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MCB 32, FALL 2000 REGULATION OF ARTERIAL BLOOD PRESSURE Reading: Chapters 8 and 9. I. Pressures and flows in the cardiovascular system Systolic pressure is the highest pressure during any one beat of the heart, while diastolic pressure is lowest pressure. Pressure gradients within the CV system: Periodic high pressure in ventricles is dissipated as blood circulates back to the veins and atria, which have only very low pressure, nearly zero. Thus, the energy of contraction of the ventricles (expressed as a pressure) has been nearly entirely dissipated as the blood has cirulated from the left ventricle through the systemic circulation back to the right atrium. Similarly, though the pressures in the pulmonary circulation are much lower than in the systemic circulation, this pressure energy is nearly entirely dissipated as it circulates through the pulmonary circulation back to the left atrium. Note also oxygen conc. changes abruptly at systemic and lung capillaries, where exchange of oxygen and carbon dioxide occurs. Note high pressures in systemic arteries and arterioles and low pressures in veins. Pulmonary circulation pressures in general are all lower than systemic circulation. Smooth blood flow is silent (laminar). Flow is proportional to the pressure gradient (e.g., between points one and two) and inversely proportional to resistance of vessel between these two points: F = (P1-P2)/R Resistance to blood flow is determined primarily by the size of the vessel, which is controlled by contraction and relaxation of blood vessel smooth muscle; larger vessel, smaller resistance and vice versa. Resistance is inversely proportional to radius to 4th power. See Figs 9.13 and 9.14. Resistance to blood flow is larger in smaller vessels. The overall resistance of the circulatory system is determined primarily by the resistance of the arterioles, even though the capillaries are much smaller at the level of each individual vessel. The low resistance of the capillaries is due to the fact that there are so many of them compared to the number of arterioles. Thus, regulation of resistance to blood flow is controlled by controlling the arteriolar resistance. People with abnormally high resistances in their arterioles often have high blood pressure. Since blood pressure averages about 100 mm Hg in the aorta and large arteries, while it is about zero in the vena cava and right atrium, the above equation is often substituted as follows: blood flow = cardiac output = 5 liters/min P1 = arterial pressure = 100 mm Hg P2 = venous pressure = 0 mm Hg R = peripheral resistance and cardiac output = CO (5 liters/min) = (Part– Pven )/PR = Part/PR Volume of blood is not distributed equally through the CV system: small amounts in heart, arteries and capillaries, large amount in veins. Small amount in lung blood vessels too. II. Control of blood flow at the local tissue level Blood flow to individual tissues can be controlled by contraction or relaxation of smooth muscles surrounding the arterioles and also around the entries to capillary beds, the pre-capillary sphincters. These smooth muscles are controlled by factors released from the tissues surrounding them. When the cells in the tissues alter their metabolic activities, they release altered amounts of the metabolic factors, which diffuse over to the smooth muscles to control their contraction and, thus, the flow of blood through the vessels. For example, during exercise, muscle metabolism increases production of lactic acid, CO2 and AMP (break down from ATP), and these diffuse from the cells to the smooth muscles of the arterioles and precapillary sphincters, causing them to relax and dilate, increasing blood flow through them. This automatically increases blood flow to a metabolically active tissue. This is called exercise hyperemia. Another example occurs during the increased blood flow following an ischemic episode (i.e., decreased blood flow). This is called reactive hyperemia and is described in the textbook on page 253. III. Negative feedback regulation of blood pressure, example of homeostasis Arterial blood pressure must be maintained at the proper level to insure blood flows properly, but it cannot get too high or there is damage to the blood vessels, leading to atherosclerosis, hardening of the arteries. Regulation occurs by negative feedback, which refers to the situation in which a change in some controlled variable (e.g., decrease in blood pressure) leads to a series of changes that results in the opposite change in the controlled variable back to its control level. This maintenance of a steady state is called homeostasis. IV. Mechanisms for controlling blood pressure Figs 9.18 and 9.19 All of the following are important for controlling arterial blood pressure: Blood volume needs to be maintained. Normal value is 5 liters. This can be decreased by about 1 liter without much effect (most of it comes from the veins, where there is little effect on pressure), but loss of too much blood will lead to a drop in blood pressure. Arteriolar constriction and relaxation are also important. Increased constriction of arterioles leads to increases in pressure due to increased peripheral resistance, while decreased constriction leads to drops in pressure due to decreased peripheral resistance. Heart rate and stroke volume, which in turn are regulated by autonomic nerves and venous return, are also important. Increased heart rate and stroke volume lead to increases in blood pressure. V. Pressure sensors: baroreceptors The body has a variety of pressure receptors for sensing arterial and venous pressures. All of them are pressure receptors that respond to changes in stretch of the vessel they are located in by sending action potentials to the central nervous system. More pressure, more stretch of the vessel, more action potentials sent to the CNS, informing the system of the state of the arterial blood pressure. The most prominent and important baroreceptors are located in the walls of the arch of the aorta and in the carotid sinus; also in heart. VI. Control center: medulla oblongata The baroreceptors send impulses to the medulla oblongata, which integrates the information and then sends out the appropriate responses. When pressure has decreased, sympathetic nerves are triggered, which then send out action potentials to the heart and the blood vessels. In the heart, sympathetic nerves release norepinephrine increase rate of depolarization increase frequency of AP in SA node, which increases rate and strength of contraction. Sympathetic nerves to the smooth muscles in the blood vessels causes them to contract more strongly, leading to increased resistance, which elicits increases in blood pressure to counteract the original decrease in pressure. When pressure increases, parasympathetic nerves are triggered. Parasympathetic nerves release acetylcholine decrease rate of depolarization reduce frequency of AP in SA node, leading to reduction in cardiac output and decrease in blood pressure. There is also a reduction in the sympathetic effects on the blood vessels, which can cause them arteriolar smooth muscle to relax, also leading to reductions in blood pressure. VII. Control of cardiac output CO (liters/min) = stroke volume (ml/beat) x heart rate (beats/min) Normal human CO = 5 l/min = 72 ml/beat x 70 beats/min Control by changing heart rate (sympathetic increase, parasympathetic decrease) and stroke volume. Stroke volume is changed by altering contractility of heart muscle, usually increased by sympathetic nerves. This increases amount of force generated by the myosin and actin, often through changes in cell [Ca]. Stroke vol also changed by alterations of size of heart. with increases in venous return leading to increases in contractility of the heart. VII. Integrated activity: hemorrhage Fig. 9.19