Key result
Isoprenaline markedly increased voltage-dependent Ba2+ and K+ currents in guinea-pig vas deferens, appearing contradictory to the suppression of contraction by beta-adrenoceptor activation.
Isoprenaline enhances both voltage-dependent Ba2+ and K+ currents in guinea-pig vas deferens, a finding that contrasts with its known suppression of contraction.
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Requires caution extrapolating guinea-pig findings to human smooth muscle; leaves open ionic mechanisms reconciling currents with contraction suppression.
In the guinea-pig vas deferens, isoprenaline (ISO) can exert significantly enhanced effects on voltage-dependent Ca2+ channel current carried by Ba2+ (IBa) via beta-adrenoceptor activation. Voltage-dependent Ba2+ (IBa) and K+ currents (I K) were recorded in the preparation voltage-clamped in a Krebs solution replaced Ca2+ by Ba2+ (Ba2+ solution) of 36 degrees C. At a holding potential of -40 mV, ISO markedly increased IBa evoked by depolarizing pulses, whereas it also increased I K at a holding potential of -20 mV so as to inactivate Ca2+ channel. This ISO-induced enhancement of IBa seems to be contradictory to the suppression of contraction by beta-adrenoceptor activation in normal Krebs solution.
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Inomata et al. (1998) studied this question. Isoprenaline was evaluated on Voltage-dependent Ba2+ (IBa) and K+ currents (IK). Isoprenaline markedly increased voltage-dependent Ba2+ and K+ currents in guinea-pig vas deferens, appearing contradictory to the suppression of contraction by beta-adrenoceptor activation.
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