Increasing concentrations of berberine from 0.1 microM to 10 microM inhibited [3H]-
yohimbine binding, shifting the saturation binding curve to the right without decreasing the
maximum binding capacity. In platelet cyclic AMP accumulation experiments, berberine at
concentrations of 0.1 microM to 0.1 mM inhibited the cAMP accumulation induced by 10
microM prostaglandin E1 in a dose dependent manner, acting as an alpha 2 adrenoceptor agonist.
In the presence of L-epinephrine, berberine blocked the inhibitory effect of L-epinephrine
behaving as an alpha 2 adrenoceptor antagonist. Thee properties are similar to those of clonidine
on human platelets, suggesting that berberine is a partial agonist of platelet alpha 2 adrenoceptors.
These findings may account for hypotensive, antisecretory, and sedative effects of berberine (Hui,
et al., 1991).
Increasing concentrations of berberine from 0.1 microM to 10 microM inhibited [3H]-yohimbine binding, shifting the saturation binding curve to the right without decreasing themaximum binding capacity. In platelet cyclic AMP accumulation experiments, berberine atconcentrations of 0.1 microM to 0.1 mM inhibited the cAMP accumulation induced by 10microM prostaglandin E1 in a dose dependent manner, acting as an alpha 2 adrenoceptor agonist.In the presence of L-epinephrine, berberine blocked the inhibitory effect of L-epinephrinebehaving as an alpha 2 adrenoceptor antagonist. Thee properties are similar to those of clonidineon human platelets, suggesting that berberine is a partial agonist of platelet alpha 2 adrenoceptors.These findings may account for hypotensive, antisecretory, and sedative effects of berberine (Hui,et al., 1991).
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