Spasmogens and cerebral vasospasm
Marilyn J. Cipolla
I commend you on your wonderful study of cerebral spasmogens. It is intesting that there was a dissociation between those factors that caused an increase in intracellular calcium in cultured smooth muscle cells, and those that caused vasospasm in vivo. I can think of several possibilities for this: cultured cells are not structurally positioned the same as those in whole arteries, which are exposed to mechanical forces such as pressure or shear stress. These mechanical forces have been shown to be important for mediating intracellular structures such as the polymerization state of actin. Actin filaments are not only important for cross-bridge formation, but are also linked to ion channels that may control intracellular calcium. It may be that the effect that you see on intracellular calcium is an artifact of cell culture, since the actin filaments would likely not be in an appropriate position or polymerization state. Do you know if calcium is required for vasospasm? The spasmogen that mediates vasospasm during SAH may be calcium-independent. There have been many substances that cause contraction without a change in intracellular calcium, mostly linked to protein kinase C. I find this very interesting and an important work.
Mon Dec 7