Bud extracts from Salix caprea L. inhibit voltage gated calcium channels and catecholamines secretion in mouse chromaffin cells.

Background: Salix caprea L. is an ornamental plant with prominent antioxidant activity. In the last decades Salix caprea bud extracts (SCBEs) have been used for the treatment of oxidative stress related disorders.

Purpose: A large part of cellular functions depends on the amount of intracellular Ca concentration which in turn is mainly determined by Ca ions movements across plasma membrane as well as by Ca released from the stores. For better evaluating the mechanism of action of SCBEs, we focused on the effect of SCBEs on voltage gated Ca channels (VGCCs) functioning and related catecholamines secretion in mouse chromaffin cells (MCCs). These latter are neuroendocrine cells that share a wide variety of functions with neurons. They are particularly interesting for studying the relationship between VGCCs activation and catecholamines secretion both in control and under stressful conditions.

Study Design And Methods: We focused on the effect of SCBEs on VGCCs being these latter considered one of the main pathway of Ca influx across plasma membrane. Ca currents and capacitance changes were measured in patch clamp experiments performed in voltage clamp configuration.

Results: We show that SCBEs inhibited VGCCs in a dose dependent manner. On average, the saturating concentration of SCBEs (SCBEs) is able to block 36% of the maximum Ca current amplitude (I) without selectivity for L (I) or non-L type (I) Ca channels. Furthermore, I inhibition is not followed by alteration of VGCCs gating kinetics, but is responsible for a marked decrease of Ca dependent catecholamines secretion.

Conclusion: We conclude that the ability of SCBEs to inhibit VGCCs function, known to be potentiated during oxidative stress, could contribute to the already known antioxidant properties of Salix caprea L. We finally suggest that the inhibitory effect of SCBEs on catecholamines secretion may contribute to treat stress dependent cellular dysfunctions.