All organs, and most sensitively the brain, depend on consistent delivery of oxygen-rich blood. When blood flow is interrupted, organs (and consequently, sometimes organisms) die. Conversely, when blood flow to an organ is excessive, blood vessels can rupture, lungs can fill with fluid, and kidneys can scar. Because cardiovascular homeostasis is thus central to life, several neural, neurohormonal, and non-neural systems act to regulate variance in cardiovascular parameters.
A key homeostatic mechanism in the cardiovascular system is the baroreflex (Kumada et al., 1990). As blood pressure rises (or falls), the baroreflex opposes the perturbation with compensatory decreases (or increases) in heart rate and vascular tone. This negative feedback system is critical for stabilizing blood pressure. In its absence, blood pressure is markedly more variable. In addition, because the baroreflex is experimentally accessible and reliably recruits the principal effectors of cardiovascular control (sympathetic and parasympathetic efferents and hormonal secretion), it has become the dominant model for understanding the neurobiology of cardiovascular homeostasis.
Broadly, the cells and circuits subserving the baroreflex have been known for decades. Blood pressure is detected by baroreceptors, primary sensory neurons whose cell bodies reside in the nodose and petrosal ganglia of the vagus and glossopharyngeal nerves (Kumada et al., 1990). Baroreceptors have sensory endings in arterial walls, prominently in the carotid sinus and aortic arch, and they communicate a heartbeat-entrained, blood pressure-dependent signal to the nucleus of the solitary tract (NTS). Baro-recipient regions of the NTS send excitatory projections to preganglionic parasympathetic neurons of the nucleus ambiguus (which lower heart rate) and also indirectly inhibit the rostral ventral lateral medulla, a key driver of sympathetic vasoconstriction. This reflex arc through the medulla, in concert with important but lesser-studied supramedullary contributions, acts to ensure consistent organ perfusion.
In recent years, molecular dissection …
Correspondence should be addressed to Jalal Kenji Baruni at baruni{at}stanford.edu.
