Appropriate systemic arterial pressure is the single most important requirement for proper operation of the cardiovascular system. Without sufficient arterial pressure, the brain and the heart do not receive adequate blood flow, no matter what adjustments are made in their vascular resistance by local control mechanisms. In contrast, unnecessary demands are placed on the heart by excessive arterial pressure (afterload, see thread "Afterload and Its Components" at http://www.tomhsiung.com/wordpress/2015/10/afterload-and-its-components/). Thus, although dramatic changes in peripheral resistance and cardiac function can and do occur normally during the course of our normal daily activities, mean arterial pressure is maintained within a narrow range and is tightly regulated.
Arterial pressure is continuously monitored by various sensors located within the body. Whenever arterial pressure varies from normal, multiple reflex responses are initiated, which cause the adjustments in cardiac output, and total peripheral resistance needed to return arterial pressure to its normal value.
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. 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.
In the sympathetic pathways, the cell bodies of the preganglionic fibers are located within the spinal cord (T1-L2). These pregangllionic 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 and spinal cord (S2-S4). Their spontaneous activity is modulated by inputs from adjacent centers in the brainstem.
Sensory receptors, called arterial barorecetpros, 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 and at the bifurcation of the common carotid artery into the internal and external carotid arteries on either side of the neck. The receptors themselves are mechanoreceptors that sense arterial pressure indirectly from the degree of stretch of the elastic arterial walls. 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 the arterial pulse pressure affect baroreceptor firing 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 nerve), which join with the glossopharyngeal nerves (cranial nerve IX) before entering the CNS. Afferent fibers from the aortic baroreceptors run to the CNS in the vagus nerves (cranial nerve X).
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 strucutures 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. And the intermediate processes involved in the actual integration of the sensory information into appropriate sympathetic and parasympathetic responses are not well understood at present. Although much of this integration takes place within the medulla, higher centers such as the hypothalamus are probably involved as well.
The major external influence on the cardiovascular centers comes from the arterial baroreceptors which supply a tonic input to the central integration centers. Increased inputs 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 (via increased arterial pressure and/or pulse pressure) causes a decrease in the tonic activity of cardiovascular sympathetic nerves and a simultaneous increase in the tonic activity of cardiac parasympathetic nerves.
Operation of The Arterial Baroreceptor Reflex
The arterial baroreceptor reflex is a continuously operating control system that automatically makes adjustments to prevent primary 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. 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 the 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.
Other Cardiovascular Reflexes and Responses
Seemingly in spite of the arterial baroreceptor reflex mechanism, large and rapid changes in mean arterial pressure do occur in certain physiological and pathological situatons. These reactions are caused by influences on the medullary cardiovascular centers other than those from the arterial baroreceptors. These inputs on the medullary cardiovascular centers arise from many types of peripheral and central receptors as well as from "higher centers" in the CNS such as hypothalamus and the cortex.
As discussed before, the analogy was made that the arterial baroreceptor reflex operates to control arterial pressure somewhat as a home heating system acts to control inside temperature. Such as system automatically acts to counteract changes in temperature caused by such things as an open window or a dirty furnace. It does not, however, resist changes in indoor temperature caused by someone's resetting of the thermostat dial – infact, the basic temperature regulating mechanisms copperate 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. Most (but not all) of the influences that are about to be discussed 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 most of these pressure disturbances but actually assists in producing them.
Reflexes From Receptors in the Heart and Lungs/Cardiopulmonary Receptors (+)
A host of mechanoreceptors and chemoreceptors that can elicit reflex cardiovascular responses have been identified in atria, ventricles, coronary vessels, and lungs. The role of these cardiopulmonary receptors in neurohumoral control of the cardiovascular system is, in most cases, incompletely understood. One general function that the cardiopulmonary receptors perform is sensing the pressure (or volume) in the atria and the central venous pool. Increased central venous pressure and volume cause receptor activation by stretch, which elicits a reflex decrease in sympathetic activity.
Chemoreceptor Reflexes (+)
Low PO2 and/or high PCO2 levels in the arterial blood cause reflex increases in respiratory rate and mean arterial pressure. These responses appear 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 CNS. 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.
- Arterial PO2 and PCO2
- Cerebral ischemic response
Reflexes From Receptors in Exercising Skeletal Muscle
Reflex tachycarida and increased arterial pressure can be elicited by stimulation of certain afferent fibers from the skeletal muscle. These pathways may be activated by chemoreceptors responding to muscle ischemia (more accurately, low PaO2 and/or high PaCO2), which occur 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 event this reflex contributes to the cardiovascular responses to dynamic (rhythmic) muscle exercise.
Aquatic animals respond to diving with a remarkable bradycardia and intense vasoconstriction in all systemic organs except the brain and the heart. 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. This is a rare exception to the general rule that sympathetic and parasympathetic nerves are activated in reciprocal fashion.
Cardiovascular Responses Associated with Emotion (+)
Cardiovascular responses are frequently associated with certain states of emotion. These responses include blushing, fight or flight, vasovagal syncope, etc., which originate in the cerebral cortex and reach the medullary cardiovascular centers through corticohypothalamic pathways.
Central Command (+)
The term central command is used to imply an input from the cerebral cortex to lower brain centers during voluntary muscle exercise. 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 a 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, that is, 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.
- Cutaneous pain
- Deep pain
Temperature Regulation Reflexes
Temperature regulation responses are controlled primarily by the hypothalamus, which can operate through the cardiovascular centers to discretely control the sympathetic activity to regulate vasoconstriction of cutaneous vessels and thus skin blood flow. The sympathetic activity to cutaneous vessels is extremely responsive to changes in hypothalamic temperature.
Long-Term Regulation of Arterial Pressure
Long-term regulation of arterial pressure is a topic of extreme clinical relevance because of the prevalence of hypertension in our society. The most long-standing and generally accepted theory of long-term pressure regulation is that it crucially involves the kidneys, their sodium handling, and ultimately the regulation of blood volume. This theory is sometimes referred to as the "fluid balance" model of long-term arterial blood pressure control. In essence, this theory asserts that in the long term, mean arterial pressure is whatever it needs to be to maintain an appropriate blood volume through arterial pressure's direct effects on renal function.
Circulating blood volume can influence arterial pressure because:
Blood volume (decreases) –> peripheral venous pressure (down) –> left shift of venous function curve –> CVP (down) –> SV (decreases) –> CO (decreases) –> arterial pressure (down)
A fact yet to be considered is that arterial pressure has a profound influence on urinary output rate and thus affects total body fluid volume. Because blood volume is one of the components of the total body fluid, blood volume alterations accompany changes in total body fluid volume. The mechanisms are such that an increase in arterial pressure causes an increase in urinary output rate (due to decreased ADH secretion) and thus a decrease in blood volume. But decreased blood volume tends to lower arterial pressure. Thus, the complete sequence of events that are initiated by an increase in arterial pressure can be listed as follows:
Arterial pressure (increases) –> urinary output rate (up) –> fluid volume (decreases) –> blool volume (decrease) –> cardiac output (down) –> arterial pressure (decreases)
Note the negative feedback nature of this sequence of events: increased arterial pressure leads to fluid volume depletion, which tends to lower arterial pressure. Conversely, an initial disturbance of decreased arterial pressure would lead to fluid volume expansion, which would tend to increase arterial pressure. Because of negative feedback, these events constitute a fluid volume mechanism for regulating arterial pressure.
Remember that the arterial baroreceptor reflex is very quick to counteract disturbances in arterial pressure, but for fluid volume mechanism hours or even days may be required before a change in urinary output rate produces a significant accumulation or loss of total body fluid volume. Whatever this fluid volume mechanism lacks in speed, however, it more than makes up for that in persistence. As long as there is any inequality between fluid intake rate and the urinary output rate, fluid volume is changing and this fluid volume mechanism has not completed its adjustment of arterial pressure. The fluid volume mechanism is in equilibrium only when the urinary output rate exactly equals the fluid intake rate. In the long term, the arterial pressure can only be that which makes the urinary output rate equal to the fluid intake rate.