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Blood pressure and volume (Extrinsic controls of blood flow (Baroreflex…
Blood pressure and volume
Intrinsic controls of blood flow
Metabolic autoregulation
Blood flow matched to tissues metabolic rate
Increased blood flow known as active hyperaemia
Paracrine control
Locally acting chemicals that alter flow rate in response to local environment
Increased blood flow velocity = Nitric oxide from endothelial cells = vasodilation
Local irritation
Prostacyclin from endothelial cells = vasodilation
Histamine from mast cells = vasodilation mediation by NO
Bradykinin from globulins = vasodilation mediation by NO
Endothelial damage
Endothelin 1 =Vasoconstriction
Thromboxane A2 from platelets = vasoconstriction
Extrinsic controls of blood flow
Temporary management of blood pressure during times of need
Preserve blood flow to essential body tissues = brain, cardiac muscle, working skeletal muscle
CNS coordinates responses via autonomic nervous system
Baroreflex
Cardiovascular centre
Maintains CO and TPR to keep arterial BP within normal limits, via ANS
Pressure receptors (how much blood vessel being stretched)
Carotid artery, carotid sinus, aortic arch
Greater stretch = greater rate of AP
Atrial volume receptors
Renin-angiotensin-aldosterone system (RAAS)
Hypothalamus
Pituitary
Metabolic autoregulation
Increased blood flow = Active hyperaemia
Oxygen = vasoconstrictor
Carbon dioxide = Vasodilator
Lactic acid = Vasodilator
K+ = Vasodilator
Absence of oxygen or presence of others will cause vasodilation (increase blood flow), there will be O2 absence when high metabolic rate in tissue
Blood vessel compression
Long-term
Ischaemia
Reduced blood flow due to long term compression
Causes pain (to cause animal to cease activity)
Reflex increase in pressure
Increases workload of heart
Infarction
Cell damage due to long term reduced blood flow
Necrosis
Cell death
Short term
Reactive hyperaemia (Blood flow interrupted, oxygen debt and build up of waste products, increase blood flow until O2 debt repaid)
Baroreflex
Response
Drop in BP = reduced APs from baroreceptors
Increased sympathetic output
Faster conduction
Increased contractility
Increased HR (with shortened systole)
Peripheral vasoconstriction
Decreased parasympathetic output
Pa=CO x TPR
Renin-angiotensin-aldosterone system (RAA)
Longer to kick in than baroreflex
Drop in BP -> Increase symp activity -> Renin from JGA -> Liver -> with angiotensinogen forms angiotensin I -> Lung -> With ACE forms angiotensin II ->Aldosterone from adrenal gland causes a) Na+ & H2O retention in kidney, b) vasoconstriction -> Increase blood pressure
Angiotensin II
Affect on hypothalamus to increase sensation of thirst
Release of anti-diuretic hormone from pituitary = conversion of water -> further vasoconstriction
Starlings law
Vasoconstriction -> Reduced blood flow in capillaries -> reduced hydrostatic capillary pressure -> More retention of fluid (less filtration/more absorption) so increase blood pressure
Reliant on normal kidney function
Altering flow
Change vascular resistance
Change perfusion pressure
In range of normal BP flow regulated by intrinsic mechanisms
In times of need intrinsic mechanisms overwhelemed by extrinsic mechanisms
System over-rides
Fight or flight response can override cardiovascular centre (psychological input > internal monitoring input in some situations)