control of the systemic blood pressure

Question 1

Flow =

Answer 1

Pressure/ Resistance

Because blood flows through the arterial system continuously, the pressure is always positive.
Blood always flows from areas of high pressure to areas of low pressure (except when the momentum transiently sustains flow)
The flow is generated by the pump-action of the heart
Blood flow varies with the cardiac cycle
Blood flow also varies in different parts of the circulatory system

Question 2

Blood pressure =

Answer 2

CO x SVR

Question 3

How can capillary fluid shift affect bloods pressure?

Answer 3

The exchange of fluid across the capillary membrane between the blood and the interstitial fluid controls blood pressure very quickly. Low blood pressure results in fluid moving from the interstitial space into the circulation in an attempt to restore the circulating volume.

Question 4

Noradrenic fibres have a variety of effects:

Answer 4

1) Vasoconstriction at the end of vessels in all parts of the body (tonic discharge)
2) A chronotropic and an inotropic effect in the heart, which increases CO
3) Suppression of vagal (parasympathetic) tone, so that when the vagus is cut the result is tachycardia

Question 5

Summary of how the autonomic nervous system regulates BP:

Answer 5

The most rapid regulator of blood pressure. All blood vessels receive sympathetic innervation, however, arterioles are the most densely innervated. Sympathetic fibres also control the capacitance vessels (where blood is ‘stored’).
- vasoconstriction
-chrono/inotropic effect
-suppression of vagal tone

When the sympathetic fibres are cut, the blood vessels dilate. Vasodilatation is achieved by reducing the rate of discharge in vasoconstrictor fibres. The resistance vessels also receive vasodilatory cholinergic fibres that have no tonic discharge.

Question 6

Where is/ what is the vasomotor centre?

Answer 6

A group of neurons in the medulla oblongata control vascular tone by controlling the discharge from the sympathetic nerves (systemic vascular resistance, stroke volume, heart rate and contractility). The neurons that mediate this sympathetic discharge project into the preganglionic neurons in the intermediolateral grey matter in the spinal cord.

Question 7

The factors that affect the activity of the vasomotor centre are:

Answer 7

1) Direct stimulation:
-CO2
-Hypoxia

2) Excitatory inputs from:
-The cortex via the hypothalamus
-Pain pathways
-Carotid and aortic chemoreceptors

3)Inhibitory inputs from:
-The cortex via hypothalamus
-The lungs
-Carotid, aortic and cardiopulmonary baroreceptors

Question 8

Where are the chemoreceptors located?

Answer 8

in the aortic and carotid bodies.

Question 9

What effect do hypoxic and hypercarbic stimuli have?

Answer 9

Hypoxic and hypercarbic stimuli increase blood pressure.

Question 10

What is the somatosympathetic reflex?

Answer 10

The somatosympathetic reflex is the pressor response to stimulation of somatic afferents.

Question 11

Where are cardiopulmonary baroreceptors located?

Answer 11

located in the low pressure part of the circulation (right and left atrium, inferior vena cava, superior vena cava and pulmonary veins).

Question 12

What are baroreceptors?

Answer 12

Stretch receptors that are stimulated by distension of adjacent anatomical structures.

Question 13

Describe the carotid and aortic arch baroreceptors:

Answer 13

located in the adventitia and are extensively branched, coiled and intertwined.

The carotid receptors respond both to sustained and pulsatile pressure, and the afferent fibres from the carotid body form a distinct branch of the glossopharyngeal nerve, known as the carotid sinus nerve.

Increased firing of baroreceptor cells in response to elevated blood pressure leads to negative feedback on sympathetic activity via the baroreceptor reflex, resulting in a subsequent fall in heart rate and blood pressure.

Question 14

Effects of the baroreceptor reflex in response to a fall in BP:

Answer 14

A. Adrenaline secretion by the adrenal glands is stimulated by increased sympathetic activity.

B. Vasoconstriction of peripheral vessels is a result of sympathetic vasomotor activity.

C. Increased secretion of vasopressin occurs when the brain responds to a fall in the blood pressure.

D. Sodium retention occurs when increased sympathetic activity leads to renin secretion.

E. Increased sympathetic vasomotor activity also causes splanchnic venoconstriction.

F. Reduced vagal activity mediates tachycardia, together with adrenaline secretion this increases myocardial contractility.

Question 15

Humoral factors

Answer 15

Catecholamines, RAAS, substances secreted by the endothelium.

Humoral factors can regulate blood pressure directly (cathecholamines) or through regulating the blood volume and hence the cardiac output (the RAA system).

Question 16

Catecholamines

Answer 16

Adrenaline and noradrenaline are produced by and released from the adrenal medulla in response to sympathetic stimulation.

This is a fast way to achieve blood pressure control.

Question 17

The Renin-angiotensin-aldosterone system

Answer 17

Renin
Produced by the kidney and production increases in response to hypotension
Facilitates the conversion of angiotensinogen to angiotensin I

Angiotensin
Angiotensin converting enzyme (ACE) facilitates the conversion of angiotensin I to angiotensin II
Angiotensin II:
Stimulates aldosterone release from the adrenal cortex (Na+ retention)
Stimulates the thirst centre in the hypothalamus
Stimulates vasopressin secretion from the hypophysis
Leads to vasoconstriction

Aldosterone
Stimulates Na+ reabsorption in the distal renal tubules in exchange for K+ and H+
This increases the circulating volume by drawing water from the renal tubules by osmosis
The response is slow

Question 18

The kidney can increase the circulating volume by:

Answer 18

1. Water retention (e.g. vasopressin stimulation)
2. Sodium retention (e.g. sympathetic, corticosteroid stimulation)
3. Increase in aldosterone production through the RAA system
4. Increase in haemoglobin production by increased erythropoietin synthesis

The kidney can also produce natriuresis when stimulated by atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)

Question 19

Physiology of the valsalva manoeuvre:

Answer 19

Phase I. (Fig 2a) BP increases at the onset of straining (increased intrathoracic pressure is added to the blood in the aorta)

Phase IIa. (Fig 2b). BP then falls due to compression of the pulmonary veins and reduction in CO

Phase IIb. (Fig 2c) The decreased BP and HR inhibit the baroreceptors, leading to tachycardia and increased SVR

Phase III. (Fig 2d) When the glottis is open and CO is restored, intrathoracic pressure falls to normal and the thoracic aorta is decompressed, leading to a fall in mean aterial pressure (MAP)

Phase IV. (Fig 2e) The higher BP stimulates the baroreceptors, which cause bradycardia and return of BP to normal

Question 20

Pathology of the valsalva manoeuvre:

Answer 20

The reflex bradycardia in Phase IV is a clinical test of baroreceptor competence.

In patients with authonomic neuropathy the Valsalva test shows:

Continuing pressure fall in Phase II
BP does not overshoot in Phase IV
There is no reflex bradycardia in Phase IV

Question 21

Does orthostasis, the adoption of an upright position, present any challenge to the circulation?

Answer 21

Yes, orthostasis presents a serious challenge to the circulation.

After standing up abruptly, the initial blood pressure drop is quickly restored by neuroendocrine reflexes.

Initially the baroreceptor reflex causes:

-Tachycardia by reducing the vagal tone
-Stroke volume remains depressed due to volume redistribution; CO falls
-Peripheral resistance increases by 30-40% due to sympathetically mediated vasoconstriction
-Mean arterial pressure is not only restored by vasoconstriction but actually raised by 10-14%

Question 22

What happens in the next half hour after orthostasis?

Answer 22

During the next half-hour the orthostasis-induced rise in capillary filtration pressure causes 12-13% fall in plasma volume. This reduces systolic BP and elicits a further increase in HR. To compensate for the fall in plasma volume, the excretion of salt and water is reduced through the RAA system and reflex vasopressin secretion.

Question 23

What happens in a case of haemorrhage?

Answer 23

The immediate effect of acute hypovolaemia is the reduction of central circulating volume, which reduces the myocardial contractility and stroke volume, as well as pulse pressure.

The reflexes that are activated to maintain mean arterial pressure, myocardial perfusion and cerebral perfusion are:

Cardiopulmonary stretch reflex
Arterial baroreceptor reflex
Arterial chemoreceptor activity increases due to acidosis and poor receptor perfusion
As a result of these, the sympathetic outflow increases circulating adrenaline, noradrenaline, angiotensin II, and vasopressin increase.

Question 24

What is the single most important regulator of vascular tone?

Answer 24

Sympathetic vasoconstriction

Question 25

What do the sympathetic fibres release (regarding control of BP)?

Answer 25

Noradrenaline

Question 26

Where is vasopressin synthesised?

Answer 26

in the magnocellular neurons of supraoptic and paraventricular nuclei.

Question 27

Substances secreted by the endothelium:

Answer 27

The endothelium secretes a number of vasoactive substances:

1. Thromboxane A2 promotes platelet aggregation and vasoconstriction
2. Prostacyclin inhibits platelet aggregation and produces vasodilatation
3. Nitric oxide is synthesized by the endothelium from L-Arginine and is a potent vasodilator
4. Adenosine, bradykinin and histamine are other vasodilating substances
5. Endothelins are the most potent naturally occurring vasoconstrictors in the body