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Modulation of Ca(v)1 and Ca(v)2.2 channels induced by nitric oxide via cGMP-dependent protein kinase
Claudio Grassi1, Marcello D'Ascenzo, Gian Battista Azzena
1Institute of Human Physiology, Medical School, Catholic University S. Cuore, Largo F. Vito 1, I-00168 Rome, Italy. grassi@rm.unicatt.it
Abstract:
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.
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