| Short-Term Regulation of Arterial Pressure Arterial Baroreceptor Reflex   The arterial baroreceptor reflex is the single most important mechanism providing short-term regulation of arterial pressure. Recall that the usual components of a reflex pathway include sensory receptors, afferent pathways, integrating centers in the central nervous system, efferent pathways, and effector organs. As shown in Figure 9 1, the efferent pathways of the arterial baroreceptor reflex are the cardiovascular sympathetic and cardiac parasympathetic nerves. The effector organs are the heart and peripheral blood vessels.
Efferent Pathways Previous chapters have discussed the many actions of the sympathetic and parasympathetic nerves leading to the heart and blood vessels. For both systems, postganglionic fibers, whose cell bodies are in ganglia outside the central nervous system, form the terminal link to the heart and vessels. The influences of these postganglionic fibers on key cardiovascular variables are summarized in Figure 9 1. The activity of the terminal postganglionic fibers of the autonomic nervous system is determined by the activity of preganglionic fibers whose cell bodies lie within the central nervous system. In the sympathetic pathways, the cell bodies of the preganglionic fibers are located within the spinal cord. These preganglionic neurons have spontaneous activity that is modulated by excitatory and inhibitory inputs, which arise from centers in the brainstem and descend in distinct excitatory and inhibitory spinal pathways. In the parasympathetic system, the cell bodies of the preganglionic fibers are located within the brainstem. Their spontaneous activity is modulated by inputs from adjacent centers in the brainstem. Afferent Pathways Sensory receptors, called arterial baroreceptors, are found in abundance in the walls of the aorta and carotid arteries. Major concentrations of these receptors are found near the arch of the aorta (the aortic baroreceptors) and at the bifurcation of the common carotid artery into the internal and external carotid arteries on either side of the neck (the carotid sinus baroreceptors). The receptors themselves are mechanoreceptors that sense arterial pressure indirectly from the degree of stretch of the elastic arterial walls.1 In general, increased stretch causes an increased action potential generation rate by the arterial baroreceptors. Baroreceptors actually sense not only absolute stretch but also the rate of change of stretch. For this reason, both the mean arterial pressure and arterial pulse pressure affect baroreceptor firing rate as indicated in Figure 9 2. The dashed curve in Figure 9 2 shows how baroreceptor firing rate is affected by different levels of a steady arterial pressure. The solid curve in Figure 9 2 indicates how baroreceptor firing rate is affected by the mean value of a pulsatile arterial pressure. Note that the presence of pulsations (that of course are normal) increases the baroreceptor firing rate at any given level of mean arterial pressure. Note also that changes in mean arterial pressure near the normal value of 100 mmHg produce the largest changes in baroreceptor discharge rate. If arterial pressure remains elevated over a period of several days for some reason, the arterial baroreceptor firing rate will gradually return toward normal. Thus, arterial baroreceptors are said to adapt to long-term changes in arterial pressure. For this reason, the arterial baroreceptor reflex cannot serve as a mechanism for the long-term regulation of arterial pressure. Action potentials generated by the carotid sinus baroreceptors travel through the carotid sinus nerves (Hering's nerves), which join with the glossopharyngeal nerves (ninth cranial nerves) before entering the central nervous system. Afferent fibers from the aortic baroreceptors run to the central nervous system in the vagus nerves (tenth cranial nerves). (The vagus nerves contain both afferent and efferent fibers, including, for example, the parasympathetic efferent fibers to the heart.) 1 Baroreceptor discharge rate can be enhanced by mechanical manipulation of the arterial walls. For example, the carotid sinus baroreceptor firing rate can be increased by massaging the neck over the carotid sinus area. Central Integration Much of the central integration involved in reflex regulation of the cardiovascular system occurs in the medulla oblongata in what are traditionally referred to as the medullary cardiovascular centers. The neural interconnections between the diffuse structures in this area are complex and not completely mapped. Moreover, these structures appear to serve multiple functions including respiratory control, for example. What is known with a fair degree of certainty is where the cardiovascular afferent and efferent pathways enter and leave the medulla. For example, as indicated in Figure 9 1, the afferent sensory information from the arterial baroreceptors enters the medullary nucleus tractus solitarius, where it is relayed via polysynaptic pathways to other structures in the medulla (and higher brain centers, such as the hypothalamus, as well). The cell bodies of the efferent vagal parasympathetic cardiac nerves are located primarily in the medullary nucleus ambiguus. The sympathetic autonomic efferent information leaves the medulla predominantly from the rostral ventrolateral medulla group of neurons (via an excitatory spinal pathway) or the raph nucleus (via an inhibitory spinal pathway). The intermediate processes involved in the actual integration of the sensory information into appropriate sympathetic and parasympathetic responses are not well understood at present. Whereas much of this integration takes place within the medulla, higher centers such as the hypothalamus are probably involved as well. In this context, knowing the details of the integration process is not as important as appreciating the overall effects that changes in arterial baroreceptor activity have on the activities of parasympathetic and sympathetic cardiovascular nerves.  Several functionally important points about the central control of the autonomic cardiovascular nerves are illustrated in Figure 9 1. The major external influence on the cardiovascular centers comes from the arterial baroreceptors. Because the arterial baroreceptors are active at normal arterial pressures, they supply a tonic input to the central integration centers. As indicated in Figure 9 1, the integration process is such that increased input from the arterial baroreceptors tends to simultaneously: (1) inhibit the activity of the spinal sympathetic excitatory tract, (2) stimulate the activity of the spinal sympathetic inhibitory tract, and (3) stimulate the activity of parasympathetic preganglionic nerves. Thus, an increase in the arterial baroreceptor discharge rate (caused by increased arterial pressure) causes a decrease in the tonic activity of cardiovascular sympathetic nerves and a simultaneous increase in the tonic activity of cardiac parasympathetic nerves. Conversely, decreased arterial pressure causes increased sympathetic and decreased parasympathetic activity.
Operation of the Arterial Baroreceptor Reflex The arterial baroreceptor reflex is a continuously operating control system that automatically makes adjustments to prevent disturbances on the heart and/or vessels from causing large changes in mean arterial pressure. The arterial baroreceptor reflex mechanism acts to regulate arterial pressure in a negative feedback manner that is analogous in many ways to the manner in which a thermostatically controlled home heating system operates to regulate inside temperature despite disturbances such as changes in the weather or open windows.2 Figure 9 3 shows many events in the arterial baroreceptor reflex pathway that occur in response to a disturbance of decreased mean arterial pressure. All of the events shown in Figure 9 3 have already been discussed, and each should be carefully examined (and reviewed if necessary) at this point because a great many of the interactions that are essential to understanding cardiovascular physiology are summarized in this figure. Note in Figure 9 3 that the overall response of the arterial baroreceptor reflex to the disturbance of decreased mean arterial pressure is increased mean arterial pressure (ie, the response tends to counteract the disturbance). A disturbance of increased mean arterial pressure would elicit events exactly opposite to those shown in Figure 9 3 and produce the response of decreased mean arterial pressure; again, the response tends to counteract the disturbance. The homeostatic benefits of the reflex action should be apparent. One should recall that nervous control of vessels is more important in some areas such as the kidney, the skin, and the splanchnic organs than in the brain and heart muscle. Thus, the reflex response to a fall in arterial pressure may, for example, include a significant increase in renal vascular resistance and a decrease in renal blood flow without changing the cerebral vascular resistance or blood flow. The peripheral vascular adjustments associated with the arterial baroreceptor reflex take place primarily in organs with strong sympathetic vascular control. 2 In this analogy, arterial pressure is likened to temperature; the heart is the generator of pressure as the furnace is the generator of heat; dilated arterioles dissipate arterial pressure like open windows lose heat; the arterial baroreceptors monitor arterial pressure as the sensor of a thermostat monitors temperature; and the electronics of the thermostat control the furnace as the medullary cardiovascular centers regulate the operation of the heart. Because home thermostats do not usually also regulate the operation of windows, there is no analogy to the reflex medullary control of arterioles. The pressure that the arterial baroreflex strives to maintain is analogous to the temperature setting on the thermostat dial. Other Cardiovascular Reflexes & Responses Seemingly in spite of the arterial baroreceptor reflex mechanism, large and rapid changes in mean arterial pressure occur in certain physiological and pathological situations. These reactions are caused by influences on the medullary cardiovascular centers other than those from the arterial baroreceptors. As outlined in the following sections, these inputs on the medullary cardiovascular centers arise from many types of peripheral and central receptors as well as from "higher centers" in the central nervous system such as the hypothalamus and the cortex. The analogy was made earlier that the arterial baroreceptor reflex operates to control arterial pressure somewhat as a home heating system acts to control inside temperature. Such a system automatically acts to counteract changes in temperature caused by such things as an open window3 or a dirty furnace. It does not, however, resist changes in temperature caused by someone's resetting of the thermostat dial in fact, the basic temperature regulating mechanisms cooperate wholeheartedly in adjusting the temperature to the new desired value. The temperature setting on a home thermostat's dial has a useful conceptual analogy in cardiovascular physiology often referred to as the "set point" for arterial pressure. The many influences that are about to be discussed all influence arterial pressure as if they changed the arterial baroreceptor reflex's set point for pressure regulation. Consequently, the arterial baroreceptor reflex does not resist these pressure disturbances but actually assists in producing them. 3 In Minnesota, an open window is an obvious temperature lowering disturbance. Reflexes from Receptors in Heart & Lungs A host of mechanoreceptors and chemoreceptors that can elicit reflex cardiovascular responses have been identified in the atria, ventricles, coronary vessels, and lungs. The role of these cardiopulmonary receptors in the neurohumoral control of the cardiovascular system is, in most cases, incompletely understood, but evidence is accumulating that they may be involved significantly in many physiological and pathological states. One general function that the cardiopulmonary receptors perform is sensing the pressure (or volume) in the atria and central venous pool. Increased central venous pressure and volume cause receptor activation by stretch, which elicits a reflex decrease in sympathetic activity. Decreased central venous pressure produces the opposite response. Whatever the details, it is clear that cardiopulmonary baroreflexes normally exert a tonic inhibitory influence on sympathetic activity and play an arguably important, but not yet completely defined, role in normal cardiovascular regulation. Certain other reflexes originating from receptors in the cardiopulmonary region have been described that may be important in specific pathological situations. For example, the Bezold-Jarisch reflex that involves marked bradycardia and hypotension is elicited by application of strong stimuli to coronary vessel (or myocardial) chemoreceptors concentrated primarily in the posterior wall of the left ventricle. There is much clinical evidence that myocardial infarctions involving this region of the ventricle can elicit the Bezold-Jarisch reflex and cause certain myocardial infarction patients to present with bradycardia. (Far more commonly, patients with myocardial infarction have hypotension, as would be expected from compromised myocardial function, and tachycardia as would be expected from an arterial baroreceptor response to hypotension.) Chemoreceptor Reflexes Low PO2 and/or high PCO2 levels in the arterial blood cause reflex increases in respiratory rate and mean arterial pressure. This appears to be a result of increased activity of arterial chemoreceptors, located in the carotid arteries and the arch of the aorta, and central chemoreceptors, located somewhere within the central nervous system. Chemoreceptors probably play little role in the normal regulation of arterial pressure because arterial blood PO2 and PCO2 are normally held very nearly constant by respiratory control mechanisms. An extremely strong reaction called the cerebral ischemic response is triggered by inadequate brain blood flow (ischemia) and can produce a more intense sympathetic vasoconstriction and cardiac stimulation than is elicited by any other influence on the cardiovascular control centers. Presumably the cerebral ischemic response is initiated by chemoreceptors located within the central nervous system. However, if cerebral blood flow is severely inadequate for several minutes, the cerebral ischemic response wanes and is replaced by marked loss of sympathetic activity. Presumably this situation results when function of the nerve cells in the cardiovascular centers becomes directly depressed by the unfavorable chemical conditions in the cerebrospinal fluid. Whenever intracranial pressure is increased for example, by tumor growth or trauma-induced bleeding within the rigid cranium there is a parallel rise in arterial pressure. This is called the Cushing reflex. It can cause mean arterial pressures of more than 200 mmHg in severe cases of intracranial pressure elevation. The obvious benefit of the Cushing reflex is that it prevents collapse of cranial vessels and thus preserves adequate brain blood flow in the face of large increases in intracranial pressure. The mechanisms responsible for the Cushing reflex are not known but could involve the central chemoreceptors. Reflexes from Receptors in Exercising Skeletal Muscle Reflex tachycardia and increased arterial pressure can be elicited by stimulation of certain afferent fibers from skeletal muscle. These pathways may be activated by chemoreceptors responding to muscle ischemia, which occurs with strong, sustained static (isometric) exercise. This input may contribute to the marked increase in blood pressure that accompanies such isometric efforts. It is uncertain as to what extent this reflex contributes to the cardiovascular responses to dynamic (rhythmic) muscle exercise. The Dive Reflex Aquatic animals respond to diving with a remarkable bradycardia and intense vasoconstriction in all systemic organs except the brain and heart. The response serves to allow prolonged submersion by limiting the rate of oxygen use and by directing blood flow to essential organs. A similar but less dramatic dive reflex can be elicited in humans by simply immersing the face in water. (Cold water enhances the response.) The response involves the unusual combination of bradycardia produced by enhanced cardiac parasympathetic activity and peripheral vasoconstriction caused by enhanced sympathetic activity that is a rare exception to the general rule that sympathetic and parasympathetic nerves are activated in reciprocal fashion. The dive reflex is sometimes used clinically (as is massage of the neck over the carotid sinus) to reflexly activate cardiac parasympathetic nerves for the purpose of interrupting atrial tachyarrhythmias. Cardiovascular Responses Associated with Emotion Cardiovascular responses are frequently associated with certain states of emotion. These responses originate in the cerebral cortex and reach the medullary cardiovascular centers through corticohypothalamic pathways. The least complicated of these responses is the blushing that is often detectable in individuals with lightly pigmented skin during states of embarrassment. The blushing response involves a loss of sympathetic vasoconstrictor activity only to particular cutaneous vessels, and this produces the blushing by allowing engorgement of the cutaneous venous sinuses. Excitement or a sense of danger often elicits a complex behavioral pattern called the alerting reaction (also called the "defense" or "fight or flight" response). The alerting reaction involves a host of responses such as pupillary dilation and increased skeletal muscle tenseness that are generally appropriate preparations for some form of intense physical activity. The cardiovascular component of the alerting reaction is an increase in blood pressure caused by a general increase in cardiovascular sympathetic nervous activity and a decrease in cardiac parasympathetic activity. Centers in the posterior hypothalamus are presumed to be involved in the alerting reaction because many of the components of this multifaceted response can be experimentally reproduced by electrical stimulation of this area. The general cardiovascular effects are mediated via hypothalamic communications with the medullary cardiovascular centers. Some individuals respond to situations of extreme stress by fainting, a situation referred to clinically as vasovagal syncope. The loss of consciousness is due to decreased cerebral blood flow that is itself produced by a sudden dramatic loss of arterial blood pressure that, in turn, occurs as a result of a sudden loss of sympathetic tone and a simultaneous large increase in parasympathetic tone and decrease in heart rate. The influences on the medullary cardiovascular centers that produce vasovagal syncope appear to come from the cortex via depressor centers in the anterior hypothalamus. It has been suggested that vasovagal syncope is analogous to the "playing dead" response to peril used by some animals. Fortunately, unconsciousness (combined with becoming horizontal) seems to quickly remove this serious disturbance to the normal mechanisms of arterial pressure control in humans. The extent to which cardiovascular variables, in particular blood pressure, are normally affected by emotional state is currently a topic of extreme interest and considerable research. As yet the answer is unclear. However, the therapeutic value of being able, for example, to learn to consciously reduce one's blood pressure would be incalculable. Central Command The term central command is used to imply an input from the cerebral cortex to lower brain centers during voluntary muscle exercise. The concept is that the same cortical drives that initiate somatomotor (skeletal muscle) activity also simultaneously initiate cardiovascular (and respiratory) adjustments appropriate to support that activity. In the absence of any other obvious causes, central command is at present the best explanation as to why both mean arterial pressure and respiration increase during voluntary exercise. Reflex Responses to Pain Pain can have either a positive or negative influence on arterial pressure. Generally, superficial or cutaneous pain causes a rise in blood pressure in a manner similar to that associated with the alerting response and perhaps over many of the same pathways. Deep pain from receptors in the viscera or joints, however, often causes a cardiovascular response similar to that which accompanies vasovagal syncope, ie, decreased sympathetic tone, increased parasympathetic tone, and a serious decrease in blood pressure. This response may contribute to the state of shock that often accompanies crushing injuries and/or joint displacement. Temperature Regulation Reflexes Certain special cardiovascular reflexes that involve the control of skin blood flow have evolved as part of the body temperature regulation mechanisms. Temperature regulation responses are controlled primarily by the hypothalamus, which can operate through the cardiovascular centers to discretely control the sympathetic activity to cutaneous vessels and thus skin blood flow. The sympathetic activity to cutaneous vessels is extremely responsive to changes in hypothalamic temperature. Measurable changes in cutaneous blood flow result from changes in hypothalamic temperature of tenths of a degree Celsius. Cutaneous vessels are influenced by reflexes involved in both arterial pressure regulation and temperature regulation. When the appropriate cutaneous vascular responses for temperature regulation and pressure regulation are contradictory, as they are, for example, during strenuous exercise in a hot environment, then the temperature-regulating influences on cutaneous blood vessels usually prevail. Summary  Most of the influences on the medullary cardiovascular centers that have been discussed in the preceding sections are summarized in Figure 9 4. This figure is intended first to reemphasize that the arterial baroreceptors normally and continually supply the major input to the medullary centers. The arterial baroreceptor input is shown as inhibitory because an increase in arterial baroreceptor firing rate results in a decrease in sympathetic output. (Decreased sympathetic output should be taken to imply also a simultaneous increase in parasympathetic output, which is not shown.) As indicated in Figure 9 4, the nonarterial baroreceptor influences on the medullary cardiovascular centers fall into two categories: (1) those that increase arterial pressure by raising the set point for the arterial baroreceptor reflex and thus cause an increase in sympathetic activity, and (2) those that decrease arterial pressure by lowering the set point for the arterial baroreceptor reflex and thus cause a decrease in sympathetic activity. Note that certain responses that have been discussed are not included in Figure 9 4. The complex combination of stimuli involved in the dive reflex cause simultaneous sympathetic and parasympathetic activation and cannot be simply classified as either pressure raising or pressure lowering. Also, temperature stimuli that discretely affect cutaneous vessels but not general cardiovascular sympathetic and parasympathetic activity have not been included in Figure 9 4.
The nonarterial baroreceptor influences shown in Figure 9 4 may be viewed as disturbances on the cardiovascular system that act on the medullary cardiovascular centers as opposed to disturbances that act on the heart and vessels. These disturbances cause sympathetic activity and arterial pressure to change in the same direction. Recall from the discussion of the arterial baroreceptor reflex that cardiovascular disturbances that act on the heart or vessels (such as blood loss or heart failure) produce reciprocal changes in arterial pressure and sympathetic activity. These facts are often useful in the clinical diagnoses of blood pressure abnormalities. For example, patients commonly present in the doctor's office with high blood pressure in combination with elevated heart rate (implying elevated sympathetic activity). These same-direction changes in arterial pressure and sympathetic activity suggest that the problem lies not in the periphery but rather with an abnormal pressure-raising input to the medullary cardiovascular centers. The physician should immediately think of those set-point raising influences listed in the top half of Figure 9 4 that would simultaneously raise sympathetic activity and arterial pressure. Often, such a patient does not have chronic hypertension but rather is just experiencing a temporary blood pressure elevation due to the anxiety of undergoing a physical examination. Systems Analysis of the Arterial Baroreflex For most purposes, the preceding "thermostat analogy" provides a sufficient understanding of how the arterial baroreflex operates. In certain situations especially when there are multiple disturbances on the cardiovascular system a more detailed understanding is helpful. Consequently, this section will analyze the operation of the arterial baroreflex with a more formal control systems approach. The complete arterial baroreceptor reflex pathway is a control system made up of two distinct portions as shown in Figure 9 5: (1) an effector portion, including the heart and peripheral blood vessels, and (2) a neural portion, including the arterial baroreceptors, their afferent nerve fibers, the medullary cardiovascular centers, and the efferent sympathetic and parasympathetic fibers. Mean arterial pressure is the output of the effector portion and simultaneously the input to the neural portion. Similarly, the activity of the sympathetic (and parasympathetic)4 cardiovascular nerves is the output of the neural portion of the arterial baroreceptor control system and, at the same time, the input to the effector portion.
A host of reasons why mean arterial pressure increases when the heart and peripheral vessels receive increased sympathetic nerve activity was discussed in Chapters 2, 3, 4, 5, 6, 7, and 8. All this information is summarized by the curve shown in the lower graph of Figure 9 5 that describes the operation of the effector portion of the arterial baroreceptor system alone. In this chapter, how increased mean arterial pressure acts through the arterial baroreceptors and medullary cardiovascular centers to decrease the sympathetic activity has also been discussed. This information is summarized by the curve shown in the upper graph of Figure 9 5 that describes the operation of the neural portion of the arterial baroreceptor system alone. When the arterial baroreceptor system is intact and operating as a closed loop, the effector portion and neural portion retain their individual rules of operation as described by their individual function curves in Figure 9 5. Yet in the closed loop, the two portions of the system must interact until they come into balance with each other at some operating point with a mutually compatible combination of mean arterial pressure and sympathetic activity. The analysis of the complete system begins by plotting the operating curves for the neural and effector portions of the systems together on the same graph as in Figure 9 6A. To accomplish this superimposition, the graph for the neural portion (the upper graph in Figure 9 5) was flipped to interchange its vertical and horizontal axes. Consequently, the neural curve (but not the effector curve) in Figure 9 6A must be read in the unusual sense that its independent variable, arterial pressure, is on the vertical axis and its dependent variable, sympathetic nerve activity is on the horizontal axis.
Whenever there is any outside disturbance on the cardiovascular system, the operating point of the arterial baroreceptor system shifts. This happens because all cardiovascular disturbances cause a shift in one or the other of the two curves in Figure 9 6A. For example, Figure 9 6B shows how the operating point for the arterial baroreceptor system is shifted by a cardiovascular disturbance that lowers the operating curve of the effector portion. The disturbance in this case could be anything that reduces the arterial pressure produced by the heart and vessels at each given level of sympathetic activity. Blood loss, for example, is such a disturbance because it lowers central venous pressure and, through Starling's law, lowers cardiac output and thus mean arterial pressure at any given level of cardiac sympathetic nerve activity. Metabolic vasodilation of arterioles in exercising skeletal muscle is another example of a pressure-lowering disturbance on the effector portion of the system because it lowers the total peripheral resistance and thus the arterial pressure that the heart and vessels produce at any given level of sympathetic nerve activity. As shown by point 2 in Figure 9 6B, any pressure-lowering disturbance on the heart or vessels causes a new balance to be reached within the baroreceptor system at a slightly lower than normal mean arterial pressure and a higher than normal sympathetic activity level. Note that the point 1' in Figure 9 6B indicates how far the mean arterial pressure would have fallen as a consequence of the disturbance had not the sympathetic activity been automatically increased above normal by the arterial baroreceptor system.5 As indicated previously in this chapter, many disturbances act on the neural portion of the arterial baroreceptor system rather than directly on the heart or vessels. These disturbances shift the operating point of the cardiovascular system because they alter the operating curve of the neural portion of the system. For example, the influences listed in Figure 9 4 that raise the set point for arterial pressure do so by shifting the operating curve for the neural portion of the arterial baroreceptor system to the right as shown in Figure 9 7A because they increase the level of sympathetic output from the medullary cardiovascular centers at each and every level of arterial pressure (ie, at each and every level of input from the arterial baroreceptors). For example, a sense of danger will cause the components of the arterial baroreceptor system to come into balance at a higher than normal arterial pressure and a higher than normal sympathetic activity as shown by point 2 in Figure 9 7A. Conversely, but not shown in Figure 9 7, any of the set-point-lowering influences listed in Figure 9 4 acting on the medullary cardiovascular centers will shift the operating curve for the neural portion of the arterial baroreceptor system to the left and a new balance will be reached at lower than normal arterial pressure and sympathetic activity. Many physiological and pathological situations involve simultaneous disturbances on both the neural and effector portions of the arterial baroreceptor system. Figure 9 7B illustrates this type of situation. The set-point-increasing disturbance on the neural portion of the system alone causes the equilibrium to shift from point 1 to point 2. Superimposing a pressure-lowering disturbance on the heart or vessels further shifts the equilibrium from point 2 to point 3. Note that, although the response to the pressure-lowering disturbance in Figure 9 7B (point 2 to point 3) starts from a higher than normal arterial pressure, it is essentially identical to that which occurs in the absence of a set-point-increasing influence on the cardiovascular center (see Figure 9 6B). Thus, the response is an attempt to prevent the arterial pressure from falling below that at point 2. The overall implication is that any of the set-point-increasing influences on the medullary cardiovascular centers listed in Figure 9 4 cause the arterial baroreceptor system to regulate arterial pressure to a higher than normal value. Conversely, the set-point-lowering influences on the medullary cardiovascular centers listed in Figure 9 4 would cause the arterial baroreceptor system to regulate arterial pressure to a lower than normal value. Several situations that involve a higher than normal sympathetic activity at a time when arterial pressure is itself higher than normal will be discussed in Chapters 10 and 11. It should be noted that higher than normal sympathetic activity and higher than normal arterial pressure can exist together only when there is a set-point-raising influence on the neural portion of the arterial baroreceptor system. 4 For convenience, we will omit continual reference to parasympathetic nerve activity in the following discussion. Throughout, however, an indicated change in sympathetic nerve activity should also be taken to imply a reciprocal change in the activity of the cardiac parasympathetic nerves unless otherwise noted. 5 In the absence of an arterial baroreflex, sympathetic nerve activity would remain constant despite changes in arterial pressure. In this case, the operating curve for the neural portion of the system would be a vertical line in Figure 9 6B ie, one fixed sympathetic nerve activity regardless of arterial pressure. | 