Abstract
The unconventional gaseous transmitter nitric oxide (NO) markedly influences most of mechanisms involved in the regulation of intracellular Ca 2+ homeostasis. In excitable cells, Ca 2+ signaling mainly depends on the activity of voltage-gated Ca 2+ channels (VGCCs). In the present paper, we will review data from our laboratory and others characterizing NO-induced modulation of Ca v1 (L-type) and Ca v2.2 (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 Ca 2+ channels.
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