Adrenergic stimulation of rat resistance arteries affects Ca²⁺ sparks, Ca²⁺ waves, and Ca²⁺ oscillations

Confocal laser scanning microscopy and fluo 4 were used to visualize local and whole Cell Ca²⁺ transients within individual smooth muscle cells (SMC) of intact, pressurized rat mesenteric small arteries during activation of α₁-adrenoceptors. A method was developed to record the Ca²⁺ transients within individual SMC during the changes in arterial diameter. Three distinct types of "Ca²⁺ signals" were influenced by adrenergic activation (agonist: Phenylephrine). First, asynchronous Ca²⁺ transients were elicited by low levels of adrenergic stimulation. These propagated from a point of origin and then filled the cell. Second, synchronous, spatially uniform Ca²⁺ transients, not reported previously, occurred at higher levels of adrenergic stimulation and continued for long periods during oscillatory vasomotion. Finally, Ca²⁺ sparks slowly decreased in frequency of occurrence during exposure to adrenergic agonists. Thus adrenergic activation causes a decrease in the frequency of Ca²⁺ sparks and an increase in the frequency of asynchronous wavelike Ca²⁺ transients, both of which should tend to decrease arterial diameter. Oscillatory vasomotion is associated with spatially uniform synchronous oscillations of cellular [Ca²⁺] and may have a different mechanism than the asynchronous, propagating Ca²⁺ transients.