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After studying this chapter, you should be able to:

  • Describe the neural mechanisms that control arterial blood pressure and heart rate, including the receptors, afferent and efferent pathways, central integrating pathways, and effector mechanisms involved.

  • Describe the direct effects of CO2 and hypoxia on the rostral ventrolateral medulla.

  • Define how the process of autoregulation contributes to control of vascular caliber.

  • Identify the paracrine factors and hormones that regulate vascular tone, their sources, and their mechanisms of action.


Multiple cardiovascular regulatory mechanisms are able to increase the blood supply to active tissues and increase or decrease heat loss from the body by redistributing the blood. In the face of challenges such as hemorrhage, they maintain the blood flow to the heart and brain. When the challenge faced is severe, flow to these vital organs is maintained at the expense of the circulation to the rest of the body. Circulatory adjustments are effected by altering the output of the pump (the heart), changing the diameter of the resistance vessels (primarily the arterioles), or altering the amount of blood pooled in the capacitance vessels (the veins). Regulation of cardiac output is discussed in Chapter 30. This chapter reviews the systemic regulatory mechanisms that synergize with the local mechanisms to adjust vascular responses throughout the body.


The cardiovascular system is under neural influences coming from several parts of the brainstem, forebrain, and insular cortex. The brainstem receives feedback from sensory receptors in the vasculature (eg, baroreceptors and chemoreceptors). A simplified model of the feedback control circuit is shown in Figure 32–1.


Feedback control of blood pressure. Brainstem excitatory input to sympathetic nerves to the heart and vasculature increases heart rate and stroke volume and reduces vessel diameter. Together these increase blood pressure, which activates the baroreceptor reflex to reduce the activity in the brainstem.


Most vascular beds receive input only from the sympathetic division of the autonomic nervous system, and the activation of these sympathetic nerves release norepinephrine that acts on α1-adrenoceptors to mediate vasoconstriction. The nerves to the resistance vessels regulate tissue blood flow and arterial pressure and those to the venous capacitance vessels vary the volume of blood “stored” in the veins. A change in the level of activity (increase or decrease) in sympathetic nerves is one of the many factors that mediate vasoconstriction or vasodilation (Table 32–1).

TABLE 32–1Summary of factors affecting the caliber of the arterioles.

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