Abstract
Although nitric oxide (NO)-mediated relaxation of vascular smooth muscle was described several years ago, the downstream effects of NO and the mechanism of relaxation of vascular smooth muscle are still not well understood. NO produced endogenously or from nitrovasodilators such as nitroglycerin or sodium nitro-prusside generates cGMP (Arnold et al. 1977; DeRubertis and Craven 1977; Gruetter et al. 1980) which in turn produces vascular smooth muscle relaxation. There have been several reviews of the roles of NO and cGMP in cellular regulation (Walter 1989; Nathan 1992; Marietta 1993; Lincoln 1994; Lincoln et al. 1996). This article is focused on the effects of cGMP-dependent protein kinase (cGMP kinase), the major receptor protein for cGMP in vascular smooth muscle, and our current understanding on how this enzyme mediates relaxation by lowering intracellular Ca2+ ([Ca2+];).
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Komalavilas, P., Lincoln, T.M. (2000). Regulation of Intracellular Ca2+ by Cyclic GMP-Dependent Protein Kinase in Vascular Smooth Muscle Cells. In: Kadowitz, P.J., McNamara, D.B. (eds) Nitric Oxide and the Regulation of the Peripheral Circulation. Nitric Oxide in Biology and Medicine, vol 1. Birkhäuser, Boston, MA. https://doi.org/10.1007/978-1-4612-1326-0_2
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