Relaxation Of Muscle Cell

Phospholipase r


Arginine + o2 Citrulline + No!

Protein kinase G

cytosolic Ca2 + . After Ca2+ binds to calmodulin, the resulting complex stimulates the activity of NO synthase, an enzyme that catalyzes formation of NO from O2 and the amino acid arginine. Because NO has a short half-life (2-30 seconds), it can diffuse only locally in tissues from its site of synthesis. In particular NO diffuses from the endothelial cell into neighboring smooth muscle cells, where it triggers muscle relaxation (Figure 13-30).

The effect of NO on smooth muscle is mediated by the second messenger cGMP, which can be formed by an intra-cellular NO receptor expressed by smooth muscle cells. Binding of NO to the heme group in this receptor leads to a conformational change that increases its intrinsic guanylyl cyclase activity, leading to a rise in the cGMP level. Most of the effects of cGMP are mediated by a cGMP-dependent protein kinase, also known as protein kinase G (PKG). In vascular smooth muscle, protein kinase G activates a signaling pathway that results in inhibition of the actin-myosin complex, relaxation of the cell, and dilation of the blood vessel. In this case, cGMP acts indirectly via protein kinase G, whereas in rod cells cGMP acts directly by binding to and thus opening cation channels in the plasma membrane.

Relaxation of vascular smooth muscle also is triggered by binding of atrial natriuretic factor (ANF) and some other peptide hormones to their receptors on smooth muscle cells. The cytosolic domain of these cell-surface receptors, like the intracellular NO receptor, possesses intrinsic guanylyl cyclase activity. When an increased blood volume stretches cardiac muscle cells in the heart atrium, they release ANF. Circulating ANF binds to ANF receptors in smooth muscle cells surrounding blood vessels, inducing activation of guanylyl cyclase activity and formation of cGMP. Subsequent activation of protein kinase G causes dilation of the vessel by the mechanism described above. This vasodilation reduces blood pressure and counters the stimulus that provoked the initial release of ANF.

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