作者: Stanley Heydrick
DOI: 10.1007/978-1-59259-002-5_3
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摘要: Nitric oxide (NO·) is an important regulatory determinant of vascular tissue homeostasis that evokes its functional effects through a broad range signaling elements, including the phospholipase C/calcium systems, tyrosine kinase pathways, G-proteinlinked receptors, ion channels, cyclic guanosine monophosphate (cGMP) and adenosine (cAMP)-dependent apoptotic pathway. Traditionally, nitric was thought to signal exclusively via stimulation guanylyl cyclase, inducing increase in intracellular cGMP levels and, turn, allosteric activation cGMPdependent (protein G [PKG]). However, more recent work has revealed some NO·’s can also be transduced by S-nitros(yl)ation nitrosation. Moreover, addition PKG, cGMP-dependent mediated other proteins whose activities are allosterically modified (e.g., phosphodiesterases channels), cross-activation cAMP-dependent A [PKA]). This chapter will cover specific on pathways smooth muscle cells, cardiomyocytes, endothelial platelets.