The two variables within the cardiovascular system that are well controlled are the mean arterial blood pressure (MABP) and the cardiac output (CO). As discussed in Chapter 19, MABP is controlled within a fairly limited range by the baroreceptor reflex. CO, however, is not controlled within a limited range but rather is linked to the workload of the body and the metabolism or oxygen consumption of the body (see Figure 13-1). CO can therefore vary from a resting level that is approximately 8% of the body weight (kg) to a level that is four- to sixfold higher. There is no one sensor for CO as there is for MABP. The CO is the result of the interaction between the pump and the vasculature into which it ejects blood. For a normal cardiovascular system, the pump has little control over the magnitude of the CO. The heart’s two properties of contractility (as altered by the sympathetic nervous system [SNS]) and length-tension (as altered by venous return) allow the heart to pump various stroke volumes. The metabolic needs of the peripheral tissues more directly determine the absolute level of CO since CO is simply the sum of the blood flow to all of the systemic organs. The distribution of the CO is independent of pump function but is dependent on the interaction of the central nervous system, via the SNS, with the local control of blood flow by individual organs. The balance between central control and local control of tissue blood flow is tailored to each tissue. For example, blood flow to some tissues, such as the brain and heart, is regulated primarily by local mechanisms. Blood flow to other tissues, such as the gastrointestinal tract, may be more influenced by the central nervous system. Local mechanisms predominate when SNS activity is low; however, SNS activity predominates over local mechanisms in many tissues when SNS activity is high.
LOCAL VERSUS CENTRAL CONTROL OF ARTERIOLES
The two control mechanisms for regulating tissue blood flow then consist of the autonomic nervous system and locally mediated factors. As discussed previously, the SNS is the major component of the central nervous system to affect the vasculature. Its effect is primarily mediated by the transmitter norepinephrine released from the sympathetic postganglionic fibers. Norepinephrine binds to alpha1 receptors and, via stimulation of phosphatidylinositol turnover resulting in increases in cytosolic calcium which increases smooth muscle contraction. In venous blood vessels, smooth muscle contraction results in a decrease in compliance and increase in venous pressure. In arteriolar vessels, increased contraction results in decreased vessel radius, increased resistance, and decreased blood flow. A tissue’s response or sensitivity to autonomic control is dependent on:
The type of receptors present on the vascular smooth muscle cells, that is, alpha1 receptors mediate vasoconstriction whereas beta2 receptors mediate vasodilation.
The density of alpha1 and/or beta2 receptors—the more alpha receptors ...