Baroreflex Dysfunction

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What is the baroreflex?

The baroreflex is a critical mechanism in the homeostatic regulation of blood pressure. Blood pressure is monitored continually by receptors located in the carotid arteries, aorta, lungs, coronary arteries, and the splanchnic vasculature of the gut, termed “baroreceptors.” These receptors consist of mechanosensory neurons that form macroscopic “claws” that circumnavigate large arteries, and are activated when increased blood pressure causes the arterial lumen to expand, stretching the arterial wall. In response, baroreceptor neuron firing rate increases ( Fig. 42.1 ). The baroreceptors have classically been separated into “high-pressure” and “low-pressure” receptors based on their relative responses to varying levels of blood pressure. The carotid and aortic baroreceptors are considered “high-pressure” receptors, and are thought to be the primary controllers of heart rate and vascular resistance. The “low-pressure” cardiopulmonary receptors sense changes in central blood volume and blood pressure.

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How does the baroreflex respond to increased blood pressure?

A rise in blood pressure stretches the arterial wall, resulting in an increase in baroreceptor action potentials. Baroreceptor afferent neurons travel via the glossopharyngeal and vagal nerves to synapse in the nucleus tractus solitarius in the medulla. From here, excitatory interneurons activate preganglionic parasympathetic neurons in the dorsal motor nucleus of the vagus, and the nucleus ambiguous. Activation of these neurons results in acetylcholine release at the sinoatrial node in the heart, reducing heart rate.

The nucleus tractus solitarius also projects to inhibitory interneurons in the caudal ventrolateral medulla. These interneurons inhibit tonically active preganglionic sympathetic neurons in the rostral ventrolateral medulla, and reduce the firing rate of sympathetic neurons. As both the heart and peripheral vasculature receive sympathetic innervation, reduced sympathetic activity reduces the heart rate and contractility, as well as systemic vascular resistance.

In summary, a rise in blood pressure is modulated by the baroreflex via two mechanisms: (1) reduced heart rate and cardiac output, due to reduced sympathetic outflow, and increased parasympathetic outflow; and (2) reduced systemic vascular resistance due to reduced sympathetic outflow only.

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How does the baroreflex respond to decreased blood pressure?

Baroreceptors are tonically active, and a reduction in blood pressure results in reduced baroreceptor firing rate. This results in increased sympathetic outflow, resulting in increased systemic vascular resistance, heart rate, and contractility. Parasympathetic outflow through the vagus nerve is reduced, causing an increase in heart rate.

In summary, during a decrease in blood pressure (such as during an active stand), tonic baroreceptor firing rate decreases, and blood pressure is maintained via (1) increased total peripheral resistance, and (2) increased heart rate and cardiac output.

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What role does the baroreflex play in the long-term control of blood pressure?

Although the baroreflex has traditionally been thought of as a short-term regulator of blood pressure, it plays a central role in the long-term regulation of blood pressure as well. The baroreflex-mediated response during hypotensive periods acts to increase renal sympathetic nerve activity, resulting in increased sodium reabsorption by the kidney via the renin-angiotensin-aldosterone system. This results in fluid retention, increased blood volume and blood pressure. Conversely, the baroreflex acts to reduce blood volume during periods of hypertension, and therefore acts as a central reflex in the long-term regulation of blood pressure.

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