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arterioles
resistance vessels
radius can be adjusted independently to
distribute cardiac output among systemic organs
help regulate arterial blood pressure
local chemicals influence of arteriola radius: intrinsic
metabolic control mechanism matches blood flow to local tissue needs
histamine release: injured organs, allergic reactions
vasodilation causes inflammatory response
active hyperemia
high metabolism → vasodilation
decreased O2
increased CO2
decreased pH
increased K+
endothelium
paracrine regulators promote vasodilation (vasoactive mediator)
nitric oxide (NO) sets resting “tone” of vessels
vasodilator drugs: nitroglycerin or viagra
endothelin 1: vasoconstrictor produced by endothelium
local physical influences on arteriolar radius
local application of heat or cold
shear stress: blood flow causes friction on endothelial lining. Cells release NO
myogenic response to stretch
vasoconstriction when stretched
vasodilation when not stretched
reactive hyperemia
autoregulation
Reactive hyperemia
bloackage (occlusion causes less blood flow → less stretch → dilation
causes a buildup of metabolites → dilation
autoregulation
MAP decreases → blood flow decreases → dilation
MAP increases → blood flow increases → constriction
both exacerbate (make worth) pressure problem, however
Extrinsic Regulation of blood flow at arterioles
ANS, Endocrine
Sympathoadrenal activation: increased CO and total peripheral resistance
blood flow to viscera is decreased
blood flow to skeletal muscles in increased
blood is shunted away from viscera and skin toward muscles
Capillaries
thin-walled, small-radius, extensively branched
sites of exchange
maximized surface area; minimized diffusion distance
velocity of blood flow through capillaries relatively slow
2 types of passive exchanges
diffusion
bulk flow