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  • 1
    ISSN: 0014-5793
    Keywords: Aerobic desaturation ; Anaerobic pathway ; Unsaturated fatty acid ; Vibrio
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1434-0879
    Keywords: Bladder detrusor muscle ; Acetylcholine ; Calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of extracellular and intracellular Ca2+ on acetylcholine-induced contraction of the bladder detrusor muscle were studied in vitro, utilizing two types of Ca2+ antagonists of different mechanisms of action; verapamil and sodium nitroprusside (NP). Acetylcholine (10-8 to 10-2 M) caused dose-dependent contractions of the detrusor muscle strips. Pretreatment of the strips with verapamil (10-7, 10-6 M) significantly inhibited the acetylcholine-induced contraction in a dose-dependent manner, whereas NP (10-7 to 10-5 M) failed so suppress the contraction. The contraction of the strips once elicited by acetylcholine (10-6 M) could be completely relaxed by verapamil (10-5 M) addition, but only incompletely by NP (10-5, 10-4 M). In Ca2+-free solution containing 0.01 mM EGTA, replenishment of Ca2+ (2.5 mM) to the medium caused contractions of the strips. Addition of acetylcholine (10-6 M) to the medium enhanced the Ca2+-induced contration, which was significantly inhibited by pretreatment with verapamil (10-6 M), but not affected by NP (10-6 M). In Ca2+-free medium containing 0.1 mM EGTA, acetylcholine caused a slight degree of tension increase of the strips in a dosedependent fashion, at higher concentrations exceeding 10-6 M. These results suggest that the detrusor muscle contraction induced by acetylcholine is mostly dependent of extracellular Ca2+ influx both in its initiation and maintenance. It is also supposed, however, that in tracellular Ca2+ fractions will partly participate in the acetylcholine-induced contration and possibly in its maintenance.
    Type of Medium: Electronic Resource
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