Effects of tetrandrine on cardiac noradrenaline release evoked by electrical stimulation.

The effects of tetrandrine (TD) on endogenous cardiac noradrenaline (NA) release evoked by electrical stimulation were investigated in perfused guinea pig hearts. The overflow of cardiac NA and its intraneuronal metabolite 3,4-dihydroxyphenylethyleneglycol (DOPEG) were determined by high pressure liquid chromatography (HPLC). In the presence of TD, the release of NA evoked by either nerve ganglion-stimulation or cardiac field-stimulation was significantly reduced (P < 0.01). The overflow of DOPEG was markedly enhanced (P < 0.01). TD inhibited cardiac endogenous NA release resulting from activation of the sympathetic nerve terminals within the myocardium, and increased the release of DOPEG, indicating that TD could result in a loss of NA from storage vesicles or activate monoamine oxidase in axoplasma, which could be detected by markedly increased DOPEG release. These effects of TD may be associated with its property of calcium antagonist.