a1-adrenergic agonists, angiotensin II, vasopressin, endothelin elicit a rapid transient increase in [Ca2+]i which subsequently declines to a steady state level that is higher than unstimulated. Resultant force is biphasic; rapid phasic component and slow sustained tonic component. Phasic contraction is activated by release of Ca2+ from intracellular stores. Tonic contraction requires the influx of Ca2+ from extracellular space, which serves to maintain MLCK in a partially activated state.