Flashcards in The cardiovascular control system Deck (42):
What are the aims of the CV control system?
Maintain BF to different organ systems
Purpose of the RAA system
Regulation of body fluids
Factors causing increased renin secretion?
Decreased perfusion pressure
Increased sympathetic drive to the kidney
Decreased sodium content in tubular fluid
Some functions of angiotensin II
- Primarily a vasoconstrictor
- Release of aldosterone = sodium reabsorption (also a direct action of aldosterone), followed by water reabsorption = increase circulating volume = maintained BP
- Increased secretion ADH
- SNS stimulant
General pathway of the RAA system?
Angiotensinogen produced by the liver
Renin coverts it to angiotensin I
ACE produced in the lungs converts it to angiotensin II
How are changes in BP sensed by the body?
Systemic aortic baroreceptors in carotid sinus and aortic body, nerve impulse firing rate increases with increased arterial pressure
What is the pattern of negative feedback to the systemic aortic baroreceptors?
Info comes back from the brain via the sympathetic cardiac nerve, is effectively the opposite of the firing rate from the carotid sinus nerve impulses
So when you have low levels of carotid sinus nerve activity you have increased sympathetic drive. vice versa
What are the neural responses to an increased BP?
Decreased sympathetic drive and increased vagal / parasympathetic drive
There is no vagal inhibitor so temporal rate changes less than sympathetic nerves
Changes to said mechanism in a hypertensive patient
baroreceptor reflex not as good
Changes in pressure either don't change carotid sinus nerve activity as much or they change change carotid sinus nerve activity enough but the output doesn't change as much
Therefore the patients are prone to having more fluctuations in blood pressure because the gain of the system is low
What is a telling prognostic indicator of outcome in hypertensive patients?
the severity of the decreased gain of the baroreceptor reflex
Threshold of the carotid sinus baroreceptor?
below 30-50mmHg a decrease in pressure doesn't alter the firing rate
Saturation of the carotid sinus baroreceptor?
increase in pressure above 150-180mmHg also has no further effect on firing frequency
rate sensitivity of the carotid sinus baroreceptor
For a given mean pressure the rate of firing is greater for pulsatile pressure than for steady pressure
Standard responses when arterial pressure falls?
Increased HR and cardiac inotropic state
Graded restriction of pre capillary resistance vessels in skeletal muscle (splanchnic, cutaneous and renal circulations) but not in cerebral and coronary arteries
Increased catecholamine secretion by adrenal medulla
Increase circulating levels of ADH, AII and other hormones
Vagal afferent in the heart sense
Sense changes in cardiac volume
A and B receptor fibres which fire off either atrial or ventricular contraction send info about the stretch in either the atria or ventricle
In most cases volume and pressure increase together but sometimes can be dissociated from each other
Steep activation of myelinated RA receptors leads to?
Reduced renal sympathetic stimulation (sympathetic drive to other organs doesn't change that much) this helps you excrete out salts and water and bring blood volume back down
Osmoreceptors in the hypothalamus?
sense changes in effective plasma osmolality by measuring their volume alteration.
this modulates the synthesis and release of ADH levels leads to net water excretion (vice versa)
Increased discharge of peripheral chemoreceptors is brought about by? and results in?
by low PaO2
Stimulates increased sympathetic drive to heart and heart vessels.
When oxygen delivery is deprive for instance by reduced arterial pressure chemoreceptor activation causes vasoconstriction and contributes to restoration of BP.
What happens in the circuitry of the brain if BP increases?
Increased activation of CVLM which sends inhibitory signals to the RVLM do decreased excitation at the RVLM and from the RVLM sympathetic drive to all the blood vessels decreases
The paraventricular nucleus and CV control
Underneath is the posterior pituitary where ADH is secreted, so cardiopulmonary receptors go up into the NTS which sends projections to the PVN which sends projections to the posterior pituitary to try and change ADH, PVN also sends projections directly and via the RVLM to the kidney to change kidney sympathetic drive
What type of vasculature has the largest relative size of smooth muscle?
small arteries and arterioles
How is the blood flow to different parts of the body regulated?
Alteration of lumen of pre capillary resistance vessels
Effects of altered pre capillary resistance of distribution of mean pressure through typical vascular network
Constriction of pre capillary resistance vessels means that energy is dissipated as blood is funnelled through a narrower opening, pressure gradient along vessels is increased and pressure within vessels is reduced this means less fluid extrusion/ more fluid absorption
Storage of blood in the systemic circulation and how does it change?
Small veins and venules
Construction reduces their capacity to store blood and increases pressure driving blood back to the right heart. vice versa.
These changes also influence post capillary vascular resistance
About vascular smooth muscle?
Local pacemaker activity because all VSM cells are electrically coupled to their neighbours and this may propagate from one side to the other
The link between blood vessel flow and metabolism is demonstrated by?
auto regulation )intrinsic tendency of organ to maintain constant blood flow despite changes in perfusion pressure
the cutaneous circulation has almost none whereas the cerebral circulation is tightly regulated
after a blood vessel is occluded for a short period, when the occlusion is released blood flow rises above the preclusion level, and is maintained for a period roughly proportional to the duration of the occlusion
How does the myogenic control work?
most potent in medium sized arterioles and in small and medium veins
Increased pressure distends the vessel walls which depolarises VSM cells (stretch sensitive membrane ion channels) causing contraction
Endothelial control of VSM?
endo cells release smooth muscle which acts on VSM to increase intracellular cGMP conc causing VSM relaxation
The end also releases endothelin a calcium chanel agonist and potent vasoconstrictor
Integrated model of local control
When tissue metabolism is increased with respect to blood supply vasodilator metabolites are produced leading to dilation of terminal arterioles which in turn increases blood flow resulting in dilation of small arteries and more proximal arterioles that are less sensitive to metabolites and more sensitive to flow
The role of co transmitters?
Produce long lasting actions that supplement the effects of primary neurotransmitter
act as a vasodilator system
Pre capillary vessels in the heart, brain, face, tongue and urogenital tract, they release Ach
bind to M3 receptors in the vascular endothelium stimulating release of NO. But when vascular endo damaged or removed they bind to M2 receptors in the VSM causing vasoconstriction
Sympathetic cholinergic fibers innervate pre capillary vessels in the skeletal muscle beds
Exogenous admin of noradrenaline causes?
Widespread vasoconstriction except for coronary and cerebral arteries
Exogenous admin or adrenaline causes?
similar vascular effects to noradrenaline but resistance vessels in skeletal muscle and splanchnic circulations vasodilate, because Beta2 andregenic receptors are present in splanchnic and skeletal muscle circulations
Other hormones that cause blood vessel changes
Angiotensin II a potent vasoconstrictor
Vasopressin / ADH is a vasoconstrictor
What happens in skeletal muscle during exercise?
substantial fall in vascular resistance Increased perivascular concentrations of vasoactive metabolites which occur in exercise i) relax smooth muscle ii) inhibit sympathetic androgenic neurotransmission
The increased levels of adrenaline in circulation will also sustain vasodilation
Histamine released dilates pre capillary vessels
Low capillary densities and large numbers of superficial arteriovenous shunts to function as heat exchangers
Blood flow at rest greater than tissue requirements, auto regulation poorly developed
Powerfully innervated by the sympathetic adrenergic system
The affinity for the alpha receptor for NA decreases as the temperature rises thus local warming will lead directly to increased skin blood flow. Vice versa
tight linkage between metabolism and blood flow, tight regulation of perfusion pressure. Normal range = 60-180mmHg Autoregulation fails when PP < 50mmHg, oxidative metabolism of the brain impaired by pp of 40mg or less
Total cerebral blood flow relatively constant but large regional variation
Cerebral BF control mechanisms
cons of pH, PCO2, PO2 and K+
How are vascular cross sectional dimensions determined?
by pressure gradient across the vessel wall = transmural pressure Pt = Pi - Pe
Pressures causing vessels to collapse
Pe > Pi = collapse
if Pe 20mmHg --> transient collapse and occlusion of post capillary vessels
However pressures will increase sufficiently throughout the vascular circuit for flow to be reinstated though possibly at a reduced level
When pressure 40mmHg there is collapse off price capillary vessels leading to impaired perfusion and sustained non-perfusion for some vascular regions
*compliancy of the compartment the vascular bed is inis significant e.g. those bounded by skin are easily distend able whereas the cranial cavity or fascial ones aren't