The control of arterial blood pressure

Pressure depends upon two factors: the flow produced by the pump, and the resistance of the flow pathway. The blood pressure, therefore, is the product of the cardiac output and the resistance of the circulation to flow. The latter is termed the total peripheral resistance (TPR). Blood pressure and cardiac output are both directly measurable; the peripheral resistance is not. It is the ratio of pressure to the cardiac output and is often given in arbitrary peripheral resistance units, or PRU, obtained by dividing pressure in mmHg of mercury by flow in ml/s. Thus the peripheral resistance in the systemic circulation is normally around 1.2 PRU (a mean pressure drop of 13.3 kPa, or 100 mmHg of mercury, divided by 83ml/min, or 51/min) and that in the pulmonary circuit, 0.2 PRU (assuming a mean pressure drop of 2.2 kPa, or 17 mm). In more conventional units one PRU is 133kPa/s/m⁻³.

If blood pressure increases, the transmural pressure in the major arteries is increased and the vessel walls stretch. Similarly, a decrease in pressure permits the vessel walls to recoil. Blood pressure can, therefore, be monitored by stretch receptors in the walls of the blood vessels. It is probable that such stretch receptors are found in many parts of the circulation including the walls of the cardiac chambers themselves. However, the best known and most important are found in the walls of the arch of the aorta and in the walls of the internal carotid arteries just after the bifurcation of the common carotid vessels (Fig. 15.1). These stretch receptors are branched nerve terminals with bulbous swellings – almost like the flower-spray type of nerve endings. The internal carotid artery is dilated to form a swelling termed the carotid sinus and the walls of the sinus are more distensible than those of the vessel before and after this point. The carotid sinus and the arch of the aorta, then, can be regarded as sensor areas for blood pressure measurement, baroreceptor areas. Pressures below 9kPa produce no response from these sensors but from that pressure up to about 20kPa their response is almost linear. Any recording of their normal activity reflects the regular cycle of systolic and diastolic pressures with a burst of action potentials at each systole superimposed upon the regular frequency of action potentials proportional to the diastolic pressure.

The input pathways of the blood pressure control system (Fig. 15.2) are a branch of the glossopharyngeal nerve from each carotid sinus and a branch of the vagus nerve from the aortic arch. These nerves are called depressor nerves since an increased input of action potentials along them to the medulla reduces the rate and strength of the heartbeat.

The impulses pass to a controlling centre within the medulla oblongata (Fig. 15.3). Cells here can be grouped into areas termed the vasomotor centre, which controls dilatation or constriction of the arterioles, and the cardiac centres, which control the activity of the heart. The ‘set level’ for blood pressure probably depends as much on the sensitivity of the receptors as on the controlling centre, and there is evidence that in hypertension – a state in which the blood pressure is continuously above normal – the sensitivity of the receptors is reduced. Adjustment of set levels in physiological systems is often achieved by altering the sensitivity of the receptors.

The output pathways of the system are the sympathetic nerves to the smooth muscle of the arteriolar walls, and the cardiac branches of the vagus and sympathetic nervous systems.

The effector systems are two-fold. Since the blood pressure is proportional to the cardiac output and the peripheral resistance, variations in one or both of these may be used to maintain blood pressure. Cardiac output may be increased by a diminution in the vagal restraint of the sinoatrial node or by an increase in the sympathetic acceleration of the rate initiated by the sinoatrial node. Sympathetic stimulation will produce positive inotropism (an increase in the force of contraction of the heart) as well as positive chronotropism (an increase in the rate at which it beats). The ventricles both fill and empty more completely so that their end diastolic volume is greater and the end systolic volume less. The stroke volume may also be increased by an increase in venous return resulting from sympathetic venoconstriction. Peripheral resistance may be increased by sympathetic stimulation of arteriolar constriction. It may be decreased by a decrease in sympathetic stimulation and hence a relaxation of the arterioles-vasodilatation (the passive word dilatation, rather than the active word dilation, is used to describe this change in calibre, because active contraction of the muscle walls can only reduce the diameter of the vessel). Thus sympathetic stimulation of the blood vessels has two effects: constriction of the arterioles to raise peripheral resistance and constriction of vessels on the venous side to increase return of blood to the heart and raise cardiac output.

The feedback control system is in fact much more complex than this (Fig. 15.4). There is evidence of other pressure receptors in both the atria and the ventricles as well as in other blood vessels. Other factors can modify the response to changes in blood pressure. The cardiovascular control areas receive inputs from the receptors in the carotid and aortic bodies which monitor the partial pressure of oxygen in the blood. These peripheral chemoreceptors will be dealt with more fully in Chap. 17 in relation to respiration. They respond to decreases in partial pressure of oxygen or to decreased blood flow. In general impulses from them cause an increase in vasomotor activity. Impulses from the aortic bodies usually cause tachycardia, but those from the carotid bodies may cause bradycardia. In the medulla itself increased partial pressures of carbon dioxide and decreased partial pressures of oxygen at first stimulate the cardiovascular control areas, but then depress nervous activity.

The feedback control system is able to maintain a fairly constant arterial blood pressure by these apparently simple components of a feedback loop. This system by itself is able to adjust the blood pressure during changes in posture, or after changes in the calibre of blood vessels, or when the venous return to the heart is varied. It does not, however, adjust the differential flow to different parts of the body, except inasmuch as the effects of sympathetic stimulation are selective in different vascular beds, and it does not adjust flow in response to external stimuli or changes in external environment. Differential flow can be controlled entirely locally, or, alternatively, may be directed by some higher centre. The activity of the medullary centres may be adjusted by interaction with other medullary or pontine centres involved in controlling other activities, such as respiration. Some integration of body systems occurs, therefore, even at medullary level. There are, in addition, controls exerted by higher centres. Biofeedback treatments make use of voluntary control of blood pressure by conscious cortical direction. Normally, however, there is no direct cortical control but the hypothalamus, which is the main area of the brain concerned in the integration of hormonal and nervous responses, and the area through which manifestations of limbic brain activity are channelled, exerts a general control over the medullary cardiovascular centres. The responses of anger and fear, and the responses to exercise, involve complex adjustment of the functioning of the cardiovascular system. Part of the response to loss of blood or a decrease in body fluids is cardiovascular (Chap. 16), and the control of body temperature, centred in the hypothalamus, demands the balancing of peripheral vasoconstriction and vasodilatation with the need to maintain the blood pressure.

The sympathetic system with its combination of activity through nervous pathways and the release of adrenaline from the adrenal medulla can control both the overall blood pressure and also flow to different organs. Both adrenaline and noradrenaline act differentially via α and β-receptors (p. 142