autoregulation of blood flow
Q1: Define the autoregulation of blood flow.
A1:
Intrinsic ability of an organ to maintain constant blood flow
Despite changes in perfusion pressure
Can be short term or long term
Q2: What is myogenic tone?
A2:
Vascular smooth muscle contracts when stretched
Sudden arterial pressure increase → Arterioles stretch and smooth muscle contracts
Results in vasoconstriction to maintain constant blood flow
Known as Bayliss Effect
Q3: Name two types of mediators released by the endothelium and their effects.
A3:
Vasoconstrictor: Endothelin
Vasodilator: NO, prostacyclins
Biosynthesis and Actions of Nitric Oxide
Q4: What is the substrate and enzyme involved in nitric oxide biosynthesis?
A4:
Substrate: L-Arginine
Enzyme: Endothelial Nitric Oxide Synthase (eNOS)
Q5: Describe the reaction catalyzed by eNOS.
A5:
eNOS converts L-arginine to nitric oxide (NO) and L-citrulline
Requires oxygen (O₂) and NADPH
Q6: How does nitric oxide diffuse and where does it go?
A6:
NO diffuses from endothelial cells
Moves to nearby vascular smooth muscle cells
Q7: What enzyme does nitric oxide activate in vascular smooth muscle cells?
A7:
Guanylyl cyclase
Q8: What is the result of guanylyl cyclase activation?
A8:
Converts GTP to cGMP (cyclic guanosine monophosphate)
Q9: How does cGMP affect vascular smooth muscle?
A9:
Triggers events leading to smooth muscle relaxation
Activates PKG
PKG phosphorylates target proteins
Decreases intracellular calcium levels
Reduces sensitivity of contractile proteins to calcium
Q10: What is the overall effect of nitric oxide on blood vessels?
A10:
Causes vasodilation
Decreases vascular resistance
Increases blood flow
Mechanisms of Hyperemia
Q11: What is active hyperemia?
A11:
Increased metabolic activity of a tissue
Produces vasodilators
High metabolic activity, high PCO2, low PO2, low pH induce vasodilator release
Increases blood flow
Q12: What is adenosine's role in vasodilation?
A12:
Breakdown product of ATP
Causes vasodilation
Q13: Define reactive hyperemia.
A13:
Decreased tissue blood flow due to occlusion
Release of metabolic vasodilators
Q14: Define inflammatory hyperemia and name some mediators.
A14:
Active process from increased arterial blood inflow
Due to inflammatory mediators
Mediators include histamine, bradykinin, prostanoids, neuropeptides
Triple Response of the Skin
Q15: Describe the first component of the triple response of the skin.
A15:
Red Line
Caused by vasodilation from histamine release
Q16: Describe the second component of the triple response of the skin.
A16:
Flare
Mediated by the axon reflex
Injury stimulates sensory nerve endings
Nerve endings release neuropeptides (substance P, CGRP)
Causes vasodilation in surrounding area
Q17: What is neurogenic inflammation?
A17:
Inflammation mediated by nerve-induced release of neuropeptides
Leads to vasodilation and redness spreading from the initial injury site
Q18: Describe the third component of the triple response of the skin.
A18:
Wheal
Localized swelling (edema)
Increased capillary and venule permeability
Fluid leakage into surrounding tissue
Caused by histamine and other inflammatory mediators