In general, endogenous vasoconstrictors such as norepi-nephrine, angiotensin II, vasopressin, and the endothelins tend to activate smooth muscle cation influx through voltage-gated Ca2+ and nonselective cation channels, activate Cl- efflux through ClCa channels, and inhibit K+ efflux through K+ channels, resulting in membrane depolarization, net Ca2+ influx, and an increase in intracellular Ca2+ leading to smooth muscle contraction (Figure 2). In addition to the mechanisms outlined in Figure 2, the vasoconstrictor-induced increase in intracellular Ca2+ bolsters depolarization by activation of the Ca2+-dependent phosphatase 2B (PP2B, calcineurin), which dephosphorylates KV and KATP channels to reduce their activity (not shown in Figure 2). Although the activity of KV and BKCa channels is somewhat blunted by the inhibitory mechanisms outlined in Figure 2, the membrane depolarization and, in the case of BKCa channels, the elevated intracellular Ca2+ lead to net activation of both KV and BKCa channels. This K+ channel activity importantly limits the depolarization and provides an effective negative feedback signal so that overstimulation and vasospasm do not occur. Thus, ion channels play a key role in vasoconstriction.
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.