Figure 2-4

in retaining water. Water tends to follow where sodium goes. Increased plasma sodium results in increased water retention. Normal adult blood volume is about 5-6 liters.

Not shown in Fig. 2-3 is the important point that blood pressure is also controlled by negative feedback of blood pressure itself. That is, decreased (or increased) blood pressure stimulates a homeostatic increase (or de crease) in blood pressure. Similar negative feedback mechanisms exist for peripheral resistance, cardiac output, and blood volume. Each entity feeds back to regulate itself in addition to influencing all the others.

The body has many intertwining mechanisms to detect and respond to changes in blood pressure, blood volume, peripheral resistance, and cardiac output, which will herewith be discussed as a whole. Receptors in the nervous system, kidney, heart, and peripheral vasculature play important roles in circulatory control:

1) Receptors in the nervous system

Both the brain stem and hypothalamus contain blood pressure regulating centers.

The brain stem contains a vasomotor center (influenced by numerous other areas of the nervous system), which increases blood pressure by firing sympathetic nerve messages (see Chapter 9, Neurophysiology, for further information on the sympathetic nervous system). Sympathetic nerves release norepinephrine, which stimulates alpha-1 receptors on the peripheral blood vessels (causing vasoconstriction) as well as beta-1 receptors on heart muscle (increasing cardiac output by increasing both stroke volume and heart rate). As veins contain most of the body's blood (largely for blood storage), the vasoconstrictive effect on the venous system can be particularly important in restoring blood pressure; venous constriction helps restore effective arterial blood volume in the rest of the body following fluid loss (as in hemorrhage). The veins hold about two thirds of the body's blood (the arteries and arterioles about 15%, and the capillaries only about 5%).

Sympathetic nerves also stimulate the adrenal medulla to secrete both norepinephrine and epinephrine, which reach the entire body through the circulation. NoRepinephrine, present also in sympathetic nerve endings, has geNeRal vasoconstrictive effects, by interacting with blood vessel alpha-1 receptors. Epinephrine vasoconstricts too, but not in all places. Like norepinephrine, epinephrine causes vasoconstriction when it acts on blood vessel alpha-1 receptors, but vasodilation when it acts on blood vessel beta-2 receptors, most notably those in skeletal muscle and heart. (The "B" in Beta stand for "Bigger diameter vessel"—not really.)

Norepinephrine does not act on beta-2 receptors. Thus it is logical to understand that sympathetic nerve endings, which rely on norepinephrine to transmit messages, do not innervate beta-2 receptors. Freely circulating epinephrine, however, does stimulate beta-2 receptors and thereby dilates skeletal and heart coronary blood vessels. This helps to ensure perfusion of the latter organs in states of sympathetic activity, as in the flight-or-fight response, where increased cardiac and skeletal circulation is critical.

Fig. 2-5. Location and effects of stimulation of adrenergic receptors.

Sympathetic nerves stimulate beta-1 receptors on cardiac muscle, including the modified muscle cells of the SA and AV nodes, which are part of the pacemaker and conduction system of the heart. This stimulation increases heart rate, conduction velocity through the AV node, and cardiac muscle contractility, with a net increase in cardiac output.

In addition, sympathetic nerves stimulate beta-1 receptors on granular cells in the kidney to cause renin secretion. Renin initiates a chain reaction that results in the production of angiotensin II and aldosterone. Both angiotensin II and aldosterone have powerful vasoconstrictive effects and, in addition, stimulate the renal tubules to reabsorb sodium (and, passively, water), thereby increasing pressure and blood volume.

The direct effect of the sympathetic nervous system on vasoconstriction throughout the body provides a more immediate control of blood pressure than does the longer range measure of altering blood volume through urine output.

The brain stem vasomotor center also contains a depressor region which connects with the parasympathetic system via the vagus nerve, thereby decreasing heart rate (and to some degree stroke volume) and, therefore, blood pressure when stimulated. Parasympathetic nerves do not significantly innervate peripheral blood vessels.

The hypothalamus releases antidiuretic hormone (ADH). ADH acts on the kidney to increase water reab-sorption from the renal tubules, thereby increasing blood volume and, hence, blood pressure. ADH also constricts blood vessels, thereby increasing peripheral resistance. Hence its other name—vasopressin.

The brain stem and hypothalamic centers are notified of the need for a change in blood pressure in several ways:

a) Venous, cardiac, and arterial baroreceptors (carotid and aortic sinuses) respond to a drop in blood pressure by reducing their normal rate of firing to the blood pressure centers in the brain stem and hypothalamus. Normally, baroreceptor firing INHIBITS the brain stem sympathetic center from issuing its sympathetic output (but stimulates the parasympathetic system), and INHIBITS the hypo-

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