Abstract
What do we really know about sympathetic outflow and blood pressure in humans? For example, in healthy normotensive young subjects, baseline sympathetic outflow can vary 2-fold to 3-fold.1,2 We also know that in healthy aging subjects, baseline sympathetic outflow can be increased dramatically with only a modest impact on vascular resistance and little or no impact on blood pressure.1 Additionally, there is no clear evidence for dramatic increases in baseline sympathetic outflow in “garden variety” essential hypertension.1 If we stop here, a position of “nihilism” about sympathetic outflow and blood pressure seems reasonable. However, when the sympathetic nervous system is destroyed by disease or surgery, blood pressure is highly labile.3 We also know that many “stressors” that evoke a pressor response also evoke marked sympathetic activation, and that the magnitude of these pressor responses can be a harbinger of future hypertension.4,5 Finally, in disease states like congestive heart failure, excessive sympathetic activation is a “bad thing.”6,7 If we emphasize these points, sympathetic vasoconstriction seems more important to blood pressure and perhaps survival. …
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