The effects of β-adrenoceptor stimulation by isoprenaline (ISO) on action potential and membrane current were studied in the guinea-pig was deferens in normal Krebs solution by using a double sucrose gap method.
In current-clamp experiments, ISO produced the membrane hyperpolarization by reducing the resistance and modified the pattern of multi-spike activity elicited by long depolarizing currents; an initial spike potential was reduced in the amplitude and the rate of rising phases and the slope of diastolic depolarization was slowered, leading to a prolongation of the spike discharge interval.
In voltage-clamp experiments, ISO greatly enhanced the late outward K
+ current (I
K2) by increasing the conductance, but hardly affected the peak outward K
+ current (I
K1). ISO also reduced the inward Ca
2+ current (I
Ca) by decreasing the conductance (g
a) as well as by reducing the driving force for Ca
2+. While it increased the leakage conductance (g
1) due to K
+ associated with hyperpolarizing voltage steps.
In the preparations treated with Ca
2+ channel blocker such as D-600, the enhanced effect of ISO on the I
K was still prominent, suggesting that Ca
2+ and K
+ channels appear to be independently regulated during β-adrenoceptor stimulation.
These results suggest that ISO exerts depressant actions on the was deferens muscle by reduction of the I
Ca as well as by prominent enhancement of the I
K2 via β-adrenoceptor activation.
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