Control of Arterial Pressure (Chapter 23 cont.)

Objectives:

Describe the arterial baroreceptor reflex
Describe other reflexes controlling blood pressure

As described in the preceding lecture, the arterial system acts as a high-pressure reservoir of blood from which the tissues can draw on demand. There is a limit to the quantity of flow that can be supplied from this system at any point in time yet; the heart and arterial system can supply sufficient blood flow to tissues over a wide range of demands. To be effective, arterial pressure must be maintained at an adequate and constant level. Therefore, control of arterial pressure is a critical part of cardiovascular function.

The Arterial baroreceptor reflex

The baroreceptor reflex is the single most important mechanism for short-term control of arterial pressure. This reflex system consists of pressure receptors in the carotid arteries and aortic arch with afferent neurons running to the medulla in the central nervous system. The integration of inputs occurs in the medulla. The efferent pathways of the baroreceptor reflex involve the parasympathetic and sympathetic nervous systems.

A rise in arterial pressure increases neural input to the medulla, which results in an increase in the parasympathetic activity (through the vagus) as well as a concomitant decrease in sympathetic activity. Increased parasympathetic tone and decreased sympathetic tone work together to reduce arterial pressure.

Reduction of arterial pressure reduces afferent input to the medulla, increases sympathetic output, and reduces parasympathetic output. These changes favor an increase in blood pressure.

Efferent pathways - The efferent segments of the baroreceptor reflex are the sympathetic and parasympathetic nervous systems. Parasympathetic stimulation causes the heart to slow. Sympathetic stimulation increases the cardiac rate (chronotropic), cardiac contractility (inotropic), and arteriolar constriction. The baroreceptor reflex is a major controller of sympathetic and parasympathetic output, but not the only one.

Central nervous system integration - Input from the pressure receptors (action potentials) ascends to the medulla, via axons of the glossopharyngeal and vagus nerves, bilaterally. These axons synapse in two bilateral nuclei (Nucleus Tractus Solitarius) in the medulla (Fig. 1). The synapse between the afferent neuron and the cell bodies of the NTS is an excitatory synapse that employs glutamate as its neurotransmitter. The neurons of the NTS also receive input, some excitatory, some inhibitory, from a host of other areas, especially the hypothalamus and cortex of the brain. NTS neurons send axons to two different areas: the bilateral vagal nuclei and the midline cardiovascular center. Action potentials coming from the NTS stimulate the vagal nuclei, especially in the Dorsal Vagal Nucleus and the Nucleus Ambiguus. This in turn increases parasympathetic output via the vagal nerves, most importantly to the heart where the effect is to slow the heart rate.

Efferent action potentials from the NTS also influence the cardiovascular center; stimulation of the NTS inhibits activity in the cardiovascular center. If the cardiovascular center is inhibited by NTS input, sympathetic output will be reduced, heart rate will slow, contractility will be reduced and peripheral resistance will fall. All these effects tend to oppose the stimulus (increasing blood pressure).

If the cardiovascular center is released from inhibition, or stimulated directly, the activity of the sympathetic nervous system increases causing increased heart rate, cardiac contractility, and peripheral resistance.

(Reprinted from Principles of Physiology 3rd ed.,(2000) by R.M. Berne & M.N. Levy, page 260 with permission from Elsevier.)

The Stretch receptors and afferent pathways

The receptors for monitoring arterial pressure are stretch receptors, nerve endings located in the wall of the aortic arch and the carotid sinus, that are stimulated by stretch. The carotid sinuses are on both sides of the neck near the bifurcation of the internal and external carotid arteries (Fig. 2). Axons arising from the stretch receptors in the carotid sinus ascend to the NTS via the glossopharyngeal nerve (cranial nerve IX). Axons from the aortic arch receptors ascend via the vagus nerve (cranial nerve X).

Action potentials are initiated when these nerve endings are stretched, such as would happen with elevated arterial pressure. The effect of stretch is to stimulate the vagal nuclei and elevate parasympathetic output, while simultaneously reducing sympathetic output. With reduced arterial pressure, fewer action potentials are generated, increasing sympathetic output and reducing parasympathetic output. The net effect of the baroreceptor reflex is to limit changes in blood pressure and to restore blood pressure toward its resting level.

(Reprinted from Principles of Physiology 3rd ed., (2000) by R.M. Berne & M.N. Levy, page 260 with permission from Elsevier.)

Characteristics of Baroreceptor Response - The baroreceptor stretch receptors respond to the degree of stretch, but respond even more to changes in stretch and the rate of change (Fig. 3 and 4).

Baroreceptors respond more strongly to changing (pulsatile) pressures than to constant pressure.
Baroreceptor response parallels mean pressure within a limited range. As blood pressure is lowered, action potential frequency falls. However, below a mean pressure of about 60 mmHg, action potential frequency is a minimum. Falling below that level does not elicit further decreases in action potential frequency. Similarly, baroreceptors reach a maximum firing rate at a mean pressure of about 160 mmHg. If blood pressure is elevated above that level the stretch receptors will not increase their firing rate further (Fig. 3).
The carotid baroreceptors are more sensitive to change than the aortic arch receptors.

The baroreceptor reflex adapts to sustained changes in blood pressure. If blood pressure is increased suddenly, the reflex will respond as described above and will buffer the changes in blood pressure. However, if an increase in blood pressure is sustained over a period of days or even hours, the baroreceptor response diminishes. Ultimately the baroreceptor will begin to regulate blood pressure around a new set point. This is seen in individuals with sustained hypertension.

The baroreceptor reflex responds within a single heartbeat; therefore it is effective in buffering sudden changes in blood pressure, such as might be seen with changing body position. Long-term control of blood pressure, however, is not a function of the baroreceptor reflex but depends on the control of vascular volume, a function of renal control of salt and fluid balance.

Other reflexes with cardiovascular significance

Cardiopulmonary baroreceptors: These stretch receptors respond to the absolute pressure in the atria and the pulmonary veins. Although they discharge at lower pressures than the arterial baroreceptors, on reaching the brain, the impulses initiate a similar response. Elevated cardiopulmonary pressure inhibits sympathetic output.
Peripheral chemoreceptors: The primary purpose of the peripheral chemoreceptors, which are located in the carotid and aortic bodies, is to control respiration. Although the peripheral chemoreceptors respond to increased PaCO2, increased H+ concentration, and decreased PaO2, the latter is most important physiologically. The increased discharge of these receptors, brought about by low PaO2, stimulates increased activity of the cardiovascular center, hence increasing vasoconstriction and blood pressure.

When elevated PaCO2 and low PaO2 occur simultaneously (as in asphyxia), the vasoconstrictor response is augmented, just as is the ventilatory response.

The chemoreceptor responses can be overridden by the baroreceptor responses.

Hypothalamic regions integrate heart rate and blood pressure in response to emotion-evoking situations. Also, elevation of the temperature of the anterior hypothalamus elicits signals that depress the cardiovascular center, thus activating vascular mechanisms of heat loss, i.e. vasodilation and sweating. This area controls some complex patterns of cardiovascular change. The output from the hypothalamus affects the baroreceptor reflex by acting on the NTS nuclei.

Bainbridge Reflex refers to the following phenomenon: when an increase in right atrial volume occurs (e.g. increased venous return), heart rate increases. The reflex appears to be mediated by vagal afferents from the heart to the cardiovascular center and by sympathetic efferents to the heart.