduce the Ca2+ dependence of the mammalian alpha4beta2 acetylcholine response.

Five nicotinic acetylcholine receptor (nAChR) mutations are currently linked to autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). The similarity of their clinical symptoms suggests that a common functional anomaly of the mutations underlies ADNFLE seizures. To identify this anomaly, we constructed rat orthologues (S252F, +L264, S256L, V262L, V262M) of the human ADNFLE mutations, expressed them in Xenopus oocytes with the appropriate wild-type (WT) subunit (alpha4 or beta2), and studied the Ca2+ dependence of their ACh responses. All the mutations significantly reduced 2 mM Ca2+-induced increases in the 30 microM ACh response (P < 0.05). Consistent with a dominant mode of inheritance, this reduction persisted in oocytes injected with a 1:1 mixture of mutant and WT cRNA. BAPTA injections showed that the reduction was not due to a decrease in the secondary activation of Ca2+-activated Cl- currents. The S256L mutation also abolished 2 mM Ba2+ potentiation of the ACh response. The S256L, V262L and V262M mutations had complex effects on the ACh concentration-response relationship but all three mutations shifted the concentration-response relationship to the left at [ACh] >= 30 microM. Co-expression of the V262M mutation with a mutation (E180Q) that abolished Ca2+ potentiation resulted in 2 mM Ca2+ block, rather than potentiation, of the 30 microM ACh response, suggesting that the ADNFLE mutations reduce Ca2+ potentiation by enhancing Ca2+ block of the alpha4beta2 nAChR. Ca2+ modulation may prevent presynaptic alpha4beta2 nAChRs from overstimulating glutamate release at central excitatory synapses during bouts of synchronous, repetitive activity. Reducing the Ca2+ dependence of the ACh response could trigger seizures by increasing alpha4beta2-mediated glutamate release during such bouts.

Acetylcholine↗