Cardiovascular Reflexes

Overview

Like many organ systems, the heart is controlled by both the sympathetic and parasympathetic branches of the autonomic nervous system. The sympathetic nervous system tends to increase blood pressure while the parasympathetic nervous system reduces it. The two systems are constantly at work making minor adjustments to blood pressure on a minute by minute basis, rather than being switched “on” or “off”. Baroreceptors in the aortic arch and carotid sinus are important sensory systems for conveying changes in blood pressure to the central nervous system. Circuitry within the medulla oblongata then make appropriate adjustments by altering heart rate and contractility as well as the calibre of resistance vessels that contribute to peripheral resistance.

Baroreceptors

Baroreceptors detect changes in blood pressure at two key points: in the aortic arch and the carotid sinus. Information from the carotid baroreceptors appears to be more important and sensory fibres from here are carried in the glossopharyngeal nerve to the brainstem. Sensory fibres from the aortic arch are carried by the vagus nerve, which is also a conduit for parasympathetic efferent fibres to the heart (Figure 1). Changes in beat-to-beat arterial pressure pulses are processed in the medulla oblongata where alterations to sympathetic and parasympathetic activity are made.

Figure 1: Reflex control of cardiac output and peripheral resistance. Baroreceptors in the carotid sinus and aortic arch send information to the brainstem via sensory nerves. Appropriate alterations to parasympathetic and sympathetic activity are made in the medulla oblongata, where preganglionic neurons are located (not shown for clarity). Parasympathetic preganglionic fibres travel in the vagus nerve and synapse onto local ganglia which subsequently release acetylcholine, reducing heart rate and contractility. Sympathetic preganglionic nerve fibres reach ganglia in the sympathetic chain adjacent to the spinal cord. Postganglionic sympathetic nerve fibres from these ganglia release noradrenaline, which increases heart rate and contractility. Other sympathetic postganglionic fibres innervate blood vessels, generally causing contraction to increase peripheral resistance. Blood pressure is the result of the balance of these differing effects on the heart and vasculature.

Autonomic innervation of the heart

Most textbooks describe the parasympathetic innervation of the heart as restricted to the sinoatrial (SA) node (see cardiac action potentials) and hence only influences heart rate, not the force of contraction of the heart. This is probably an oversimplification; parasympathetic input can influence the speed of conduction of action potentials through the bundle of His. However, the sympathetic innervation of the heart is certainly more extensive and has more influence beyond the pacemaker cells in the SA node. Furthermore, adrenergic receptors in the heart (mainly β₁) can respond to circulating adrenaline as well as neuronally-released noradrenaline. By contrast, acetylcholine has a very short half-life in blood (imagine the consequences if it didn’t) and can only act as a discrete messenger where it is released.

Autonomic innervation of the vasculature

Again, the influence of the parasympathetic nervous system is weaker than that of the sympathetic nervous system when it comes to the vasculature. Nearly every blood vessel receives some kind of sympathetic innervation, whereas the parasympathetic nervous system innervates only a few vascular beds (e.g. cerebral and urogenital). It’s important to dispel the myth that the sympathetic and parasympathetic control of the cardiovascular system are equal and opposite, being turned on and off as required. They serve different roles and are both active most of the time. The “on-off” myth is probably perpetuated by the limited number of examples of blood vessels being innervated by both branches of the autonomic nervous system. Where this does occur, each has opposite effects. However, most vessels only receive a sympathetic innervation.

Veins are innervated by sympathetic nerves and have a thin wall of smooth muscle. In their position on the “wrong side” of the capillaries it might at first appear that contracting veins would have little impact on the cardiovascular system since venous blood pressure is so low. However, by changing the volume of the veins it is possible to change the volume of venous blood in a given organ or tissue. This is because most blood volume is stored in veins, rather than arteries. Furthermore, when veins contract, their volume is forced towards the heart, increasing the volume in the right atrium and increasing contractility via the Frank-Starling relationship. This will increase cardiac output and hence blood pressure, by shifting blood volume from the venous pool to the arterial side of the circulation.

Sympathetic neurohumoral control

The sympathetic nerve system can also control levels of adrenaline released by the adrenal gland and renin production by the kidneys. Its roles here are again unopposed by the parasympathetic nervous system.

The chromaffin cells in the medulla of the adrenal gland are essentially adrenergic neurons with no axons. Instead, when activated by sympathetic preganglionic fibres from the spinal cord, these cells release adrenaline into the blood. This is the famous “adrenaline rush” that we associate with the “flight or fight” reflex. Circulating adrenaline differs in its effects on the vasculature since it can bind to receptors on cells that are not “innervated”. Noradrenaline released by sympathetic nerves acts near the point of release from each of the varicosities along the nerve where release occurs. Reuptake mechanisms (and degradation) limit the overflow of noradrenaline at these sites so that predominantly receptors nearby are activated (Figure 3). By contrast, circulating adrenaline has access to all receptors on the each smooth muscle cell. What the overall result of sympathetic nerve activation and adrenaline release will be (contraction or relaxation) will depend on how many receptors of each type are present. In muscle for example, adrenaline tends to overpower sympathetic neurotransmission, whilst in the splanchnic circulation the opposite occurs. This makes some physiological sense, since during a “flight or fight” response, blood flow to the muscles needs to be maximised, while blood flow to organs of digestion can be minimised.

Figure 2: Differences in the effects of sympathetic nerve-derived noradrenaline and circulating adrenaline. Noradrenaline acts near the site of release, generally by activation of α adrenoceptors, and is transported back into the nerve varicosity or metabolised. By contrast, adrenaline has access to the entire cell surface, activating both β and β adrenoceptors. In this way, adrenaline can overpower sympathetic neurotransmission and have the opposite effect on myocyte contractility and hence blood flow.

Consider the following situation. You are sitting watching television and gently tapping your foot. Most of the muscles in your leg require minimal blood flow and the sympathetic nervous system will limit flow to them. By contrast the muscles performing the foot-tapping manoeuvre will require a bit more blood and the sympathetic drive to blood vessels supplying them will be less. This sort of fine control is constantly occurring. Suddenly, there is an almighty explosion nearby. The surge of adrenaline in blood overpowers the sympathetic control of blood to your legs and dilates all blood vessels ready for you to run in whatever direction is required.

The renin-angiotensin system (RAS) provides endocrine (so more sluggish) control of blood vessel contractility and kidney function to maintain blood pressure. The sympathetic nervous system and the RAS interact. Circulating adrenaline activates juxtaglomerular cells in the kidney (via β₁ receptors) to release renin, triggering the activation of the RAS. The final result of this is the production of angiotensin II which exerts several effects to increase blood volume and blood pressure, including directly contracting vascular myocytes. Angiotensin II also causes increased release of noradrenaline from sympathetic nerves innervating blood vessels. So, the two systems – working over different time scales – interact constantly as a team.