Pressure and Flow Control Flashcards
Primary source of nitric oxide
endothelium
Intrinsic Mechanism
Local control
Often does not affect systemic blood pressure; only affects local mechs
Autoregulation - tissues can control their own blood flow to meet their metabolic needs
Extrinsic Control
Autonomic NS and circulating hormones regulate BP
Essential driving force for blood flow and redistribution
Mechanisms involved in autoregulation (keeping flow constant)
- Myogenic - smooth muscle
- Metabolic
- Paracrine - substances released locally
How does flow stay constant
Changing resistance
MEtabolic Autoregulation
Matching flow with tissue metabolic activity
Metabolites = local vasodilation
Inc them, inc blood flow to wash out the metabolites
Then blood flow will decrease until metabolites accumulate again
Hyperemia
Increase in flow
- Active - dilation in response to inc metabolic activity (exercise)
- Reactive - increase in accumulation of vasodilator metabolites due to occlusion (happens every single beat - BP cuff)
Myogenic Autoregulation
Inc transmural pressure causes smooth muscle vasoconstriction
Activation of stretch will activate the stretch activated channels on the VSM
This induces depolarization and Ca influx
Decrease in transmural pressure would cause smooth muscle ____
dilation
Inc in arterial and transmural pressure —>
Stretch of smooth muscle –> contraction of the muscle –> arteriolar constriction –> dec in blood flow
Paracrine Mechanism - major dilators
Nitric Oxide
Prostacyclin
EDHF
Paracrine Mechanism - major constrictors
Angiotensin II
Thromboxane A2
Endothelium
Metabolic - dilate or constrict
Vasodilator
metabolites
Myogenic Control - dilate or constrict
Can do either
Depends on the stress
Inc pressure = constrict
Dec pressure = dilate
Paracrine - shear stress will cause
NO release from endothelium
Paracrine Dilators
Relax
- NO
- Prostacyclin
- EDHF
Paracrine Relaxer - NO
Ach stimulates NO release
NO is produced from reaction with L-Arg (amino acid) and NOS (nitric oxide synthase - synthesizes NO)
NO then uses cGMP to produce relaxation
Paracrine Relaxer - Prostacyclin
From arachadonic acid
Inc cAMP to cause relaxation
Paracrine Relaxer - EDHF
Endothelium derived hyperpolarized factor
Takes membrane potential further away from potential by allowing K to leave the cell and therefore relax
What happens prior to symptoms of cardiovascular disease
Endothelial dysfunction
Key underlying Mechanisms - Endothelial Dysfunction
- Arginase also competes for L arg (like NO)
if arg is elevated will produce less NO - Could have less L-Arg around - so less NO
- Missing BH4 - get superoxide - free radical - oxidative stress
- Elevation of Rho Kinase - leads to dec in NO by inhibiting myosn light chain phosphokinase and keeps myosin in contracted state
Risk factors for cardiovascular disease
Hypertension Hypercholesterolemia Diabetes Mellitus Aging Obesity Smoking Meopause