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2 main sources of arteriolar tone
- natural properties of arteriole wall: elasticity of smooth muscle surrounding arterioles
- baseline sympathetic activity: resting activity
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intrinsic control of vasoconstriction/dilation
chemical changes: histamine, local metabolic changes
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sensors for vasodilation
within the endothelium, sense local changes in tissue and release nitric oxide which acts on smooth muscle to cause relaxation
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sensors for vasoconstriction
also in the endothelium, releases endothelin which reduces blood flow by constricting smooth muscle around the arterioles
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meta-arterioles
- larger vessels in the capillary beds that allow for more rapid transport
- only use when tissue doesn't need high level of perfusion
- use pre-capillary sphincters to open/close routes
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precapillary sphincters
- bands of smooth muscle that sit at gates between meta-arterioles and capillary beds
- can constrict and keep blood only in the meta-arterioles
- local controls only- levels of O2, CO2, free adenosine, acidity, temperature
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cardiac suction
ventricles contract, atrial volume increases and causes negative pressure that promotes movement of blood from veins into atria
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short term BP regulation
- use baroreceptors in aortic arch and carotid sinus- they sense stretch in vessels from increase in BP
- sense change and can make changes but if it lasts more than 4 minutes, they will adapt
- adjust baseline para and symp nerve stimulation to adjust MAP and BP
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extrinsic control of arteriolar diameter
- neuronal or hormonal control
- sympathetic stimulation ( no para) to smooth muscle
- release of norepinephrine that binds to alpha-1 or beta-2 receptors
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effects of epinephrine on arteriolar diameter
- binds to beta-2 receptor and causes vasodilation
- decreased sympathetic stimulation
- decreases TPR and BP
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effects of norepinephrine on arteriolar diameter
- binds to alpha-1 receptor and causes vasoconstriction
- increased sympathetic stimulation
- increases TPR and BP
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