Calmidazolium chloride is a small molecule CaM antagonist and calcium channel protein inhibitor. Calmidazolium chloride demonstrates noncompetitive inhibition of platelet and sarcoplasmic reticulum Ca2+-ATPase activity and shows inhibition of Ca2+ transport activity in platelet microsomes. In HeLa cells, calmidazolium chloride stimulates a mechanism of cellular Ca2+ influx distinct from store-operated Ca2+ entry and unaccompanied by Ca2+ store depletion, mobilizing stores and evoking a Ca2+ signal through activation of phospholipase C. Calmidazolium chloride is described to inhibit constitutive nitric oxide synthase (NOS) activity without affecting inducible NOS in rat aorta. The dependence upon calmodulin of neuronal NOS (nNOS) in neuroblastoma N1E-115 cells was probed with calmidazolium chloride, where it was demonstrated to increase cGMP levels indirectly indicating an increase in NO output by nNOS. Calmidazolium chloride is also described to inhibit the activity of calmodulin N-methyltransferase.
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