LAUSR

See related article, pp 465–472 In this issue, Johansson et al1 find that markers of atherosclerosis and inflammation (which is present in atherosclerotic plaques) are associated with postural hypotension. When we stand, >500 mL of blood descend into the legs, decreasing blood pressure. The baroreflex is the initial mechanism called into play to stabilize blood pressure. Blood pressure changes are sensed by the baroreceptors in the carotids and aortic arch and signaled to the brain stem, which initiates an increase in heart rate in a single heartbeat. Sympathetic nerves then lead to vasoconstriction so that blood pressure returns toward baseline levels in ≈20 seconds after standing. When this system fails, postural hypotension ensues. Postural hypotension is not just a risk for falls, it is also associated with an increased incidence of stroke and myocardial infarction.2 Baroreflex control of blood pressure slowly deteriorates with advancing age, diminishing both sympathetic3 and parasympathetic4 nervous responses to hypertension and hypotension. Loss of baroreflex function is accelerated in hypertension and atherosclerosis. Consequently, the incidence of postural hypotension and episodic hypertension also increases with age and vascular disease. The baroreflex is impaired in subjects with carotid plaque and coronary atherosclerosis.5 Diminished heart rate variability is a sign of baroreflex loss and is associated with excess cardiovascular mortality and total mortality6 and predicts coronary artery disease. After a myocardial infarction, depressed baroreflex sensitivity predicted a 280% increase in cardiac mortality.7 Johansson et al1 report that proteins associated with atherosclerosis are also associated with impaired blood pressure control. Why should this be so? Baroreceptors are …