Calcium Sparklets Regulate Local and Global Calcium in Murine Arterial Smooth Muscle

In arterial smooth muscle, protein kinase C (PKC) coerces clusters of L‐type calcium channels to operate in a high open probability mode resulting in sites of nearly continual calcium influx called “persistent calcium sparklets”. Here, we tested the hypothesis that steady‐state calcium entry into arterial myocytes is regulated by calcium influx via channels operating in this high activity mode. Consistent with this, we found that persistent calcium sparklets produced local and global elevations in calcium. Depolarization increased calcium influx via low and high activity persistent calcium sparklets. Our data indicate that calcium entering arterial smooth muscle through persistent calcium sparklets accounted for about 50% of the total dihydropyridine‐sensitive calcium influx at a physiologically‐relevant membrane potential (−40 mV) and external calcium concentration (2 mM) and inhibition of basal PKC‐dependent persistent calcium sparklets decreased global calcium by about 50% in arterial myocytes and intact arteries. These data support the conclusion that in arterial smooth muscle, steady‐state calcium entry and global calcium are regulated by low activity and PKC‐dependent, high activity, persistent calcium sparklets.