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  • 1
    ISSN: 1432-1912
    Keywords: α1A-adrenoceptors ; α1B-adrenoceptors ; Rat kidney ; Inositol phosphates ; G protein ; Calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have compared the coupling mechanisms of rat renal α1A- and α1B-like adrenoceptors to inositol phosphate formation. The experiments were performed in parallel in native renal tissue preparations and in those where α1B-adrenoceptors had been inactivated by treatment with 10 μmol/l chloroethylclonidine for 30 min at 37°C; renal slices were used in most experiments but isolated renal cells were also used in some cases. The Ca2+ chelating agent, EGTA (5 mmol/l), reduced noradrenaline-stimulated inositol phosphate formation in native but enhanced it in chloroethylclonidine-treated renal slices. The inhibitory effect of EGTA was not mimicked by 100 nmol/l nifedipine. Inactivation of 87% of cellular Gi by 16–20 h treatment with 500 ng/ml pertussis toxin did not significantly affect noradrenaline-stimulated inositol phosphate formation in isolated renal cells but abolished the inhibitory effect of chloroethylclonidine. The adenylate cyclase activator, forskolin (20 μmol/l), inhibited noradrenaline-stimulated inositol phosphate formation in native and chloroethylclonidine-treated slices, and the inhibitory effects of chloroethylclonidine treatment and forskolin were additive. We conclude that in rat kidney inositol phosphate formation via α1B-like adrenoceptors may involve the influx of extracellular Ca2+ and a pertussis toxin-sensitive G-protein but is insensitive to inhibition by forskolin. In contrast α1A-like adrenoceptor-mediated inositol phosphate formation does not require the presence of extracellular Ca2+ or of Gi and is sensitive to inhibition by forskolin. In comparison to published data from other model systems we further conclude that the signaling mechanisms of α1-adrenoceptor subtypes may depend on their cellular environment.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1009
    Keywords: Acid precipitation ; Biomass nutrients ; Calcium ; Clearcutting ; Magnesium ; Nitrogen ; Phosphorus ; Potassium ; Soil leaching ; Soil nutrients ; Timber harvest ; Weathering ; Whole-tree harvest
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering
    Notes: Abstract Both harvest removal and leaching losses can deplete nutrient capital in forests, but their combined long-term effects have not been assessed previously. We estimated changes in total soil and biomass N, Ca, K, Mg, and P over 120 years from published data for a spruce-fir site in Maine, two northern hardwood sites in New Hampshire, central hardwood sites in Connecticut and Tennessee, and a loblolly pine site in Tennessee. For N, atmospheric inputs counterbalance the outputs, and there is little long-term change on most sites. For K, Mg, and P, the total pool may decrease by 2%–10% in 120 years depending on site and harvest intensity. For Ca, net leaching loss is 4–16 kg/ha/yr in mature forests, and whole-tree harvest removes 200–1100 kg/ha. Such leaching loss and harvest removal could reduce total soil and biomass Ca by 20%–60% in only 120 years. We estimated unmeasured Ca inputs from rock breakdown, root-zone deepening, and dry deposition; these should not be expected to make up the Ca deficit. Acid precipitation may be the cause of current high leaching of Ca. Although Ca deficiency does not generally occur now in acid forest soils, it seems likely if anthropogenic leaching and intensive harvest removal continue.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2013
    Keywords: Crayfish neuromuscular junction ; Veratridine ; Excitatory synapse ; Asynchronous quantal release ; Quantal store of transmitter ; Calcium ; Noise analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract At single voltage-clamped opener muscle fibres of crayfish claw, 10–100 μmol/l veratridine increased within a few seconds the rate of asynchronous quantal release, ñ, of excitatory transmitter from ñ〈1 quantum/s to ñ≃10,000 quanta/s. Thereafter ñ declined exponentially either with a single, τ(2)≃50 s, or with two time constants τ(1)≃19 s, τ(2)≃50 s. In total (t→∞), about 0.3 million quanta were released by veratridine in a single short fibre of about 1 mm length. These values were estimated by means of the noise analysis technique and they agreed with equivalent parameters of release when 100 mmol/l K+ were used as release stimulus. Strong quantal release could be elicited only once in a single muscle by veratridine. Furthermore, the effect of veratridine on quantal release could be completely prevented by pretreatment with tetrodotoxin. In another nerve-muscle preparation of crayfish, the abdominal superficial extensor muscle, up to 3 million excitatory quanta could be released by veratridine in a single fibre. In the latter muscle veratridine-induced asynchronous quantal release was strongly dependent on the extracellular concentration of Ca2+ whereas in the claw opener dependence of quantal release on extracellular Ca2+ was negligible.
    Type of Medium: Electronic Resource
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