Heavy metal to lower the pressure?

This editorial refers to ‘Tungstate activates BK channels in a β subunit- and Mg2+-dependent manner: relevance for arterial vasodilatation’ by A.I. Fernández-Mariño et al., pp. 29–38, this issue. Activation of the large conductance, Ca2+-dependent K+ channel [KCa1.1+β-subunits, generally known as the Big K (BK) or maxi K channel] is an important negative feedback on depolarization and Ca2+-induced contraction of smooth muscle and thus arterial vasoconstriction (Figure 1). Intriguingly, altered function of BK and/or polymorphism in human BK α- and β-subunit genes have been associated with hypertension,1,2 and, from the therapeutic perspective, it is generally believed or hoped that improving BK channel function helps to ease vasodilation and to lower blood pressure in hypertension. The study by Fernández-Mariño et al.3 demonstrates that the heavy metal salt tungstate has vasodilator capabilities by stimulating BK activity (Figure 1). At the molecular level, the authors showed that this positive gating modulation is conferred by the β1-subunit of the BK channel complex and interactions with the magnesium control of channel activity. Hence, the study makes a significant contribution to a better understanding of the regulation of BK channels by a heavy metal salt. From the translational perspective, the study fosters the potential utility of tungstate as a new type of antihypertensive ‘drug’, perhaps as food additive or component of the daily diet.