Posted by Cam W. on April 25, 2000, at 19:57:58
In reply to Norvasc (calcium channel blocker) as AD ??? WHAT !, posted by Andy on April 25, 2000, at 19:11:02
Calcium channel blockers (CCBs) have be tried as adjuncts to mood stabilizers with limited success. The fat-soluble, L-type ones (like nimodipine) seem to work better than the one's used for hypertension (diltiazem or verapamil).The theory behind using CCBs to augment mood stabilizers is that one proposed mechanism of action of mood stabilizers is to interfere with an overactive phosphoinositol cycle (PIC)-(cAMP manufacturer and intracellular calcium regulator) in neurons. By blocking calcium ion channels (that the PIC open) you are helping to regulate the influx of calcium into the nerve cell.
In bipolar disorder the PIC is overactive and allows calcium ions to enter from outside the nerve cell, as well as releasing them from the endoplasmic reticulum. This extra intracellular calcium interferes with the conduction of the electrical signal along the axon of the nerve cell.
In theory CCBs should work, in real life they have a modest effect. I have a theory why CCBs don't work in vivo as well as they do on paper (therefore the theory is probably not totally correct). CCBs have an affinity for vascular smooth muscles (arteries) and cardiac striated muscles, more so than for neurons (I think), so the affect in neurons is not that pronounced. Can anyone corroborate or disclaim this theory. I would be extremely interested to understand what is really going on with mood stabilizers and CCBs.
Thanks - Cam W.
poster:Cam W.
thread:31247
URL: http://www.dr-bob.org/babble/20000420/msgs/31268.html