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It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles. [2] Blood vessel walls are composed of endothelial tissue and a basal membrane lining the lumen of the vessel, concentric smooth muscle layers on top of endothelial tissue, and an adventitia over ...
When blood pressure is increased in the blood vessels and the blood vessels distend, they react with a constriction; this is the Bayliss effect. Stretch of the muscle membrane opens a stretch-activated ion channel. The cells then become depolarized and this results in a Ca 2+ signal and triggers muscle contraction. No action potential is ...
Regardless of the subtype, the result of hyperemia is an increase in blood flow to the affected skeletal muscle. [4] Active hyperemia is one subtype, which occurs in response to increased metabolic demand, meaning high oxygen requirements within the tissue. It follows the principle of metabolic control, with the release of vasodilatory ...
An arteriole is a small-diameter blood vessel in the microcirculation that extends and branches out from an artery and leads to capillaries. [1] Arterioles have muscular walls (usually only one to two layers of smooth muscle cells) and are the primary site of vascular resistance. The greatest change in blood pressure and velocity of blood flow ...
Generalized vasoconstriction usually results in an increase in systemic blood pressure, but it may also occur in specific tissues, causing a localized reduction in blood flow. The extent of vasoconstriction may be slight or severe depending on the substance or circumstance. Many vasoconstrictors also cause pupil dilation.
The main endogenous agonist of these cell receptors is norepinephrine (NE). The adrenergic receptors exert opposite physiologic effects in the vascular smooth muscle under activation: alpha-1 receptors. Under NE binding alpha-1 receptors cause vasoconstriction (contraction of the vascular smooth muscle cells decreasing the diameter of the ...
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 ...
The cells of the macula densa are taller and have more prominent nuclei than surrounding cells of the distal straight tubule (cortical thick ascending limb).. The close proximity and prominence of the nuclei cause this segment of the distal tubule wall to appear darker in microscopic preparations, [5] hence the name macula densa.