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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 287-294 
    ISSN: 1432-1912
    Keywords: Endothelium ; Calcium fluxes ; Alpha ; Adrenoceptor agonist ; Rat aorta ; Carbachol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Preincubation with carbachol (10 μM) did not affect basal 45Ca accumulation by rat isolated aortic segments complete with endothelium, although 45Ca accumulation was enhanced by removal of endothelium. This confirms the observation that in the presence of endothelium Ca2+ influx in rat aorta is antagonized, and indicates that the basal release of an endothelial derived factor might be sufficient to maximally antagonize basal Ca2+ influx, or alternatively that EDRF released as a result of muscarinic stimulation does not have identical effects to the factor released under basal conditions. Accumulation of 45Ca stimulated by B-HT 920 but not that stimulated by phenylephrine was antagonized in the presence of endothelium. Contractions elicited by B-HT 920 were abolished in the presence of endothelium while contractions evoked by phenylephrine were reduced by about 50%. Preincubation with 10 μM carbachol antagonized both phenylephrine (1 μM) stimulated 45Ca accumulation and contractile responses in the presence of endothelium to about the same extent. Therefore, it might be concluded that the inhibitory effect of EDRF in this tissue is due to an inhibition of stimulated Ca2+ influx. However, while addition of carbachol to tissues precontracted with phenylephrine elicited an immediate relaxation in the presence of endothelium, this relaxation could not be correlated with a reduction in tissue accumulation of 45Ca. Carbachol also antagonized the phenylephrine-induced reduction of tissue 45Ca content (i.e. efflux of Ca2+), in tissues preloaded with 45Ca. This implies that the initial endothelial-mediated relaxant effect of carbachol in precontracted tissues cannot be explained either by reduced influx or by an enhanced efflux of Ca2+ from the smooth muscle cells. Therefore, it is concluded that although EDRF mediates a reduction in agonist-induced Cat2+ uptake it also exerts other effects, one of which may be an initial redistribution of intracelllar Ca2+, resulting in a reduction in free intracellular Ca2+ levels and therefore in relaxation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 15 (1990), S. 407-417 
    ISSN: 1573-6903
    Keywords: Endothelin ; calcium ; calcium entry blockers ; smooth muscle ; nerve
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The recently identified endothelium-derived peptide, endothelin, is a potent vasoconstrictor, but also binds specifically to many types of smooth muscle and to nerve tissue. Endothelin has been detected in plasma and may have physiological or pathological functions. Like other agonists, endothelin increases the turnover of phosphatidyl inositol and liberates intracellular stocks of Ca2+. It also increases plasmalemmal Ca2+ permeability, an effect that is antagonized by calcium entry blockers in some tissues. However, the characteristics of this antagonism are not always typical of that seen when other types of agonists are employed. It seems that in at least some cell types endothelin might activate specific L-type Ca2+ channels indirectly, perhaps secondarily to the activation of another type of cation channel. The endothelin originally described is one of a family of peptides that are closely related to the sarafotoxins. The comparative pharmacology of these peptides and of some analogues of the originally described endothelin have revealed some surprising differences and may indicate the existence of different endothelin receptors.
    Type of Medium: Electronic Resource
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