PSL301H1 Lecture Notes - Lecture 10: Windkessel Effect, Blood Vessel, Venule
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PSL301H1 Full Course Notes
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Where is blood pressure greatest: tunic intima endothelium, tunica media smooth muscle, tunic externa connective tissue, capillary, venule. Windkessel effect arteries expand and store pressure in the elastic walls. Because of semilunar valve being closed and preventing backflow there is an elastic recoil that squeezes blood forward. In veins (70%) acts a reservoir during hemorrhage: metarteriole, true capillaries exchange vessels. Direct flow between arteriole and venule bypassing tissue cells: pressure gradient increases flow, resistance decreases flow. Aorta: resistance increases as length increases, resistance increases as viscosity increases, resistance decreases as radius increases. Increase in transmitter release on alpha receptor causes vasoconstriction and decrease in frequency of transmitter release causes vasodilation. No just contraction via gpcr pathway: thin actin filaments, thick myosin filaments. Intermediate filaments: roc channel, vdcc channel, ryr channel on sr, serca atpase on sr, na/ca2+ exchanger, mhc atpase activity, mlc1 essential light chain, mlc2 regulatory light chain.
