Modulation of Ca(v)1 and Ca(v)2.2 channels induced by nitric oxide via cGMP-dependent protein kinase.
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.
Grassi
Claudio
C
Institute of Human Physiology, Medical School, Catholic University S. Cuore, Largo F. Vito 1, I-00168 Rome, Italy. grassi@rm.unicatt.it
D'Ascenzo
Marcello
M
Azzena
Gian Battista
GB
D000818:Animals; D020746:Calcium Channels, L-Type / Q000187:drug effects*; D020864:Calcium Channels, N-Type / Q000187:drug effects*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology*
D020746:Calcium Channels, L-Type; D020864:Calcium Channels, N-Type; D009569:Nitric Oxide; D017868:Cyclic AMP-Dependent Protein Kinases