Aim: 

We have described in rat basilar artery that L type Ca²⁺ channel activation can activate Ca²⁺ release from sarcoplasmic reticulum (SR) in the absence of extracellular Ca²⁺ through a metabotropic pathway (mechanism denoted as Calcium-Channel Induced Calcium Release, CCICR) (Del Valle-Rodríguez et al, 2003). This calcium-release mechanism depends on the conformational change of L-type Ca²⁺ channels and the downstream activation of the G protein/phospholipase C (PLC) cascade, leading to synthesis of InsP₃ and Ca²⁺ release from the SR. Because previous results were obtained in isolated myocytes bathed in free Ca²⁺ medium, the aim of this work was to study the functional role of CCICR in physiological conditions (i.e. in arteries bathed in medium containing Ca²⁺).

Methods: 

Isometric force and cytosolic Ca²⁺ concentration ([Ca²⁺]_i) was measured in rat basilar arterial rings and in intact arteries.

Results: 

Ca²⁺ channel activation produced an initial rapid rise in cytosolic Ca²⁺ and a second plateau phase that was maintained until the end of the stimulus. Concomitant with this change in [Ca²⁺]_i, a reduction of the arterial diameter was detected. Both signals were transitory when Ca²⁺ was eliminated from the extracellular medium. Thapsigargin, U73122 and ryanodine, inhibitors of SR Ca²⁺ pump, PLC and ryanodine receptors respectively, reduced the maintained phase of contraction although the transient component was not significantly affected.

Conclusion: 

Ca²⁺ channel-induced contraction of the basilar artery can be mediated by Ca²⁺ influx from the extracellular medium (ionotropic function of Ca²⁺ channel) and Ca²⁺ release from the SR through a metabotropic pathway.

References: 

Del Valle-Rodríguez A., López-Barneo J and Ureña J. Ca²⁺ channel-sarcoplasmic reticulum coupling: a mechanism of arterial myocyte contraction without Ca²⁺ influx. EMBO J. 22: 4337-4345 (2003)