- 1 Learning outcomes
- 2 Blood pressure
- 3 Short-term control of blood pressure
- 4 Coordinating areas
- 5 Parasympathetic innervation of heart
- 6 Sympathetic innervation of heart
- 7 Sympathetic innervation of blood vessels
- 8 Summary of the baroreceptor reflex (short term control of blood pressure)
- 9 Long term control of blood pressure
- 10 Summary
- 11 See also
- Know the elements of the arterial baroreceptor reflex which controls blood pressure on a moment-to-moment basis.
- Understand that blood pressure in the long term is controlled by changes in blood volume, and that the kidney has a vital role in this process.
- Know the three mechanisms by which the body responds to changes in blood volume; pressure diuresis, the volume reflex (mediated by atrial baroreceptors); the renin-angiotensin system.
- ‘Vital sign’ - homeostasis.
- Too low - inadequate perfusion of tissues/organs. End-organ damage.
- Too high - strain, damage to heart, vessels. Risk factor for CV disease.
- Q = P/R; P = Q x R (Ohm's law)
- BP = CO x TPR (Total peripheral resistance)
- =120 / 80 mmHg (systolic / diastolic) Mean arterial pressure (MAP) ~ 93 mmHg
- Control mechanisms are divided into short-term and long-term.
Short-term control of blood pressure
- Moment-to-moment control of arterial blood pressure is through baroreceptor reflex
- Reflex = a neural feedback loop: stimulus, a detector, an afferent neural pathway (takes signal from detector to coordinating centre), an efferent neural pathway (to an effector) and a response
- Baroreceptor = pressure receptor
- Coordinating centre is the 'vasomotor centre' or 'cardiovascular control area' in the upper medulla
- Produces a response in the autonomic nervous system (sympathetic nerves and parasympathetic nerves)
- Two key effects to lower BP: 1. decrease heart rate and 2. causes vasodilation
- There are two groups of baroreceptors: aortic arch and carotid sinuses. They are bare nerve endings; very simple; buried in aortic wall. (Note also chemoreceptors that detect oxygen and carbon dioxide). (Carotid sinus is just where the common carotid artery branches into the internal and external carotid arteries). (The carotid body is the yellow dot in the diagram, and has chemoreceptors in it, not baroreceptors).
- Sensory fibres from the aortic arch baroreceptors go up in the Lt and Rt vagus nerve (CNX) to travel up to the CV control area. Baroreceptors in the carotid sinus are connected via the sinus nerve (or Hering's nerve) to the glossopharyngeal nerve (CNIX) to travel up to the CV control area.
- Baroreceptors sense pressure within vessels by stretch of vessel wall.
- Pulse pressure
- Static pressure
- Has a basal level of stimulation. During systole, this stimulation increases. During diastole, this stimulation decreases. Similar for static pressure.
- When pressure is increasing, a rapid burst of firing occurs. If the stimulus is maintained, the frequency of firing decreases to a stable level of firing. This is because the baroreceptors adapt or desensitise over time in response to a maintained stimulus, which is part of the reason they're not good for maintaining blood pressure.
- Range of action:Below 80 mmHg there is not much activity. Above 160 mmHg, they're fully active
- Vasomotor centre, receiving input from chemoreceptors and pressure receptors. Also connected to motor cortex (increase CVS output during exercise), cingulate gyrus/limbic system (emotional response - stress increases HR and BP, relaxation decreases them), orbital/temporal lobe/hypothalamic nuclei (important for sensing blood osmolality, has responses for the kidney etc), and mesencephalon/reticular substance (diurnal rhythms: BP decreases at night).
- Hence there are a LOT of inputs into the CVS control centre (vasomotor centre) other than what we focus on today
- Dorsal view of vasomotor control area
- Various groups of nerve bodies: vasodilator (inhibit sympathetic nerve traffic). Cardioinhibitor gives rise to parasympathetic nerves to slow the heart
- Right diagram
- Dotted = vagus nerve, to slow the heart down
- Dark lines = sympathetic nerves, that have their own ganglia alongside the spinal column, and run to the heart (increase HR and BP), and to the blood vessels (causing constriction)
Parasympathetic innervation of heart
- Xth cranial nerve (vagus)
- Innervate atria, primarily (very little evidence they innervate the ventricles)
- Slows heart rate (bradycardia) - by slowing the discharge of SA node cells
- Predominant influence under resting conditions (no neural influence: HR ~ 110 bpm) - if you cut all the nerves to the heart, HR jumps to 110 bpm
- Acetylcholine - increases K+ in ECF
Sympathetic innervation of heart
- Cardiac accelerator nerves (thoracic). Innervate atria and ventricles
- Increases heart rate (tachycardia) and force (positive inotropic).
- Noradrenaline - increase Ca2+ in ECF
Sympathetic innervation of blood vessels
- Sympathetic nerve activation causes constriction of blood vessels (smooth muscle contraction).
- arteries, arterioles and veins
- not capillaries (not innervated) - don't have smooth muscle in the wall
- Only sympathetic nerves innervate blood vessels (at least w.r.t. blood pressure)
Summary of the baroreceptor reflex (short term control of blood pressure)
- Baroreceptor reflex is a negative feedback loop:
- Activation stimulates:
- bradycardia (reduced heart rate)
- dilation of peripheral arteries (reduced resistance)
- negative inotropy (reduced heart force; minor effect)
- Because baroreceptors are tonically active, reduction in blood pressure produces opposite effect:
- Artificially perfused, anaesthetised rat. Increasing blood pressure decreases sympathetic, increases cardiac vagal (p- symp.) nerve activity.
- Note the integral shows you the mean integrated activity of the cardiac vagal and T12 sympathetic nerves
- Second example shows how important the baroreceptor reflex is necessary for moment-to-moment blood pressure maintenance.
- Baroreceptor reflex is vital in cardiovascular response to changes in posture.
- Lying down (recumbent) to upright position may greatly decrease venous return: fall in CO, BP.
- Blood drains from cerebral circulation: fainting
- Stand from recumbent position (orthostasis): Gravity forces blood to drain from upper body and pool in lower body (veins distensible).
- Decreased cardiac output when you stand is mainly due to a reduce in stroke volume (less blood is feeding into the heart)
Long term control of blood pressure
- Baroreceptors are not effective for long-term control of blood pressure (they adapt, see above - they'll reset control around a new setpoint)
- Goal of long term control is to maintain the water volume control of your body
- Accomplished by blood volume regulation.
- Number of mechanisms involved.
- Kidneys are vital in this role.
Pressure diuresis (diuresis: increased urine formation)
- Note that stroke volume increases with increased venous return due to Starling's law of the heart
- Quite small increases in blood pressure can double urine formation (similarly for halving urine formation)
- After exercise, you need to urinate due to blood pressure increases
- Located in the right atrium and walls of the VC are the atrial baroreceptors (volume receptors). These respond mainly to blood volume (rather than pressure).
- NB: 60% of blood volume is in venous system, so a good place to monitor
- Blood volume goes up --> stretches VC and right atrium wall --> stimulates A (firing during atrial contraction) and B (in VC, stimulated by atrial diastole or ventricular systole, while the atrium is filling) fibres of atrial baroreceptors --> sends sensoring nerve inputs to vasomotor control centre and hypothalamus --> 1. CV control centre increases sympathetic nerve activity to heart: rate/force/CO (to drive increased blood volume from the venous system to the arterial side; the Bainbridge reflex) 2. hypothalamus: reduces sympathetic nerve activity from CV control area to renal arterioles, so we get more blood flow to the kidney, to get more urine formation (diuresis). hypothalamus also decreases the secretion of ADH, to increase water excretion from the kidney --> increase urine formation and excretion; blood volume falls
- 3 key components: increase in heart rate (move from veins to arteries) 2. decrease blood flow to kidney 3. reduce ADH. 2+3 --> more urine
What if blood volume/pressure is too low?
- Pressure diuresis/volume reflex are for pressure too high
- E.g. hemorrhage; diarrhoea; dehydration
- less pressure diuresis, volume reflex not active.
- activate renin - angiotensin system (RAS). Hormonal mechanism.
- Low blood volume = low BP --> low GFR in kidney --> stimulates release of renin (enzyme) from the kidney --> goes into bloodstream, to act on angiotensinogen and convert it into the angiotensin 1 --> ACE (on endothelium, particularly in the pulmonary circulation) converts angiotensin 1 into angiotensin 2.
- AT2 does 3 things to increase blood pressure:
- Vasoconstriction - constriction of veins particularly increases venous return, SV and CO (Starling's law)
- Increase Na+ reabsorption (directly) - increased water reabsorption (salt first), increasing plasma volume and venous return --> SV and CO (Starling's law)
- Adrenal gland: Aldosterone --> Increased Na+ retention --> higher water retention
- Adrenal medulla stimulation - strong when rapid decrease in blood volume (e.g. hemorrhage).
- Adrenaline release is tightly coupled to blood volume
- High adrenaline causes vasoconstriction, and increases heart rate and force
- Fed into by sympathetic nerves in response to atrial/arterial baroreceptors
- Arterial blood pressure is tightly regulated as part of homeostasis. Blood pressure (BP) is the product of cardiac output (CO) and total peripheral resistance (TPR).
- The autonomic nervous system is the main modulator of the cardiovascular system. Sympathetic nerves increase heart rate and force, increasing cardiac output, and constrict (most) blood vessels, increasing peripheral resistance. Parasympathetic nerves reduce heart rate, reducing cardiac output
- Baroreceptors, located in the aortic arch and carotid sinuses, are stimulated by an increase in blood pressure. They cause a reflex slowing of heart rate and reduced sympathetic nerve activity to blood vessels, thus reducing both CO and TPR.
- Low-pressure baroreceptors located in the vena cavae and right atrium are activated by an increase in blood volume; they act to decrease blood volume by increasing water loss through the kidney.
- Long-term increases in blood pressure are opposed by a reduction in blood volume, through diuresis; the renin-angiotensin system acts to increase blood volume and peripheral resistance should blood pressure fall, through production of the hormone angiotensin II. Adrenaline is also released from the adrenal gland as a result of blood volume loss.