 This video will cover the following objective from cardiovascular physiology part 2, blood vessels, discuss the factors that affect blood flow, and how they relate to blood pressure and resistance, distinguish between intrinsic and extrinsic controls of arterial diameter. The heart functions as a pump driving blood flow through the blood vessels. As the heart beats with each contraction, the blood forced into the arteries causes an increase in the blood pressure inside of the arteries. Then blood flows from an area of high pressure to low pressure from the elastic arteries into muscular arteries, then into arterioles and capillaries, then from the capillaries blood continues flowing into lower pressured veins, then drain into the atria of the heart where the pressure is the lowest. And so blood pressure drives the flow of blood, blood flows from areas of high pressure to low pressure. Pussy's equation describes the rate of blood flow as a function of change in pressure, radius, viscosity, and blood vessel length. So we can see the equation here, blood flow equals pi delta P r to the fourth divided by 8 eta lambda. Pi is just a constant 3.14. Delta P is the change in pressure between two points in a blood vessel. So it could be the two ends of a blood vessel. What is the change in pressure? Between those two ends of a blood vessel and since pressure is the force driving blood flow, increasing pressure will increase blood flow. Now r stands for the radius, which is one half of the diameter of the vessel. And notice that in this equation, radius is raised to the fourth power. So a small increase in the radius of a blood vessel can create a large increase in the rate of blood flow. Now in the denominator of the equation, we can see 8 is just a constant and the Greek letter eta represents the viscosity of blood. If the blood is thicker, if there are more cells and less liquid that the cells are suspended in, or more protein relative to the amount of liquid that it's suspended in, this would create thicker blood that flows more slowly through the vessel. So increasing viscosity decreases the rate of flow. And similarly, we see the Greek letter lambda representing the length of a blood vessel is in the denominator of the equation. So increasing the length of the blood vessel would lead to a decrease in the rate of blood flow. So another equation that describes flow is Ohm's law. Ohm's law states that blood flow is equal to the change in pressure divided by the resistance. And so resistance is the opposition to blood flow, whereas pressure is what drives blood flow resistance opposes blood flow. And resistance results from the friction of the blood vessel wall against the blood as it flows through. So we can also convert Ohm's law into the equation. Cardiac output equals mean arterial pressure divided by total peripheral resistance. Where the cardiac output is the volume of blood pumped out of the heart per unit time. So milliliters of blood pumped into the arteries per minute. And the mean arterial pressure is essentially the force that's driving the blood flow. The mean arterial pressure is much higher in the arteries than the veins. And so it's roughly the entire value of the change in pressure and the majority of the resistance is what we call the total peripheral resistance. So we can calculate the total peripheral resistance if we know the cardiac output and the mean arterial pressure. And so we can rearrange this equation if we multiply both sides by the resistance and then divide both sides by the blood flow. We can calculate that resistance equals the change in pressure divided by blood flow. And then if we substitute Poise's equation for blood flow into that, we'll have change in pressure on the numerator and denominator. And those will cancel out. Leaving us with resistance equals 8 eta lambda divided by pi r raised to the fourth power. Now this equation allows us to see how these variables influence resistance. If viscosity or the length of the blood vessels increased, that would cause an increase in resistance. In contrast, if the radius were to increase, that would cause a decrease in resistance. And because radius is raised to the fourth power, we could see that a very small increase in resist, very small increase in radius, would create a large decrease in the resistance. And so I want you to think about what of those variables, which of those variables would change in the body under what circumstances? Which of these variables would we expect to be changing rapidly and be regulated by the nervous system? And so the length of the blood vessels in the body doesn't normally change very quickly. As we grow, the length of the blood vessels becomes longer, but that takes a long time. So it's not a variable that changes a rapidly under control of the nervous system. Similarly, the viscosity of blood doesn't normally change rapidly, although if we have, if we're dehydrated, for example, we could have a higher viscosity of blood. And then if we drink some water and dilute the blood a little, that could decrease the viscosity of the blood. But what is being regulated rapidly by the nervous system in order to regulate resistance is the radius of our blood vessels or the diameter of the blood vessels. The smooth muscle in the wall of the blood vessel can contract in order to decrease the radius, which leads to an increase in resistance. And this is the primary way that the blood vessels are able to contribute to regulation of blood flow and blood pressure. The graph in the top left here shows us the vessel diameter as we move through the blood vessels from the elastic arteries that have a large diameter into smaller muscular arteries and arterioles, these small vessels that are the capillaries, then as blood flows into the venules and veins, the diameter increases until we reach the largest diameter vessels, the large vein, the vena cava, the superior and inferior vena cava, which have the largest diameter of all the blood vessels in the body. The cross-sectional area is shown on the graph in the top right here. So we can see that maybe at first, surprisingly, there's a much larger cross-sectional area. If we take the total cross-sectional area of all of the capillaries in the body and add that together, it's much more than the cross-sectional area of any of the other vessels. So even though capillaries have a very small diameter individually, there are so many capillaries that if we add it all up, it's a much larger total cross-sectional area of capillaries than there are of arteries or veins. And of course, this is because when an artery branches, it branches into two arteries that are only slightly smaller than the artery that supplies both of the branches, and so every time a blood vessel is branching into smaller and smaller vessels, we're getting an increased total cross-sectional area of the vessels. The bottom left shows us a graph of the blood pressure as it falls from the elastic arteries to the veins. The blood pressure drops as blood is flowing through the vessels, but we see that the steepest decline in the blood pressure is in the arterioles. And this is because the arterioles have a small diameter relative to the amount of high-pressure blood that is flowing through them. The arterioles provide the greatest resistance to blood flow and therefore the blood pressure decreases most dramatically as the blood is flowing through the arterioles. Now in the bottom right, the graph shows us the velocity of blood flow through each of the vessels, and we can see that the blood is flowing most rapidly through the arteries as we would expect. Bloods flowing quickly through elastic arteries and a little slower in the muscular arteries and then slows down dramatically as the blood flows into the arterioles. And then blood flows most slowly through the capillaries as we have that very large cross-sectional area allowing the blood to flow very slowly through the numerous capillaries allowing a large amount of time for exchange. Then as blood flows into the larger diameter veins, blood flow starts to increase as a result of the low resistance of the large veins. Regulation of the diameter of blood vessels is the primary way that blood vessels can regulate blood flow and blood pressure. When the smooth muscle in the wall of a blood vessel contracts, this is called vasoconstriction and vasoconstriction leads to an increased resistance and decreased flow rate through a vessel. In contrast, vasodilation is when the vascular smooth muscle relaxes, leading to an increased diameter, decreasing resistance and increasing flow. The vascular smooth muscle is regulated through both intrinsic and extrinsic control mechanisms. One intrinsic control mechanism is known as myogenic activity occurs when the blood vessel is stretched and that stretching stimulates contraction of the smooth muscle. Therefore, if a blood vessel has a low flow rate, the smooth muscle will be stretched less and that will allow the smooth muscle to relax thereby increasing the diameter and increasing the flow rate through that vessel. So this is a homeostatic mechanism that helps to maintain a stable flow rate and a stable pressure inside of the vessel. Another intrinsic control mechanism that regulates vascular smooth muscle locally is a response to metabolic activity when blood oxygen level is low, which is also known as hypoxia and when blood carbon dioxide concentration is high, which is also known as hypercapnia, this stimulates the vascular smooth muscle to relax, allowing the blood vessels to vasodilate, increasing blood flow, carrying away metabolic waste and carrying in nutrients to support metabolic activity. This figure summarizes the intrinsic control mechanisms regulating blood flow, the auto-regulation or local intrinsic regulation mechanisms where local receptors within the blood vessel detect metabolic activity or stretching and while a high metabolic activity would be one of the things that would stimulate vasodilation as receptors detect decreasing oxygen levels and increasing carbon dioxide levels. Other stimuli include metabolic acids like lactic acid, another vasodilator that can be increasing levels during high metabolic activity is nitric oxide, and the increasing levels of potassium in the blood, which can result as potassium is flowing out of cells that are excitable cells like skeletal muscle cells, one they're contracting, in order to have repolarization in the action potential, potassium flows out of the cells, but as that potassium is accumulating outside of the cells, that's another thing that will stimulate vasodilation to help increase blood flow through that metabolically active tissue, increase in hydrogen ion concentration, a low pH in a tissue is a thing that stimulates vasodilation in order to help carry away the excess hydrogen ions, and as we study the lymphatic and immune system as we study the functions of the immune system in defending against infection, we'll see the process of inflammation involves stimulating vasodilation, which increases blood flow through the tissue in order to help leukocytes move into that tissue and defend against infection. Another thing that will stimulate and increase blood flow through a tissue is rising body temperature will cause vasodilation of the blood vessels in the skin in order to help with the homeostatic control of our body temperature, so in contrast the mechanisms that stimulate contraction of the vascular smooth muscle include the myogenic mechanism where stretching stimulates contraction, but receptors also detect local chemical signals such as prostaglandins, which are released when leukocytes become activated during an inflammatory response to help defend against infection, and also when blood vessels are damaged, there are vasoconstricting messages released, paracrine signals released from the endothelial cells, which are known as endothelins, which will stimulate vasoconstriction in order to help reduce bleeding, and when the platelets are exposed to the damaged blood vessel wall, platelets will also release signals that stimulate vasoconstriction in order to help with the mechanism of hemostasis to prevent bleeding. The vascular smooth muscle is also regulated by extrinsic control mechanisms. One of the major extrinsic control mechanisms that stimulates vasoconstriction is the sympathetic nervous system releasing the neurotransmitter norepinephrine and stimulating the adrenal gland to release the hormone epinephrine. Norepinephrine and epinephrine then bind to alpha-adrenergic receptors on the surface of vascular smooth muscle cells, stimulating retraction, leading to vasoconstriction, increasing resistance and decreasing flow. And this is a mechanism that will help to increase the blood pressure as arterioles constrict all through the body, it will stimulate an increase in the blood pressure, and this is used as a mechanism to help maintain a homeostatic. Stable, mean arterial pressure in the arteries.