After studying this chapter, youshould 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.
In humans and other mammals, multiple cardiovascular regulatory mechanisms have evolved. These mechanisms 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. The caliber of the arterioles is adjusted in part by autoregulation (Table 32–1). It is also increased in active tissues by locally produced vasodilator metabolites, is affected by substances secreted by the endothelium, and is regulated systemically by circulating vasoactive substances and the nerves that innervate the arterioles. The caliber of the capacitance vessels is also affected by circulating vasoactive substances and by vasomotor nerves. The systemic regulatory mechanisms synergize with the local mechanisms and adjust vascular responses throughout the body.
TABLE 32–1Summary of factors affecting the caliber of the arterioles. ||Download (.pdf) TABLE 32–1 Summary of factors affecting the caliber of the arterioles.
|Vasoconstriction ||Vasodilation |
|Local factors |
Decreased local temperature
Increased CO2 and decreased O2
Increased K+, adenosine, lactate
Decreased local pH
Increased local temperature
|Endothelial products |
Locally released platelet serotonin
|Circulating neurohumoral agents |
Epinephrine (except in skeletal muscle and liver)
Endogenous digitalis-like substance
Epinephrine in skeletal muscle and liver
Calcitonin G-related protein
Atrial natriuretic peptide
Vasoactive intestinal polypeptide
|Neural factors |
|Increased discharge of sympathetic nerves || |
Decreased discharge of sympathetic nerves
Activation of sympathetic cholinergic vasodilator nerves to vasculature of skeletal muscles of the limbs
The terms vasoconstriction and vasodilation are generally used to refer to constriction and dilation of the resistance vessels. Changes in the caliber of the veins are referred to as venoconstriction or venodilation.
NEURAL CONTROL OF THE CARDIOVASCULAR SYSTEM
INNERVATION OF THE BLOOD VESSELS