Titlebook: Nitric Oxide and the Regulation of the Peripheral Circulation; Philip J. Kadowitz,Dennis B. McNamara Book 2000 Springer Science+Business M

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Role of Na+-K+-ATPase in Nitric Oxide-Induced Relaxationee cytoplasmic Ca. and relaxation of vascular smooth muscle (Lincoln and Cornwell 1993). Nitric oxide also causes relaxation of vascular smooth muscle by increasing the activity of Ca.-activated K. channels by a cGMP-independent mechanism (Bolotina et al., 1994).

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PALSY

Nitric Oxide Derived from Perivascular Nerves and EndotheliumPalmer et al. (1988b), enabled us to clarify the physiological roles of endogenous NO. This lipophilic gas molecule is now recognized to be a new intercellular messenger not only in the circulatory system but also in the central nervous and immune systems.

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Regulation of Intracellular Ca2+ by Cyclic GMP-Dependent Protein Kinase in Vascular Smooth Muscle Ce994; 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 Ca. ([Ca.];).

Commission

Oxidants and Vascular Nitric Oxide Signalingesent and by the function of antioxidant and metabolizing systems that interact with each active species. This chapter will focus on processes shown in Figure 3.1, which are likely to contribute to the control of vascular tone and organ blood flow in the peripheral circulation.

Graves’-disease

G. M. Owen,A. L. Owenection 4.5 sketches a dynamic model that explains how these cognitive factors act to distort critical decision-making. Section 4.6 closes by identifying the cognitive biases that most strongly influence the phases of the critical decision-making process presented in Chap. 2.

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