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• W2155534824 abstract "1. The effects of membrane potential and the dihydropyridine calcium channel inhibitor, nisoldipine, on single calcium channels in the presence of Bay K 8644 and contraction in the presence and absence of Bay K 8644 were examined in the rabbit mesenteric artery. 2. Membrane depolarization decreased the peak average single calcium channel current that could be elicited by a test pulse to 0 mV. The steady-state inactivation relationship could be described by the Boltzmann equation, [1 + exp[Vm-V0.5)/k)]-1, with a steepness factor, k, of 7.1 mV. Nisoldipine shifted the steady-state inactivation curve to more negative potentials by increasing the fraction of test pulses without openings. 3. The degree of nisoldipine inhibition of average single calcium channel currents increased with membrane depolarization. Depolarization of the holding potential from -100 to -55 mV decreased the concentration of nisoldipine needed for 50% inhibition (Kapp) from 12.1 to 1.9 nM in the presence of 1 microM-Bay K 8644. 4. Membrane depolarization by external potassium (K+) of the intact artery in the presence of nisoldipine decreased contractions evoked by depolarizing test pulses. The relationship between membrane potential and contraction could be empirically described by the Boltzmann equation, with a steepness factor, k, of 7.1 mV. Increasing the nisoldipine concentration from 0.25 to 2.0 nM shifted the mid-point of this relationship from -20.5 to -33.0 mV, without affecting the steepness factor. 5. Nisoldipine inhibition of contraction increased with membrane depolarization. Membrane depolarization from -68.6 to -30.0 mV decreased the Kapp of nisoldipine for contractions from 3.02 to 0.69 nM. Bay K 8644 (1 microM) elevated Kapp about 9.3-fold at 5 mM-K+. In the presence of Bay K 8644, membrane depolarization from -68.6 to -30.0 mV reduced Kapp from 28.4 to 4.0 nM. 6. In the presence of nisoldipine, the effect of membrane depolarization on the time course of development of inhibition was examined. In 3 nM-nisoldipine, after membrane depolarization with 20 mM-K+, the time course of development of inhibition of force could be described by a single exponential with a time constant of 16.5 min. Membrane depolarization to a more positive potential accelerated the development of inhibition. 7. The results were interpreted by a model in which nisoldipine binds with higher affinity to the inactivated state than to the resting state of calcium channels in the mesenteric artery. The approach presented here can be used to estimate the properties of steady-state calcium channel inactivation and dihydropyridine interactions in smooth muscle cells in the intact artery under physiological conditions.(ABSTRACT TRUNCATED AT 400 WORDS)" @default.
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• W2155534824 date "1989-05-01" @default.
• W2155534824 modified "2023-09-25" @default.
• W2155534824 title "Dihydropyridine inhibition of single calcium channels and contraction in rabbit mesenteric artery depends on voltage." @default.
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• W2155534824 doi "https://doi.org/10.1113/jphysiol.1989.sp017604" @default.
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