Central nervous system control of cardiovascular function

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Chapter 7 Central nervous system control of cardiovascular function

After reading this chapter, you should:

• understand the basic patterns of brain control over sympathetic cardiovascular pathways

• be able to predict how cerebral arousal and exercise affect blood pressure and regional blood flows

• appreciate the different effects of dynamic and resistive exercise on these parameters

The brain exerts powerful effects on cardiovascular behaviour, predominantly by altering sympathetic motor drive to the heart and to vascular smooth muscle. While you may read about sympathetic activation specifically in relation to cardiac function or arteriolar resistance or venous capacitance, depending on the topic being discussed, the truth is that centrally mediated sympathetic activation almost always involves increased drive to both heart and blood vessels and in non-selective increases in vasomotor drive to arteries and veins. Therefore, heart rate and blood pressure usually change in parallel. This parallelism is convenient because it means that changes in any of these parameters can be used as an (approximate) index of sympathetic activation. In practice, the parameter used routinely is the change in heart rate, because ECGs can be recorded continually in moving subjects so much more easily than blood pressure.

ORGANIZATION OF CENTRAL CARDIOVASCULAR CONTROL

Although sympathetic outflow to the cardiovascular system can be affected by pathways arising in many areas of the brain, there are for our purposes three primary sources of this activation (Fig. 7.1). The first is the cardiovascular control centre lying in the medulla of the hindbrain, which is the final common pathway for all descending sympathetic information. This hindbrain centre receives reflex inputs directly from peripheral sensory nerves, but also receives descending inputs from two areas of the forebrain. The most important of these are the limbic system, which includes the hypothalamus and several neighbouring nuclei, mediates emotional arousal and determines levels of consciousness, and the motor cortex from which all instructions for muscle movement must originate.

Figure 7.1 Diagrammatic saggital view of the brain, showing the locations of the hindbrain cardiovascular control centre and the two most powerful forebrain activators of hindbrain sympathetic drive; the limbic system and the motor cortex.

Neuroscientists are still unravelling the specific neural connections and neurotransmitters involved in mediation of hindbrain regulation of the cardiovascular system. However, we can regard the cardiovascular control centre as consisting of two sets of tonically active descending neurons, one producing continual activation of the sympathetic outflows to heart and blood vessels and one producing continual inhibition of heart rate via the vagus (Fig. 7.2). As a result of this ongoing activity, there is usually some degree of vasoconstrictor tone in both arterial and venous vessels, while the heart rate at rest reflects the algebraic sum of inputs to the sinoatrial node of both sympathetic and vagal activity.

Figure 7.2 A simplified version of the neural circuitry of the hindbrain cardiovascular control centre and its baroreceptor inputs. Primary sensory inputs from baroreceptive neurons communicate via a series of interneurons as shown, to activate vagal outflow and to inhibit sympathetic outflow. Excitatory and inhibitory synaptic inputs are indicated by (+) and (−).

LOW-PRESSURE AND HIGH-PRESSURE BAROREFLEXES

Baroreflex effects on sympathetic cardiovascular control

The moment-to-moment regulation of blood pressure is via reflexes that operate through inputs to the hindbrain centre from mechanosensitive sensory axons monitoring pressure in the aorta and the carotid arteries (high-pressure baroreceptors) and in the atria (low-pressure baroreceptors). In all cases, increased distension results in increased sensory firing and the sensory neurons inhibit activity of the hindbrain centre sympathetic neurons. In consequence, either increased blood pressure or increased central blood volume will reduce peripheral resistance, while falls in blood pressure or central blood volume have the opposite effects.

With high pressure baroreflexes, parallel changes in cardiac and vascular sympathetic drive are seen, so that a reflex fall in peripheral resistance is accompanied by bradycardia. Although for ease of measurement the magnitude of baroreflex responses is usually assessed in terms of heart rate changes, it should be remembered that the end-point of the reflex is blood pressure regulation and that adjustment of peripheral resistance rather than heart rate is the dominant factor in achieving this.

Low-pressure baroreflexes have a distinct pattern of cardiac and vascular responses, with reflex falls in peripheral resistance caused by increased atrial filling being usually accompanied by tachycardia. However, increases in atrial volume that raise stroke volume will also induce an arterial baroreflex and bradycardia. This means that heart rate changes may be an uncertain index of baroreflex activity since their magnitude will vary depending on the algebraic sum of low-pressure and high-pressure receptor inputs.

Although the arterial and atrial pressure-sensitive sensory axons are commonly referred to as baroreceptors, they are in fact simple stretch receptors that react to vessel wall distortion rather than to the transmural pressure itself. For this reason, arterial baroreceptors cannot detect intravascular pressures below around 40 mmHg because there is insufficient wall stretch. Further, increased stiffness of the arterial wall by smooth muscle contraction, loss of elastic tissue or infiltration with inorganic precipitates such as calcium can greatly dampen recognition of intravascular pressure changes. As mechanoreceptors, the baroreceptors also respond to the rate of distortion as well as to its magnitude, so that during the arterial pulse wave they fire more during the rising phase than at equivalent absolute pressure levels during the falling phase.

Because the purpose of the baroreflex is to achieve restoration of arterial or atrial pressure to its operating point as efficiently as possible, it is not surprising that baroreflex activation involves the regulation of vasoconstrictor tone in large vascular beds that can contribute most to total peripheral resistance – skeletal muscle, digestive tract and kidneys. All three of these beds are equally involved in arterial baroreflex responses. Atrial baroreflexes appear to have a preferential effect on renal resistance, reflecting their involvement in blood volume regulation.

The cutaneous circulation, which is the other large vascular bed in the body, is recruited to only a small extent by baroreflex adjustments, allowing it to be reserved entirely for thermoregulatory regulation. Notwithstanding, thermoregulatory and baroreflex demands can interact, since the vascular response to body heating involves withdrawal of sympathetic vasomotor tone not only from the cutaneous arterioles, but also from both small and large superficial veins in the limbs. The consequent increase in venous volume reduces circulating blood volume and so reduces the efficiency with which baroreflex adjustments are able to compensate for postural change.

Baroreflex effects on hormonal cardiovascular control

The immediate neural compensations to altered blood pressure or blood volume are supplemented by concomitant changes in hormone release that provide longer-term reinforcement of the response. If blood pressure or atrial pressure falls, increased sympathetic discharge to the kidney not only increases renal vascular resistance, but also activates release of the enzyme renin from juxtaglomerular cells in the afferent arteriolar wall. Released renin cleaves the octapeptide angiotensin I from the circulating liver derived precursor angiotensinogen, and the angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE) in the pulmonary endothelium. Angiotensin II is a potent vasoconstrictor agent. It also stimulates release of aldosterone from the adrenal cortex, so retarding renal excretion of sodium and increasing blood volume.

Activation of low-pressure baroreceptors by atrial distension sends inhibitory inputs to the hypothalamus that depress release of vasopressin (antidiuretic hormone, ADH) from the posterior pituitary gland. As a result, less water is reabsorbed from the renal collecting ducts and plasma volume is reduced. Conversely, reduced atrial baroreceptor activity due to lower atrial pressure will increase vasopressin release, retaining water and elevating plasma volume.

Baroreflexes and ‘resting’ cardiovascular status

In most experiments concerned with human cardiovascular responses, it is essential to obtain baseline values for heart rate and blood pressure at rest. Standardization of posture is an important factor here, since upright posture inevitably results in heightened sympathetic drive. This is due to baroreflex recognition of reduced venous return because of venous pooling in the legs and splanchnic area. Ideally, baseline data should be obtained with subjects supine so as to ensure complete abolition of gravitational forces on the venous system. However, in practical terms this is often difficult to reconcile with the other requirements of the experiment – access to equipment, comfort of the subject while viewing a display screen, etc. – and the majority of studies use the seated position as a realistic compromise.

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