Guanethidine transported into adrenergic nerve endings appears to increase permeability to Na+, thereby leading to a reduction in noradrenaline efflux.
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Supports intracellular mechanism of guanethidine sympatholysis in animal nerves; leaves open clinical translation.
When guanethidine was applied to rabbit ventricular slices at 37 degrees C for an initial 30 min incubation period, doses of 4 X 10(-5) and 8 X 10(-5) M irreversibly inhibited increases in efflux of noradrenaline induced by the subsequent reduction of external sodium concentrations to 18 mM. This inhibition was prevented if the temperature was reduced to 0 degrees C during the drug application period. Guanethidine transported into adrenergic nerve endings appears to increase permeability to Na+, thereby leading to the reduction in efflux.
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Hosotani et al. (1978) studied this question.
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