Review Note

Last Update: 11/10/2024 07:52 PM

Current Deck: Geneeskunde::3e bachelor::long & hart::ZSO 33 Microcirculatie

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Question
Flow-mediated dilation of the brachial artery is impaired in patients with chronic hypercholesterolemia, primary hypertension, or atherosclerosis compared to that seen in normal healthy adults. The primary mechanism responsible for this impaired dilation in such patients is:
Title
QType (0=kprim,1=mc,2=sc)
2
Q_1
increased sensitivity of brachial artery smooth muscle to CO2.
Q_2
loss of beta-adrenergic receptors in brachial artery smooth muscle.
Q_3
decreased responsiveness of the brachial artery to acetylcholine.
Q_4
decreased shear stress–induced NO production in the brachial artery.
Q_5
idc
Answers
0 0 0 1 0
Sources
the point
Extra 1
Rationale: Flow-mediated dilation of the brachial artery is caused by high shear stress on vascular endothelium whenever blood flow velocity is high. The high shear stress causes the release of NO by the arterial endothelium, which causes relaxation of the underlying arterial smooth muscle. High flow velocities occur in the brachial artery during a reactive hyperemic response, such as that used to produce flow-mediated vasodilation in a clinical determination. Hypercholesterolemia, high blood pressure, and atherosclerosis either impair the ability of the endothelium to make NO (hypertension) or reduce its bioavailability (atherosclerosis). As a result, flow-mediated dilation is impaired in these disease states. Beta-adrenergic receptors do not mediate flow-mediated arterial dilation. Alteration of vascular smooth muscle sensitivity to CO2 is similarly not involved in flow-mediated dilation nor is it known to be altered in hypertension, atherosclerosis, or hypercholesterolemia. Endothelium-dependent dilation in response to acetylcholine would be expected to be diminished in the brachial artery in the aforementioned cardiovascular diseases, in species where acetylcholine is a primary vasodilator, but flow-mediated dilation does not involve cholinergic receptors. Reactive oxygen species production in arteries is increased in hypertension, hypercholesterolemia, and atherosclerosis.

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