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Regulation of Arterial Blood Pressure 1 George D Regulation of Arterial Blood Pressure 1 George D. Ford, Ph.D. OBJECTIVES: 1. State why it is important to maintain arterial pressure at its normal value. 2. Name the 8 blocks which make up the renal-body fluid blood pressure regulating system; show how they are coupled together; and describe the function of each block. 3. Define the following abbreviations: Q or CO, Pa, E, Pms, TPR, dEo/dt, dEi/dt, dE/dt. 4. Describe how changes in renal function (increase or decrease) affect: E, Pms, Q, and Pa. 5. Describe the anatomical connections in the arterial baroreceptor reflex. 6. Describe how pressure is transduced by baroreceptors. 7. Describe how the information generated by baroreceptors is processed by the central nervous system. 8. Describe the cardiopulmonary baroreflexes. I. OVERVIEW There are three levels of regulation, neural, humoral, and intrinsic. The latter is often referred to volume regulation in most textbooks. They operate in very distinct time frames. Traditionally, they are covered in the order listed above, but these two lectures will reverse that order. II. (MEAN) ARTERIAL PRESSURE IS THE PRODUCT OF CARDIAC OUTPUT AND TOTAL PERIPHERAL RESISTANCE. Pa = C.O. x TPR In this equation Pa = arterial pressure (mm Hg), C.O. = cardiac output (liter/min), and TPR total peripheral resistance (mm Hg x min/liters). This seductively simple equation may be one of the most dangerous equations in cardiovascular physiology because C.O. and TPR are not, as suggested by the equation, independent variables. Unfortunately changes in TPR strongly affect C.O. as we have just finished discussing. Changes in C.O. also affect TPR. Thus it cannot be stated that a doubling of TPR will double Pa at the steady state. III. THE INDEPENDENT VARIABLES REGULATING ARTERIAL BLOOD PRESSURE ARE: 1) CONTRACTILITY OF VASCULAR SMOOTH MUSCLE, 2) CONTRACTILITY OF THE HEART, AND 3) RENAL FUNCTION. Regulation of these three independent variables determines arterial blood pressure. The levels at which these variables are regulated are: 1) intrinsic, 2) neurogenic, and 3) hormonal. The regulation of arterial blood pressure will be presented at these three levels and in that order. The intrinsic level is taught first because the neurogenic and hormonal mechanisms operate on top of and regulate components of the intrinsic system. The intrinsic system is often called the Renal Body-fluid system. IV. INTRINSIC REGULATION OF ARTERIAL BLOOD PRESSURE INVOLVES INTERACTIONS BETWEEN: HEART, VASCULAR SYSTEM, AND KIDNEYS. WHEN LINKED TOGETHER THEY BECOME THE BODY FLUID SYSTEM. It is particularly the view of Arthur Guyton and many others that the kidney, heart, and vascular system interact, even in the absence of neural or hormonal control, in such a way that a nearly normal blood pressure can be achieved. These components (heart, kidney, and vascular system) possess intrinsic properties which allow them to adjust blood pressure at a slow rate (days to years). Neural and endocrine factors increase the rate of response markedly (minutes to days). With the neural mechanisms, responses occur after about 10 seconds. In the intrinsic system the kidney, heart and vascular system are coupled in series. Figure 1. Diagram of the intrinsic Renal Body-fluid blood pressure regulating system. For explanation see the following discussion. An explanation of this diagram starts with blocks that are already familiar. A. Block 1. The blood volume-mean systemic pressure relationship. This block shows the relationship between blood volume (Vb) and means system pressure (Pms). Blood volume is one determinant of mean system pressure. The other determinants are the unstressed volume and the capacitance of the stressed volume. B. Block II. The mean system pressure-cardiac output relationship. Mean system pressure anchors the vascular function curve and the intersection of this curve with the cardiac function curve determines cardiac output (Q). The curves shown are for the intrinsic contractility of the heart and vascular system. C. Block III. The cardiac output-total peripheral resistance relationship. The major determinant of total peripheral resistance is the caliber of arterioles. This caliber is determined by the contraction of vascular smooth muscle. The contraction of vascular smooth muscle is subject to influences which can be categorized as: a) intrinsic or b) extrinsic (neural or hormonal). The Intrinsic autoregulation of total peripheral resistance [TPR] is a concept that I hope Dr. Pittman has already discussed with you. The next paragraph is intended only to be a quick review of his more thorough discussion. Arterioles, if completely devoid of neural or hormonal regulation still have the capacity to alter their caliber. The phenomenon thereby produced is termed autoregulation of blood flow. The mechanism(s) responsible are not well established. At least two hypotheses have been proposed and each may play a role. The two hypotheses are: 1) the myogenic hypothesis and 2) the metabolic hypothesis. These hypotheses, in brief, are: 1. The myogenic hypothesis states that arterioles contract in response to pressure induced stretch (tension). This decreases the caliber (radius) of the arteriole and increases resistance to flow. (Recall that Poiseuille's Law states that resistance to flow is inversely related to the fourth power of the radius of the vessel). 2. The metabolic hypothesis states that increases in flow through an arteriole decrease the concentration of metabolically produced vasodilators, in particular nitric oxide (NO). The decreased concentration of vasodilators causes contraction of arteriole smooth muscle. Contraction of the arteriole smooth muscle decreases arteriole caliber and increases resistance to flow (Poiseuille's Law). Note in block III that TPR remains constant until Q reaches a certain value. After that value of Q is reached TPR increases as Q increases. D. Block IV. Pa = CO x TPR This block states that arterial pressure (Pa) is the product of cardiac output (CO) and total peripheral resistance (TPR). E. Block V. The arterial pressure-renal excretion of extracellular fluid (dEo/dt) relationship. (Renal Function Curve) Increases in Pa increase the rate at which extracellular fluid (E) is lost (dEo/dt). Note that dEo/dt is zero until Pa reaches 60 - 80 mm Hg. The kidney does not excrete extracellular fluid per se. Rather, it excretes components of extracellular fluid. The component of most importance is sodium. The regulation of the extracellular fluid volume takes place primarily by the regulation of the sodium content of the body. We are interested in extracellular fluid volume because one compartment of extracellular fluid is blood. Interstitial fluid is the second major compartment. F. Block VI. Net Change in the dE/dt is the sum of inputs and outputs This block states that the algebraic sum of the rate of input of extracellular fluid (dEi/dt) and the rate of loss of extracellular fluid (dEo/dt) determines whether the rate of gain of E, dE/dt, may be positive or negative. The rate of input of extracellular fluid (dEi/dt) is determined by the rate at which sodium and fluid enters the body, i.e., dietary choices. G. Block VII. The volume of the extracellular fluid is the integral (algebraic sum) of all gains and losses of E. H. Block VIII. The blood volume/extracellular fluid volume relationship. The volume of extracellular fluid (Ve) is the sum of blood plasma volume (Vp) and interstitial fluid volume (Vi). Ve = Vp + Vi Blood is normally composed of about 42 per cent red blood cells and 58 per cent plasma. Thus plasma volume is a determinant of blood volume (Vb). Typically Vb is about 1/3 of Ve. Later we will consider conditions which can shift interstitial fluid into or out of the vascular space. V. THE RENAL BODY-FLUID SYSTEM COMES TO A STEADY-STATE WHEN dEo/dt = dEi/dt. It is important to recognize that the renal body-fluid system can only stop changing, i.e., come to a steady-state, when dEo/dt = dEi/dt. Whenever they differ, E will either be increasing or decreasing. Changes in E cause changes in Vb, Pms, Q, TPR, and Pa. Thus, none of these can come to a steady-state until dEo/dt equals dEi/dt. VI. PATHOLOGICAL INTERVENTIONS CAN CHANGE THE VALUES OF Q (CARDIAC OUTPUT), Pa (ARTERIAL BLOOD PRESSURE), Vb (BLOOD VOLUME), E (EXTRACELLULAR FLUID VOLUME), TPR (TOTAL PERIPHERAL RESISTANCE), dEo/dt (THE RATE OF LOSS OF EXTRACELLULAR FLUID), OR Pms (MEAN SYSTEM PRESSURE). By way of example consider the effect of cardiac failure on E, CO, and Pa. The effects on each block would be as follows: A. Block II. Cardiac failure shifts the cardiac function curve to the right. This will increase right atrial pressure (RAP) and decrease Q. B. Block III. The decrease in Q will decrease TPR. C. Block IV. The decrease in Q and TPR will decrease Pa. D. Block V. The decrease in Pa will decrease dEo/dt. E. Block VI. The decrease in dEo/dt will increase dE/dt. F. Block VII. The increase in dE/dt will increase E. G. Block VIII. The increase in E will increase Vb H. Block I. The increase in Vb will increase Pms (mean system pressure). I. Block II. The increase in Pms will shift the vascular function curve to the right and shift the equilibrium point (the intersection of the vascular function curve and cardiac function curve )upward on the cardiac function curve. If the heart is not severely failed, CO, Pa, and dEo/dt will be returned to nearly normal. When dEo/dt is nearly returned to normal, it will equal dEi/dt and the system will be in a new steady-state. Values which will have changed are E, Vb, Pms and Pra. The elevated Pra is a strong clinical indication of heart weakness even in the face of near normal blood pressure and cardiac output.
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