Grassi Claudio, D'Ascenzo Marcello, Azzena Gian Battista
Institute of Human Physiology, Medical School, Catholic University S. Cuore, Largo F. Vito 1, I-00168 Rome, Italy.
Neurochem Int. 2004 Nov;45(6):885-93. doi: 10.1016/j.neuint.2004.03.019.
The unconventional gaseous transmitter nitric oxide (NO) markedly influences most of mechanisms involved in the regulation of intracellular Ca2+ homeostasis. In excitable cells, Ca2+ signaling mainly depends on the activity of voltage-gated Ca2+ channels (VGCCs). In the present paper, we will review data from our laboratory and others characterizing NO-induced modulation of Ca(v)1 (L-type) and Ca(v)2.2 (N-type) channels. In particular, we will explore experimental evidence indicating that NO's inhibition of channel gating is produced via cGMP-dependent protein kinase and examine some of the numerous cell functions that are potentially influenced by the action of NO on Ca2+ channels.
