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Baroreflexes

Physiology and Pharmacology

QuestionAnswer
Key concepts Local blood flow is determined by tissues In vascular beds flow is auto regulated to match metabolic demand and is independent of perfusion pressure Tissues have adaptations to regulate flow Reflexes hold arterial pressure constant
Cardiac output Heart rate x stroke volume Does not explain how blood flow is distributed locally
Tissue blood flow (arterial blood pressure - venous blood pressure)/resistance
Regulation of perfusion pressure Cardiac contraction - hormones, nerves, starlings law water/salt balance - volume e.g. drink, urine, sweat Vessel compliance - pressure volume relationship Changes in BP are often pathological not physiological regulation of flow
Resistance vessels Greatest fall in pressure is at arterioles Site of control of capillary flow Vasoconstriction - increase in arterial BP and decrease in capillary perfusion Vasodilation - decrease in arterial BP and increase in capillary perfusion
Capillary recruitment Some capillaries are always open Other capillaries are closed at low pressures and only open under higher pressure Important in skeletal muscle and reduces diffusion distance
Diverting blood The systemic circulation has parallel circuits Constricting one circuit can divert blood to other vessels Does not work in pulmonary circulation as there are no parallel circuits Vasoconstriction would mean blood cannot move
Changes in resistance and tissue perfusion Flow can increase an order of magnitude by vasodilation Allows flow to be responsive to demand But a certain basal, minimal perfusion must be maintained
Why do we need a minimum basal flow Blood flow is vulnerable at very low ABP Standing up and sitting down Changes in circulating volume Changes in external pressure etc Particularly damaging for kidney and cerebral vascular beds
Myogenic autoregulation Tissues controlling their perfusion independently of arterial blood pressure Arterioles show a small increase in flow with an increase in pressure but this decreases due to Bayliss effect
Bayliss effect As pressure increases radius decreases to maintain flow Only a small change in radius is needed This is myogenic Allows flow to stay in a constant range
Mechanism of Bayliss effect Stretch increases tension Opens non-specific cation channels Opens voltage gated calcium channels Raises Ca conc and triggers contraction Major mechanism in cerebral, renal and coronary Not in pulmonary and cutaneous
Metabolic autoregulation Matching local perfusion with local metabolism Perfusion often matches metabolic rate Kidney and skin are relatively over perfused Brain and heart are relatively under perfused
Flow pressure plots Arterioles are sensitive to metabolic demand of tissue Metabolic effects can override myogenic autoregulation Important in cerebral skeletal and coronary
Adenosine release Falling ATP supply leads to AMP release from cells Adenosine activates A2a receptor increasing cAMP and PKA Increases SERCA and decreases Ca Leads to vasodilation Used in coronary circuation
Acidity High oxidative phosphorylation Hight CO2 Acidity Decreased MLCK activity Vasodilation Used in cerebral circulation
Extracellular K conc Increase in K indicates increase in AP frequency Leads to hyperkalaemia as it takes time for K to be take up Important in skeletal muscle vasculature Should depolarise VSM but low concs increase K permeability and moves Vm closer to Ek - hyperpolarises
Reactive hyperaemia Important in skeletal muscle Following occlusion there is a mass increase in blood flow due to vasodilation to wash away metabolites
Factors affecting local flow Metabolic - high K, Acidity, adenosine, temp, peroxide, hypoxia, NO and osmolarity Local autacoids - histamine, bradykinin, prostaglandins and leukotrienes Extrinsic factors - adrenaline, angiotensin, noradrenaline and Ach
Reflexes Overlaid on top of auto-regulatory mechanisms Hold ABP constant allowing local mechanisms to act independently Help sustain cerebral perfusion during postural changes
Vasomotor nerves Sympathetic vasodilator Parasympathetic vasodilator Sympathetic vasoconstrictor
Sympathetic vasoconstrictor nerves Manifest basal activity High activity - vasoconstriction Low activity - vasodilation Vasomotor centre in medulla activates spinal cord, triggering sympathetic ganglion and alpha receptors on arterioles Inhibited by nucleus tractus solitarius
Baroreceptors Detect pressure changes All above the heart - this area is most sensitive to pressure changes e.g. Glossopharyngeal, Carotid baroreceptor, Vagus, Aortic baroreceptor, Cardiac baroreceptor and veno-atrial baroreceptor
Properties of aortic/cardiac baroreceptors Increase in pressure increases firing rates of receptors Can detect changes not steady state Mostly using type A myelinated fibres When baroreceptors denervated control of BP is lost
Orthostasis Gravity redistributes venous blood towards feet Reduces venous return and stroke volume by starlings law Yet blood arterial BP does not fall Increased vasoconstriction to increase peripheral resistance and an increase in heart rate
Skin perfusion Relatively over perfused Sympathetic ganglion activate alpha 2 receptors to cause AVA closure Heat inhibits this to open AVA and increase heat loss Temp decreases affinity of NA for receptors Important in cutaneous circulation
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