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  • 1
    Electronic Resource
    Electronic Resource
    Fast and slowly inactivating components of Ca-channel current and their sensitivities to nicardipine in isolated smooth muscle cells from rat vas deferens (1988)
    Springer
    Pflügers Archiv 411 (1988), S. 289-295 
    Details
    ISSN: 1432-2013
    Keywords: Vas deferens ; Isolated smooth muscle cells ; Whole cell recording ; Ca-channel current ; Inactivation ; Sensitivity to nicardipine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract (1) Fast and slowly inactivating components of Ca-channel current were compared to clarify whether more than one type of Ca-channel exists in smooth muscle cells from rat vas deferens using the whole cell variant of the patch clamp technique. The pipette was filled with 150 mM Cs solution to eliminate outward current and Ba was used as the charge carrier for Ca-channel current. (2) When activated by a 5 s test pulse to 0 mV from a holding potential of −60 mV, the inactivation process of Ba-current was well fitted by the sum of two exponentials. The time constant of the faster inactivating component was 100–300 ms and that of the slower inactivating component was 1.5–3 s. Steadystate inactivation curves of the fast- and slow-components were very similar. (3) The inward current activated at 0 mV from −80 mV was inactivated faster than that from −30 mV. The voltage-dependencies of the peak current from holding potentials of −30 mV and −80 mV were similar. Both had voltage threshold at −30 mV and were maximal at +10 mV. (4) Low concentrations of nicardipine (10−9 to 10−7 M) preferentially inhibited the slow component while higher concentration (10−6 to 10−5 M) were required to block the fast component. The current activated from a holding potential of −30 mV was almost fully suppressed by 10−7 M nicardipine whereas that from −80 mV was blocked only slightly. The voltage dependencies of the peak currents before and during the superfusion with nicardipine (10−7 M) were similar although the peak amplitude was suppressed in the presence of the drug. (5) These results suggest that the existence of either (a) two populations of Ca channels that differ in the time course of inactivation and the sensitivity to nicardipine, but have nearly identical dependence on membrane potential or (b) one population of Ca channel having two different states of inactivation and the sensitivity of nicardipine, in rat vas deferens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00585117
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  • 2
    Electronic Resource
    Electronic Resource
    5-Hydroxytryptamine is emetogenic in the house musk shrew, Suncus murinus (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 344 (1991), S. 564-567 
    Details
    ISSN: 1432-1912
    Keywords: Vomiting ; 5-HT ; 2-Me-5-HT ; 5-HT3 Receptor antagonism ; Cancer Chemotherapy ; House musk shrew (Suncus murinus)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The emetic effects of 5-hydroxytryptamine (5-HT) and 5-HT3 receptor agonists were investigated in the house musk shrew, Suncus murinus. 5-Hydroxytryptamine (5-HT; i.p., i.v., s.c.) and 2-methyl-5-HT (2-Me-5HT; i.p.) but not 5-hydroxyindoleacetic acid (i.p.) or 5-ethoxytryptamine (i.p.) induced emesis with very short latency. Tropisetron (ICS 205-930, a 5-HT3 receptor antagonist, s.c.) blocked the emesis induced by 5-HT (10 mg/kg, i.p.) and 2-Me-5-HT (5 mg/kg, i.p.) with respective ID50 values of 7.8 and 70.9 μg/kg. Pindolol (5-HT1 receptor antagonist) and ketanserin (5-HT2 receptor antagonist) were about 100 times less potent than tropisetron. The emesis induced by 5-HT was prevented by surgical vagotomy but not by pretreatment with a combination of atropine (0.1 mg/kg, s.c.) and hexamethonium (10 mg/kg, s.c.). These results clearly indicate that 5-HT is emetogenic probably through a stimulation of peripheral 5-HT3 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170653
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    Paper (German National Licenses)
    Fulltext
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