HK 3810 Package 1 notes.docx

Resistance is a function of length and number of

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Resistance is a function of length and number of vessels, viscosity, and vessel radius o Radius can be changed form msec/sec/min timescale to alter flow and resistance; it is a powerful regulator bc its effect is to the 4 th power o Length, number of vessels – vessel growth can take days/weeks
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HK 3810 Package 1 o Viscosity – a function of %RBCs (haematocrit, Hct) present in blood; can be changed in hours/days o Resistance is proportional to 1/r 4 , messing with radius is changing/controlling vascular smooth muscle contractile state Regulation of arteriolar radius Neural influences o All blood vessels are innervated by SNS, except capillaries (bc it doesn’t have smooth muscle, so no innervation) o Arteries are more innervated than veins (more sympathetic control in terms of impact of SNS) o Influences of SNS is not equally distributed o Vasoconstriction powerful on skin, gut, kidney, and less powerful in brain, skeletal muscle o Branches of the SNS cause vasodilation o Neural innervation increases Ca2+ Autocrine o Vascular smooth muscle cells can produce products that can affect themselves o Nitric oxide is released and diffuses back into the vascular smooth muscle to affect cGMP which is the second messenger decrease Ca2+ Paracrine o From cells of the tissue Release vasoactive compounds from surrounding tissue cells Working tissue will release products to influence blood vessel diameter Increase metabolism increase ADO decrease Ca2+ vasodilation Metabolic vasodilators: increase CO2, decrease O2, increase ADO, K+, increase Pi, H+ o From endothelial cells ECs are a rich source of vasoactive compounds Blood environment can stimulate ECs, BK shows up in the blood to stimulate ECs RBCs cause shear across ECs to release products Products released are (blood Q) prostaglandins, endothelin, NO Endocrine o SNS can stimulate the adrenal glands to release EPI/NE into bloodstream attach to membrane receptor population on VSM cells o Depending on membrane receptor a = constrict B = vasodilation o Not good to vasoconstrict arterioles of the heart or lungs o For no response, decorate cell with: No membrane receptor population Equal number of a and B membrane receptors o A II and ADH-VP are bloodborne vasoconstrictors, ANP is a vasodilator
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HK 3810 Package 1 Autoregulation o Intrinsic control of radius o Range of pressures where the vascular adjusts resistance to keep Q constant o When P1 increases resistance increased radius decreases to keep Q constant o Myogenic response stretch of smooth muscle results in contraction of smooth muscle Physical factors o Transmural pressure (PT) o Different between luminal pressure and tissue pressure (environmental pressure) o If P1 = P2 then diameter is constant o During systole, flow to the heart decreases due to an increase in tissue pressure during contraction o During diastole, there is an overshoot where flow increases; “reactive hyperaemia”
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