Blood vessel function and the distribution of cardiac output Flashcards Preview

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Flashcards in Blood vessel function and the distribution of cardiac output Deck (12):

Pressure, flow and resistance

Flow = pressure difference/ resistance
Friction between walls and liquid flow generate resistance


Resistance in circulation

Circulation is a combination of resistance in series and parallel
Serial resistance provides fine control of blood flow distribution
Parallel resistance minimises overall resistance- reduces the requirement for the heart to generate pressure


How resistance to flow is arranged

Resistance in series (flow through tissues)
Resistance controlled by increasing or decreasing the radius of blood vessels
Resistance in parallel (overall flow in the CNS)
Total resistance is minimised, flow is regulated by altering resistance through tissues


Mechanisms for changing vascular diameter

Local control: myogenic response, flow-induce shear stress, metabolic control
Central control: sympathetic nervous system (A1 receptors = contraction, B2 receptors = relaxation), parasympathetic nervous system (ACh on M3 receptors), vasoactive hormones (e.g. angiotensin)


Local control: myogenic contraction

Increase in intra-luminal pressure causes contraction
Decrease in intra-luminal pressure causes relaxation


Flow-induced shear stress

Increase in flow increases shear stress
Activates eNOS to make NO
NO diffuses into muscle and reduces free intracellular Ca2+
Reduced free intracellular Ca2+ = relaxation
Flow becomes more laminar thereby reducing shear stress


Endothelium Derived Hyperpolarising Factor (EDHF)

Endothelium-dependent relaxation still seen when eNOS is blocked
Relaxation is associated with hyperpolarisation of the underlying smooth muscle


Metabolic control of vascular diameter

Increase in metabolic rate leads to an increase in oxygen demand, decreasing transient tissues oxygen
Acidosis, hypoxia, adenosine release and an increase in extracellular potassium all cause vasorelaxation
Contraction is active (uses ATP), a lack of oxygen decreases the ability to make ATP so vascular relaxation is due to a lack of ATP


Sympathetic nervous output

Sympathetic drive to different tissues can be independently regulated
Sympathetic fibres are tonically active
Overall, reduced activity leads to vasodilation, increased activity leads to an increase in peripheral resistance, decrease in local blood flow and decrease in volume


Smooth muscle contraction: A1 adrenoceptor stimulation

Stimulation of alpha adrenoceptors activates Gq
Gq activates phospholipase C
PLC converts PIP2 into IP3 and DAG
IP3 causes release of intracellular Ca stores
Increased free intracellular Ca drives actin/myosin interactions resulting in contraction
Contraction is sustained until stimulus removed
Net effect = vasoconstriction


Smooth muscle relaxation: B2 adrenoceptor stimulation

Stimulation of B2 adrenoceptors activates Gs
Gs activates adenylyl cyclase
AC converts ATP into cAMP
Elevated levels of cAMP activate protein kinase G
Targets phosphorylated by protein kinase G
Net effect = vasodilation


Parasympathetic mediated vasodilation

Stimulation of muscarinic receptors on endothelium activates Gq
Gq activates phospholipase C increasing IP3 production
IP3 causes release of intracellular Ca2+
eNOS is Ca2+ sensitive and so rate of NO production increased
NO and EDRF cause relaxation of underlying smooth muscle