Regulation of blood pressure

What is the equation for mean arterial pressure (MAP)?

MAP = cardiac output (CO) × total peripheral resistance (TPR).

Which laws is the MAP equation another way of expressing?

Darcy's and Poiseuille's laws.

What is the equation for cardiac output?

CO = heart rate (HR) × stroke volume (SV).

What does total peripheral resistance reflect?

The net state of constriction and dilation in the systemic circulation, primarily the arterioles.

What three variables can the body control to regulate MAP?

Heart rate, stroke volume and total peripheral resistance.

What is the primary objective of cardiovascular regulation?

To maintain a stable MAP, ensuring adequate blood flow to the vital organs, especially the brain.

What are the arterial baroreceptors?

Sprays of non-encapsulated nerve endings in the adventitial layer of the arterial walls in the carotid sinus and aortic arch.

What type of receptor is an arterial baroreceptor?

A mechanoreceptor, sensitive to stretch rather than pressure per se.

How does a rise in arterial pressure excite baroreceptors?

It increases the distending pressure on the arterial wall, causing increased stretch, which excites the baroreceptors.

Who discovered the carotid baroreflex and when?

Hering, in 1923.

What did electrical stimulation of the carotid sinus nerve cause in Hering's work?

Reflex hypotension and bradycardia.

Which cranial nerves carry baroreceptor afferents to the cardiovascular centre?

The glossopharyngeal (IX) and vagus (X) nerves.

How does increased baroreceptor afferent input affect the heart?

It increases parasympathetic stimulation and decreases sympathetic stimulation of the heart.

How does increased baroreceptor input affect blood vessels?

It decreases sympathetic stimulation of the blood vessels.

What type of mechanism is the baroreflex?

A homeostatic mechanism driven by negative feedback.

What is the baroreflex set point for MAP in young adults?

About 95 mmHg.

What is the baroreflex latency for vagal bradycardia?

About 0.5 s.

How quickly are sympathetic vasomotor nerve activity changes complete in the baroreflex?

Within about 1.5 s.

What is orthostasis?

Changing from a supine to a standing position.

Why does orthostasis challenge the cardiovascular system?

Gravity affects the distribution of venous blood, and extra mechanical energy is needed to keep up cerebral perfusion when the head is above the heart.

What happens to dependent venous volume on standing?

It increases by about 500 ml.

What happens to intrathoracic blood volume on standing?

It decreases by about 20%.

What is the chain of events that leads to syncope on standing?

Cardiac filling pressure falls, EDV falls, stroke volume falls by 30-40% (Frank-Starling), pulse pressure and MAP fall, cerebral perfusion falls, causing syncope (fainting).

How much does stroke volume fall on standing?

By 30-40%, due to the Frank-Starling mechanism.

What happens to baroreceptor stimulation on standing?

It decreases, due to reduced pulse pressure and carotid sinus pressure (effects of gravity).

How does the cardiovascular centre respond to standing?

It decreases vagal outflow to the heart and increases sympathetic outflow in cardiac and vasomotor nerves.

How much does heart rate rise on standing?

By 15-20 bpm.

How much does the cardiac output fall on standing after compensation?

The fall is limited to about 20%.

How much does TPR rise on standing?

By 30-40%, due to vasoconstriction.

What is the net result of the baroreflex response to standing?

MAP rises by 10-15 mmHg above the supine level and cerebral perfusion is preserved.

Why doesn't the baroreflex oppose the rise in MAP during exercise?

Baroreceptors can reset.

Are arterial baroreceptors vital for long-term regulation of MAP?

No. They are responsible for acute buffering of blood pressure.

What happens if the baroreceptor afferent nerves are cut?

Blood pressure becomes less stable, but there is little change in MAP over hours to days.

What is the most important long-term determinant of arterial pressure?

Blood volume.

Which organ ultimately regulates blood volume?

The kidney.

How does renal arterial perfusion pressure affect urine production?

The greater the renal arterial perfusion pressure, the greater the glomerular filtration rate and urine production.

What are the two key mechanisms for long-term regulation of blood volume?

Veno-atrial stretch receptors (with ADH/vasopressin) and the renin-angiotensin-aldosterone system (RAAS).

Where are veno-atrial stretch receptors located?

In the atria and pulmonary arteries.

What other names are used for veno-atrial stretch receptors?

Cardiopulmonary stretch receptors, cardiopulmonary baroreceptors and low-pressure baroreceptors.

How do veno-atrial stretch receptors differ from arterial baroreceptors?

They respond to lower pressures.

What is the primary role of veno-atrial stretch receptors?

To regulate blood volume, a primary determinant of cardiac output.

What happens when both arterial baroreceptors and veno-atrial stretch receptors are denervated?

There is a marked increase in MAP, in addition to the short-term instability seen when baroreceptors alone are denervated.

What happens to veno-atrial stretch receptors when blood volume falls?

Central venous and atrial pressure drop, receptors are stretched less and reduce their firing rate.

What are the two reflex responses when veno-atrial receptor firing falls?

Constriction of the afferent renal arterioles (reducing glomerular filtration) and reflex release of ADH from the hypothalamus.

What does ADH (vasopressin) do in the kidney?

It increases the reabsorption of fluid from the renal tubules.

What is the overall effect of reduced veno-atrial receptor firing?

Reduced fluid loss in urine, increased blood volume and increased arterial pressure.

What stimulates the RAAS?

A fall in blood volume or in renal blood flow.

Which cells detect a fall in blood volume or renal blood flow for the RAAS?

The juxtaglomerular cells of the kidney.

Which enzyme do juxtaglomerular cells release?

Renin.

What is the main chain of events in the RAAS?

Renin converts angiotensinogen to angiotensin I, ACE converts this to angiotensin II, which causes vasoconstriction and aldosterone release.

Which drugs are a primary treatment for hypertension in relation to the RAAS?

ACE inhibitors.

What does angiotensin II-mediated vasoconstriction do?

It raises total peripheral resistance.

What does aldosterone do in the kidney?

It increases Na+ reabsorption from the renal tubules, which draws water in down the osmotic gradient.

What is the effect of aldosterone on blood volume and cardiac output?

It raises blood volume and therefore cardiac output.

How do the RAAS effects elevate MAP?

Angiotensin II raises TPR and aldosterone raises blood volume and cardiac output, so both combine to raise MAP.

What is the adrenal medulla?

A functional extension of the sympathetic nervous system.

What triggers adrenaline and noradrenaline release?

Stimulation of sympathetic preganglionic fibres.

How do adrenaline and noradrenaline raise cardiac output?

Via β1-adrenergic receptors, increasing both HR and SV.

How do adrenaline and noradrenaline cause vasoconstriction?

Via α1-adrenergic receptors, increasing TPR.

Why does adrenaline have a minimal effect on MAP?

It causes vasodilation via β2-adrenergic receptors in cardiac muscle, skeletal muscle and liver, decreasing TPR.

What is atrial natriuretic peptide (ANP)?

A peptide released by atrial cells in response to high cardiac filling pressures (increased blood volume).

What does ANP do?

It reduces MAP by causing vasodilation and promoting Na+ excretion (and hence water loss) in the kidneys.

How strong is the effect of ANP at physiological concentrations?

Weak.

What is pressure natriuresis?

Increased salt and water excretion (reducing blood volume) in response to a rise in capillary pressure in the kidneys.

How does pressure natriuresis occur?

Increased capillary pressure raises interstitial pressure, which blocks reabsorption of tubular fluid.

How certain is the importance of pressure natriuresis?

It is controversial.

What do muscle work receptors do?

They help drive HR and BP responses during exercise.

What do arterial chemoreceptors do in blood pressure regulation?

They support blood pressure during asphyxia and clinical shock.

What do lung stretch receptors contribute to?

Asphyxia responses, sinus arrhythmia and the inspiratory gasp reflex.

How do the external senses affect HR and BP?

Pain affects HR and BP, and cold can cause a rise in BP (which can cause angina).

What did Julius Comroe say about regulatory mechanisms?

"If a job is worth doing, the body has more than one way of doing it."

What are the three key MAP control mechanisms to study?

The baroreflex, veno-atrial stretch receptors with ADH/vasopressin, and the RAAS.