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Normal blood vessel (left) vs. vasodilation (right) Vasodilation, also known as vasorelaxation, is the widening of blood vessels. [1] It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles. [2]
The pressure drop of the arterioles is the product of flow rate and resistance: ∆P=Q xresistance. The high resistance observed in the arterioles, which factor largely in the ∆P is a result of a smaller radius of about 30 μm. [24] The smaller the radius of a tube, the larger the resistance to fluid flow.
The muscle tension in the afferent arteriole is modified based on the difference between the sensed concentration and a target concentration. [5] Vasodilation of the afferent arteriole, which results in increased glomerular filtration pressure and tubular fluid flow, occurs when MD cells detect a chloride concentration that is below a target value.
The myogenic mechanism is how arteries and arterioles react to an increase or decrease of blood pressure to keep the blood flow constant within the blood vessel.Myogenic response refers to a contraction initiated by the myocyte itself instead of an outside occurrence or stimulus such as nerve innervation.
Vascular resistance occurs when the vessels away from the heart oppose the flow of blood. Resistance is an accumulation of three different factors: blood viscosity, blood vessel length and vessel radius. [30] Blood viscosity is the thickness of the blood and its resistance to flow as a result of the different components of the blood.
First, metabolites that are produced by active muscle use can alter skeletal muscle tone. Second, skeletal muscle can undergo hyperemia, which is a mechanism of local blood flow regulation with two major subtypes. Regardless of the subtype, the result of hyperemia is an increase in blood flow to the affected skeletal muscle. [4]
When renal blood flow is reduced (indicating hypotension) or there is a decrease in sodium or chloride ion concentration, the macula densa of the distal tubule releases prostaglandins (mainly PGI2 and PGE2) and nitric oxide, which cause the juxtaglomerular cells lining the afferent arterioles to release renin, activating the renin–angiotensin–aldosterone system, to increase blood pressure ...
Flow-mediated dilation (FMD) refers to dilation (widening) of an artery when blood flow increases in that artery. [1] [2] The primary cause of FMD is release of nitric oxide by endothelial cells. [1] To determine FMD, brachial artery dilation following a transient period of forearm ischemia is measured using ultrasound. [3]