Arterial blood pressure is perhaps the key regulated variable in the cardiovascular system. This concept is especially true in the short term on a beat-to-beat, or moment-to-moment, basis. Because blood flow to vital organs, such as the brain and heart, is under significant autoregulatory control, this means that flow to these organs is generally adequate as long as mean arterial pressure stays within a modest range. In this context, the brain and heart are usually considered the "vital" organs because ischemia and/or severe hypoxia can do irreversible damage to these organs faster than almost any other and because severe brain or heart dysfunction leads rapidly to permanent disability or death. Thus, fainting when blood pressure falls during orthostatic stress can be seen as a protective mechanism that is activated when blood pressure regulation fails. In summary, arterial and perhaps cardiopulmonary receptors play a key role in the short-term regulation of arterial pressure in humans. Stimulation of these receptors by stretch associated with increased arterial pressure or central blood volume inhibits sympathetic outflow to blood vessels and stimulates vagal outflow to the heart. When blood pressure falls, there is less baroreceptor afferent activity and, therefore, more sympathetic outflow to vessels and withdrawal of vagal tone to the heart; responses that tend to maintain or increase arterial pressure.
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