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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 ]
In the kidney, the macula densa is an area of closely packed specialized cells lining the wall of the distal tubule where it touches the glomerulus.Specifically, the macula densa is found in the terminal portion of the distal straight tubule (thick ascending limb of the loop of Henle), after which the distal convoluted tubule begins.
Prostaglandins are powerful, locally-acting vasodilators and inhibit the aggregation of blood platelets. Through their role in vasodilation, prostaglandins are also involved in inflammation . They are synthesized in the walls of blood vessels and serve the physiological function of preventing needless clot formation, as well as regulating the ...
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Vasodilation and vasoconstriction are complex phenomena; they are functions not merely of the fluid mechanics of pressure and tissue elasticity but also of active homeostatic regulation with hormones and cell signaling, in which the body produces endogenous vasodilators and vasoconstrictors to modify its vessels' compliance.
Vasodilation and vasoconstriction are also used antagonistically as methods of thermoregulation. [23] The size of blood vessels is different for each of them. It ranges from a diameter of about 30–25 millimeters for the aorta [24] to only about 5 micrometers (0,005 mm) for the capillaries. [25]
Diagram of the circulatory system. SVC/IVC - Superior/Inferior vena cava. The heart is the driver of the circulatory system, pumping blood through rhythmic contraction and relaxation. The rate of blood flow out of the heart (often expressed in L/min) is known as the cardiac output (CO).
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 ...