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Vasoactive substances are produced by endothelial cells
Released under normal conditions in response to ACh or sheer stress of blood flow
Utilizes a cGMP mechanism
Released from endothelial cells in response to hypoxia, ACh, sheer stress
Utilizes a cAMP mechanism
Endothelium-derived hyperpolarizing factor
Does NOT involve a cGMP or cAMP mechanism
Stimulated by Ang II, EPI, sheer stress of blood flow
Normally there is a balance between these factors, where the vasodilators predominate. In sick endothelium, the balance can be shifted towards the constrictors.
Recall both beta 2 and alpha receptors are on the coronary vessels
Beta 2 dilates, and alphas constrict.
The way all these factors work together determines the net coronary tone.
OXYGEN DEMAND DEPENDS ON
ventricular wall stress: increased wall stress increases O2 needs
definition: tangential force acting on the myocardial fibers tending to pull them apart; energy is needed to oppose that force.
Wall stress = intraventricular pressure (P) times the radius of the vent. (r) divided by 2 times the vent. wall thickness (h).
Wall stress = P x r / (2h)
Wall stress is increased with more LV filling (mitral or aortic regurg)
Wall stress also increases with increased systolic pressure in the LV (aortic stenosis or HTN)
Increased thickness of the vent. wall will decrease wall stress (hypertrophy)
increasing HR consumes more ATP and O2 requirement increases
increasing force of contraction increases O2 utilization