Short-term blood pressure regulation

Your blood pressure changes every time you stand up, strain, laugh or start to run, and it is back near normal within a few heartbeats. The baroreceptor reflex, explained step by step on this page, does most of that fast correction. This page starts with the equation that shows every lever your body can pull on blood pressure. It then follows the reflex from its pressure sensors to the heart and vessels, and covers what happens when it fails on standing (orthostatic hypotension). It ends with the atrial reflex, local control of blood flow by the tissues themselves, and how all of these work together during exercise.

Three levers set blood pressure

You already know the flow equation: flow equals the pressure difference divided by resistance, F = ΔP / R. Apply it to your whole systemic circuit:

• The flow through the circuit is your cardiac output (CO).
• The pressure difference is mean arterial pressure (MAP) in the aorta minus the pressure in the right atrium. Right atrial pressure is close to zero, so the difference is about equal to MAP.
• The resistance is the total peripheral resistance (TPR) of all your systemic vessels, set mostly by the radius of the arterioles.

Rearranging F = ΔP / R gives ΔP = F × R. So:

MAP = CO × TPR

Because CO = heart rate × stroke volume, you can also write MAP = HR × SV × TPR. Every fast mechanism that raises or lowers blood pressure works on at least one of those three: heart rate, stroke volume, or resistance.

Baroreceptors: the pressure sensors

Press gently on the side of your neck just below the angle of your jaw and you can feel your carotid pulse. Just above that spot, where the common carotid artery forks, the start of the internal carotid artery is slightly widened. This widening is the carotid sinus, and its wall holds one of your two main sets of pressure sensors.

Baroreceptors (baro- = pressure, from Greek baros = weight) are stretch-sensitive sensory receptors: the branched endings of sensory neurons, woven into the elastic wall of a large artery. They are a kind of mechanoreceptor. When pressure inside the artery rises, the wall stretches, mechanically gated channels in the nerve endings open, and the neurons fire more action potentials. When pressure falls, the wall stretches less and firing slows.

The main arterial baroreceptors sit in two places:

• The carotid sinuses, one at the base of each internal carotid artery. Their signals travel to the brainstem in the glossopharyngeal nerves (cranial nerve IX). They report the pressure of the blood heading to your brain.
• The aortic arch. Some textbooks call this group the aortic sinuses. Anatomists use that name for something else: the three small bulges at the root of the aorta, just above the valve cusps, where the coronary arteries begin. The sensory receptors described here sit in the arch, not in those bulges. Their signals travel in the vagus nerves (cranial nerve X). They report the pressure of the blood leaving your heart.

Three features of baroreceptors matter for what comes next:

1. They fire at normal pressure. At a typical MAP they are already firing steadily, so they can report a fall as well as a rise.
2. They respond most to change. A rapidly rising pressure makes them fire harder than a steady high one. That is why they fire in a burst with each heartbeat, and why they catch sudden changes best.
3. They reset. If pressure stays at a new level for a day or two, the baroreceptors adjust and treat the new level as normal. That makes them sensors for fast changes, not for the long-term level of your blood pressure.

The baroreceptor reflex, step by step

The baroreceptor reflex (also called the baroreflex) is the negative feedback loop that uses baroreceptor signals to correct fast changes in blood pressure. It works through the parts of any feedback loop you have met: a stimulus, a sensor, an afferent pathway, a control center, efferent pathways, effectors and a response (Figure 1).

When pressure falls

1. Stimulus: MAP falls, for example when you stand up and blood pools in your leg veins.
2. Sensor: the walls of the carotid sinuses and aortic arch stretch less, and the baroreceptors fire fewer action potentials.
3. Afferent pathway: fewer impulses arrive in the medulla oblongata through the glossopharyngeal and vagus nerves.
4. Control center: the cardiovascular center in the medulla. Baroreceptor input normally boosts vagal output and holds back sympathetic output, so less input does the reverse: sympathetic output rises and parasympathetic (vagal) output falls.
5. Efferent pathways and effectors:
   • SA node. More norepinephrine acting on beta-1 receptors, and less acetylcholine from the vagus, speed the pacemaker potential. Heart rate rises.
   • Ventricular muscle. Norepinephrine on beta-1 receptors increases contractility, so stroke volume rises at any given end-diastolic volume.
   • Arterioles. Norepinephrine on alpha-1 receptors in vascular smooth muscle causes vasoconstriction, so TPR rises. This happens strongly in the skin, gut, kidneys and resting skeletal muscle, and very little in the brain and heart.
   • Veins. Sympathetic vasoconstriction of the veins squeezes blood out of the venous reservoir toward the heart. Venous return and end-diastolic volume rise, so stroke volume rises by the Frank–Starling mechanism.
   • Adrenal medulla. Sympathetic stimulation releases epinephrine into the blood, which reinforces all the effects above.
6. Response: heart rate, stroke volume and TPR rise, so by MAP = HR × SV × TPR, pressure climbs back toward its set point. The rise in pressure restores baroreceptor firing, which removes the stimulus: negative feedback.

Each step runs through nerves, so the whole loop takes effect within a few heartbeats, and fully within about 30 seconds.

When pressure rises

Every step runs the other way. More stretch means faster baroreceptor firing, which increases vagal output and reduces sympathetic output. Heart rate and contractility fall, arterioles and veins relax, cardiac output and TPR drop, and MAP comes back down.

The effects of the reflex on the heart, from baroreceptors and from the atria (below), are sometimes grouped as the cardiac reflexes.

Standing up: the orthostatic reflex

Stand up from lying down and gravity pulls about half a liter or more of blood into the veins of your legs and abdomen within seconds. Veins stretch easily, so they hold that blood without much rise in pressure. Follow the chain:

1. Less blood returns to the heart, so venous return falls.
2. End-diastolic volume falls, so stroke volume falls by the Frank–Starling mechanism.
3. Cardiac output falls, so MAP falls, and it falls most in the arteries of the head, which are now above the heart.
4. Baroreceptor firing falls, and the baroreceptor reflex raises heart rate and constricts arterioles and veins.

In a healthy person, heart rate rises by about 10 to 20 beats per minute and pressure recovers within a few heartbeats. You may never notice. The baroreceptor reflex responding to a change in posture is called the orthostatic reflex (ortho- = straight, upright; stat- = standing).

Orthostatic hypotension

Orthostatic hypotension (also called postural hypotension; hypo- = below, tens- = stretched, pressure) is a sustained fall in blood pressure on standing: a drop of at least 20 mm Hg systolic or at least 10 mm Hg diastolic within 3 minutes of standing up. Mr. Alvarez in the lesson dropped from 128/76 lying down to 98/62 after standing, a fall of 30 systolic and 14 diastolic, so he meets both criteria.

The symptoms all come from reduced blood flow to the brain: lightheadedness, dimming or graying of vision, weakness, and sometimes fainting. Fainting ends the problem in a way: lying flat removes the pull of gravity, venous return recovers, and blood reaches the brain again.

Every cause is a failure somewhere in the loop you just traced:

• Too little blood to start with. Loss of fluid from heavy sweating, vomiting or bleeding leaves less blood in the veins, so standing drops venous return further than the reflex can make up.
• Effectors that cannot respond. Drugs that block alpha-1 receptors or beta-1 receptors, or that relax arteriole smooth muscle directly, stop the reflex from raising TPR or heart rate.
• Damaged pathways. Long-standing diabetes mellitus and some nervous system diseases damage autonomic nerves, so the efferent signals never reach the heart and vessels.
• Aging and deconditioning. Stiffer arteries in older adults stretch less, so baroreceptors signal changes less strongly. After days of bed rest, the reflex and blood volume both adapt to lying down.

The atrial reflex

Suppose a nurse runs a liter of IV fluid into a patient quickly. Venous return rises and the right atrium fills and stretches. Within seconds, heart rate goes up. That is the atrial reflex, also called the Bainbridge reflex after Francis Bainbridge, who described it in 1915.

1. More venous return stretches the walls of the atria and the large veins where they join them.
2. Stretch-sensitive sensory receptors in those walls fire more, sending impulses up the vagus nerves to the cardiovascular center.
3. The center raises sympathetic output to the SA node and lowers vagal output.
4. Heart rate rises. Stretch of the SA node itself also speeds its pacemaker potential a little.

More heart rate means more of the incoming blood is pumped on each minute, so less of it backs up in the veins. Atrial stretch also releases atrial natriuretic peptide (ANP) from atrial muscle cells, which ties this sensor to the long-term control of blood volume on the next page.

The atrial reflex and the baroreceptor reflex can pull heart rate in opposite directions. A large infusion raises atrial stretch, which tends to speed the heart, and may also raise arterial pressure, which tends to slow it. Which wins depends on the starting heart rate and how much each sensor is stretched.

Local autoregulation of blood flow

Wrap a blood pressure cuff tightly around your upper arm for two minutes, then release it. Your forearm flushes red, and for a minute or so its blood flow is several times normal. No nerve told it to do that. The tissue did it by itself.

Local autoregulation of blood flow (also just autoregulation; auto- = self) is the ability of a tissue to adjust its own blood flow, by changing the radius of its own arterioles, with no help from nerves or hormones. Two mechanisms do it.

Metabolic autoregulation

When a tissue is working hard, or when its blood flow has been cut off, it changes the chemistry of its own interstitial fluid:

• oxygen falls;
• carbon dioxide and hydrogen ions (acid) rise;
• potassium ions, released from active cells, rise;
• adenosine, from the breakdown of ATP, and lactic acid rise;
• endothelial cells release more nitric oxide.

Each of these relaxes the smooth muscle of nearby arterioles. The arterioles dilate, resistance falls, and blood flow into that tissue rises. The extra flow brings oxygen and washes the metabolites away, which removes the stimulus. That is metabolic autoregulation, a local negative feedback loop. In the cuff example, metabolites piled up while flow was blocked, so the arterioles were wide open when the cuff came off.

The myogenic response

Now suppose the pressure in an arteriole suddenly rises. The rise stretches the smooth muscle in its wall. Stretch opens mechanically gated channels, calcium enters, and the smooth muscle contracts. The arteriole narrows, raising its resistance just enough to offset the higher pressure, so flow stays nearly the same. When pressure falls, the muscle relaxes and the arteriole widens. This is the myogenic response (my/o = muscle, -genic = produced by): a property of the smooth muscle itself.

Together, these two mechanisms keep flow nearly constant over a wide range of pressure in the brain, heart and kidneys, from a MAP of roughly 60 to 150 mm Hg (Figure 2). Outside that range, flow follows pressure again.

Local control and the reflex together

Local control decides how the cardiac output is shared out. The baroreceptor reflex decides how much pressure is available to share. Each tissue shows a different balance of the two. The brain and heart rely almost entirely on local control, and sympathetic vasoconstriction barely affects them, so their flow is protected when pressure falls. The skin, gut and kidneys respond strongly to sympathetic signals, so their flow is cut first. In working skeletal muscle, local metabolites override sympathetic vasoconstriction, so the muscle keeps its high flow.

The two also interact through MAP = CO × TPR. When many tissues dilate at once, TPR falls, and MAP would fall unless cardiac output rises to match. That is exactly what happens in exercise.

The cardiovascular response to exercise

Picture a 30-year-old starting a steady run. Here is what changes, and what drives each change.

Before and at the start

Even before the first step, signals from the motor areas of the brain reach the cardiovascular center, which cuts vagal output. Heart rate rises almost at once. As the muscles start to work, mechanoreceptors and chemoreceptors inside them report movement and metabolite buildup, and sympathetic output rises further.

Cardiac output rises

• Heart rate rises with sympathetic stimulation and vagal withdrawal.
• Stroke volume rises for two reasons. Sympathetic stimulation raises contractility. The skeletal muscle pump and deeper breathing (the respiratory pump) push more blood back to the heart, so end-diastolic volume rises.
• Cardiac output rises from about 5 L/min at rest to about 20 L/min in a young untrained adult at peak effort, and up to about 35 L/min in elite endurance athletes. The difference between resting and maximum output is the cardiac reserve.

Blood flow is redistributed

• Working skeletal muscle: metabolic autoregulation dilates its arterioles, and its share of cardiac output rises from about a fifth at rest to more than three quarters at peak effort.
• Heart muscle: its own metabolites dilate the coronary arterioles, so coronary flow rises with the heart's workload.
• Gut, kidneys and inactive muscle: sympathetic vasoconstriction reduces their flow.
• Skin: flow first falls with sympathetic vasoconstriction, then rises as body temperature climbs and the skin vessels dilate to shed heat.
• Brain: autoregulation keeps flow roughly constant.

Pressure rises, but less than you might expect

The dilation of large muscle beds lowers TPR, while cardiac output rises several-fold. Because cardiac output rises more than TPR falls, MAP rises, but only modestly. Systolic pressure rises a lot, because stroke volume is larger and ejected more forcefully. Diastolic pressure stays about the same or falls a little, because resistance is low. Pulse pressure widens. The baroreceptor reflex keeps working during exercise, but around a higher set point.

Maximum and target heart rate

Your maximum heart rate is the highest rate your heart reaches at all-out effort. It falls with age. A common estimate is 220 minus your age in years. That rule is only a rough guide: real maximum heart rates vary by 10 beats per minute or more either side of it, and another estimate, 208 − (0.7 × age), fits measured values somewhat better, especially in older adults.

A target heart rate is a range, set as a percentage of maximum heart rate, used to aim for a chosen exercise intensity. Common guidance puts moderate exercise at about 50 to 70 percent of maximum and vigorous exercise at about 70 to 85 percent.

Regular endurance training lowers resting heart rate and raises resting stroke volume, so the same cardiac output comes from fewer, larger beats, and the cardiac reserve grows.

Summary

MAP = CO × TPR, and CO = HR × SV, so fast control of blood pressure works on heart rate, stroke volume and arteriole radius. Baroreceptors in the carotid sinuses and aortic arch fire in proportion to arterial stretch. When pressure falls, their firing drops, the medulla raises sympathetic output and lowers vagal output, and heart rate, contractility, arteriole tone and venous tone all rise, restoring pressure within seconds. They reset within days, so they cannot set long-term pressure. Orthostatic hypotension is a failure of this reflex on standing. The atrial reflex speeds the heart when the atria are stretched. Local autoregulation, metabolic and myogenic, lets each tissue set its own flow, and in exercise it works with the reflex to raise cardiac output and send most of it to working muscle.