Regulation of Blood Pressure Flashcards
Why is it important to maintain tissue perfusion across the whole body?
- To keep a relatively constant arterial blood pressure.
- When too low, blood flow to organs fails.
- When too high, there can be damage to vessels and organs.
- To control distribution of the total cardiac output.
- 5L/minute is not sufficient to perfuse the entire body.
- Needs to respond to tisue demands.
- Satisfied by local control mechanisms.
Describe the nervous control of arterial pressure.
- Nervous control of arterial pressure is rapid.
- It can increase arterial pressre to 2x normal within 5-10s.
- It can decrease arterial pressure to 50% normal within 10-40s.
What are the fundamental components of a reflex control system?
- Internal variable to be maintained.
- Receptors sensitive to change in the variable.
- Afferent pathways from the receptors.
- An integrating centre for the afferent inputs.
- Efferent pathways from the integrating centre.
- Target effectors that alter their activities.
How is mean arterial blood pressure calculated?
- Total peripheral resistance is the factor which varies most in maintaining mean arterial blood pressure.

Describe the feedback control of mean arterial pressure.
- Main baroreceptor locations:
- Walls of the aorta
- Afferent fibres follow the vagus nerve (CNX).
- Carotid artery
- Afferent fibres follow glossopharyngeal nerve (CNIX).
- Walls of the aorta
- Baroreceptor activity:
- Stretch receptors
- Firing rate increases when BP increases.
- Firing rate decreases when Bp decreases.
- Sensitive around a ‘set-point’.
- Set point can change (e.g. hypertension).
Describe the rate of baroreceptor firing and the relationship this has with phasic aortic pressure.

What is the primary purpose of baroreceptor control of blood pressure?
- To reduce the minute-to-minute variations of arterial pressure

What is the role of cardiopulmonary baroreceptors?
- Cardiopulmonary baroreceptors are ‘low-pressure’ receptors which sense central blood volume.
- Atria, ventricles, veins and pulmonary vessels.
- If the rate of cardiopulmonary baroreceptors firing decreases, (signalling decreased blood volume), then:
- Sympathetic nerve activity to the heart and blood vessels increases.
- Parasympathetic nerve activity to the heart decreases.
Describe the integrated control of BP (medullary cardiovascular control (MCVC) ‘vasomotor’ centre).
- Medullary cardiovascular control (MCVC) ‘vasomotor’ centre:
- Sensory area
- Input from baroreceptors
- Lateral portion
- Efferent sympathetic nerves
- Medial portion
- Efferent parasympathetic (vagal) nerves
- Sensory area

What are the sympathetic and parasympathetic effects on the heart?
- Both control heart rate and normally function simultaneously.
- At rest, parasympathetic - predominate tone.
- Sympathetic can significantly affect stroke volume and rate.
What are the sympathetic and parasympathetic effects on blood vessels?
- Sympathetic effects on blood vessels:
- Continuous low-level tone affects total peripheral resistance.
- ‘Sympathetic vasoconstrictor tone’ exerts ‘vasomotor tone’ on vessels.
- Therefore, vessels are kept partially constricted.
- Remember veins are also innervated by the sympathetic NS.
- Decreased capacitance, therefore increased venous return, therefore increased stroke volume, therefore increased cardiac output.
- Continuous low-level tone affects total peripheral resistance.

Describe the CNS ischaemic response.
- Emergency pressure control system
- ‘Last ditch stand’
- When blood flow to the medullary CVCC is massively decreased:
- Increased peripheral vasoconstriction
- Almost completely occludes some peripheral vessels.
- Increased sympathetic stimulation of the heart.
- Greatly increased systemic arterial pressure.
- As high as 250mmHg for 10 minutes.
- Increased peripheral vasoconstriction
Describe the fine control of blood flow.
- Local control superimposed on organ dist. of CO
- Tissues auto-regulate blood flow.
- Build-up of local factors (e.g. adenosine)
- Independent of innervation / hormonal control
- Tissues auto-regulate blood flow.
- Intrinsic ability to maintain blood flow safely across capillaries if BP is raised.
- Myogenic theory (acute auto-regulation)
- Stretch-induced vascular depolarisation of smooth muscle due to increased arterial pressure.
- Myogenic theory (acute auto-regulation)
- Remember not all capillaries in an organ are perfused simultaneously.
Summarise cardiac output.

Summarise total peripheral resistance.

How is blood pressure regulated long-term?
- Control of body fluid volume by the kidneys - renal body fluid feedback system.
- When arterial pressure increases, urine production increases.
- When arterial pressure decreases, urine production decreases.

Describe the long-term regulation of blood pressure.
- 2 primary determinants:
- The renal output curve for salt and water
- The level of salt and water intake
- It is impossible to change long-term mean arterial blood pressure without changing one or both of these.

Describe the effects of anti-diuretic hormone (ADH).
- A.K.A. arginine vasopressin.
- Released by the pituitary gland in response to:
- Increased osmotic pressure
- Sensed by hypothalamic osmoreceptors.
- Hypovolemia (10% loss of greater)
- Atrial baroreceptors normally inhibit ADH release.
- Decreased volume leads to decreased firing rate, therefore increased ADH release.
- Hypotension
- Decreased arterial baroreceptor firing.
- Increased sympathetic activity and increased ADH release.
- Angiotensin II
- Increased osmotic pressure
What is the effect of ADH on blood volume?
Describe the mechanism.
- ADH increases blood volume by:
- Causing increased water permeability in renal collecting ducts.
- Therefore decreased urine production.
- Causing increased water permeability in renal collecting ducts.
What is the effect of ADH in severe hypovolemic shock?
- ADH release is high
- Causes vasoconstriction
- Therefore increased total peripheral resistance
Summarise the regulation of blood osmolarity.

Describe Renin.
- Proteolytic enzyme released from the kidneys in response to:
- Sympathetic nerve activation
- Mediated by baroreceptor feedback
- Renal artery hypotension
- Independent of baroreceptor feedback
- Decreased sodium in kidney distal tubules
- Sympathetic nerve activation
Summarise the renin-angiotensin-aldodterone system (RAAS).

Describe the action of the RAAS.
- Renin released from kidney juxtaglomerular cells.
- Angiotensin II acts on resistance vessels.
- Therefore increased total peripheral resistance.
- Angiotensin II acts directly on the kidneys.
- Constricts renal arteries, therefore decreased blood flow via kidneys.
- Angiotensin II causes release of aldosterone from the adrenal glands.
- This causes increased Na+ and water reabsorption.
- Angiotensin II stimulates release of ADH from the pituitary.

What is atrial-natriuretic hormone?
Describe its mechanism of action.
- 28 amino acid peptide synthesised and stored in muscle cells of the atria.
- Released in response to stretch of the atria.
- Helps oppose the effects of the RAAS.
- May help counteract volume overload.
What are the other factors which affect blood pressure control?
- Cortex
- Conscious effects of emotions
- Nerves from cortex to medullary CVC centre.
- Conscious effects of emotions
- Time of day
- Diurnal variations due to hormones and cortical input.
- Respiration
- Via mechanical movements
- Via chemoreceptors
- Aortic and carotid bodies detect changes in pO2
- If pO2 is decreased, rate of firing is increased