"Control of arterial blood pressure"

Arterial blood pressure is probably the most important variable in the circulation. As the arterial pressure follows a periodic rise and fall in each cardiac cycle, it is useful when referring to the arterial pressure to have a single value to consider. The value usually referred to is the mean arterial pressure. This is approximated to by:

Where,

P_a= mean arterial pressure.

P_d=diastolic pressure

P_s=systolic pressure.

It is not the direct mean of the systolic and diastolic pressures simply because the heart spends longer in diastole than in systole.

There are two values that directly affect mean arterial pressure. These are the arterial blood volume and the arterial compliance. Actions of physiological control mechanisms act to change these variables through various methods. Arterial blood volume is affected by both the cardiac output and by changes in the peripheral resistance. That is an increase in peripheral resistance will cause, transiently, a slower flow of blood out of the arterial system into the venous channels. Thus the arterial blood volume increases, and stretches the arteries. The elastic recoil of which increases the arterial pressure. Eventually the increase in arterial pressure will increase the flow of blood through the peripheral resistance and the system will reach a new state of equilibrium at the higher pressure. An increase in cardiac output will affect the arterial pressure through the same mechanism.

Further changes in effective arterial blood volume can be achieved through constriction of the vascular beds in the liver and spleen. These two organs provide a blood reserve to compensate for haemorrhage, although this is more marked in other species, for example, dogs.

The mean arterial pressure is not affected by changes in the arterial compliance, as the flow of blood through the system must, over large periods of time, match at both extremes. That is cardiac output must be matched to the flow of blood through the peripheral resistance. Flow of blood through the peripheral resistance is determined by two things:- arterial pressure (or rather the pressure difference between arterial and venous pressure although venous pressure can be considered constant in this case) and the peripheral resistance. Any increase in cardiac output must be met by an increase in flow through the peripheral resistance. If the peripheral resistance remains constant this can only occur through an increase in arterial blood pressure. Not only that but regardless of the compliance of the arteries there is only one value the arterial pressure can take.

Changes in compliance do, however, affect pulse pressure. Noticeable effects of this are in old age. As the arteries lose their compliance and become stiffer it takes less blood volume to reach higher pressures. The heart is faced with pumping blood into a higher arterial pressure. The left ventricle has more work to do and partly in reaction to this begins to hypertrophy in old age.

Short term control mechanisms exist to control the blood pressure during postural changes, haemorrhage or other acute stresses. Long term controls exist that adjust blood volume and microcirculatory architecture to adjust to long term changes in circulatory pressure. I will mainly be looking here at short term controls of arterial blood pressure.

Peripheral resistance

Most reflex control of arterial blood pressure is performed through regulation of the peripheral resistance. The main vessels responsible for changes in peripheral resistance are the arterioles. They react in response to either extrinsic, neural signals or in reaction to local conditions in the tissues. The balance of which control method dominates depends on the tissues in question; for example the skin and splanchnic regions are under considerable neural control whereas the brain and heart are controlled more by local mediators.

Local changes in the peripheral resistance mediated redistributions of the blood flow through various tissues. It is rare for this to effect overall arterial pressure. Overall arterial pressure is more often controlled by the CNS.

The parts of the brain involved in regulating cardiovascular output reside in the medulla. It has both a pressor region that when stimulated increases vasoconstriction, cardiac acceleration and enhances myocardial contractility. It also has a depressor region that lowers blood pressure when stimulated. Fibres from the vasoconstrictor region pass to the respective blood vessels via the sympathetic chains.

The medulla exerts its control in response to signals arising in the baroreceptors, chemoreceptors, hypothalamus, cerebral cortex and skin. The medulla can also be affected directly by changes in blood concentrations of CO₂ and O₂.

Arterial

These are stretch receptors located in the carotid sinus and the transverse aortic arch. They consist of a mesh of nerve fibres in the adventitia of their respective blood vessels. (The carotid sinus being a small thinning of the arteries in the junction between the interior and exterior carotid arteries.) Stretching of the arterial wall (in response to an increase in arterial pressure) leads to an increase in the firing frequency of these receptors. In an isolated preparation as the pressure rises a rapid serious of impulses is given out, settling down to a high frequency of firing once the pressure has settled again. In vivo this means that on the upstroke of systole the baroreceptors give off a rapid series of three or four pulses and then fall silent and the pressure drops in diastole. It has been found that the baroreceptors in the carotid sinus are more sensitive to changes in pressure than the aortic ones. On the other hand the aortic baroreceptors retain their ability to distinguish pressure differences for much higher arterial pressures.

Impulses from the carotid sinus pass up to the glossopharyngeal nerve to the nucleus of the tractus solitarius in the medulla. The aortic baroreceptors reach this region by the vagus nerves. Stimulation of this region inhibits sympathetic nerve impulses to the peripheral blood vessels. Legions sin this region produce vasoconstriction. An increase in firing frequency causes inhibition of vasoconstrictor regions. Thus there is a lowering of blood pressure. The lowering of the arterial pressure is also aided by stimulation of the vagal nerves which brings about a bradycardia.

Cardiopulmonary

These exist in parallel to the arterial receptors and come in two versions. A receptors are activated by tension developed during atrial contraction. B receptors are activated by the tension developed during atrial filling. Signals are sent up vagal fibres to the vagal centre in the medulla. Activation of these receptors causes a lowering of blood pressure by inhibiting the vasoconstriction centre in the medulla. They would appear to operate by inhibiting angiotensin, aldosterone and vasopressin release. They are also involved in long term blood pressure regulation by mediating blood volume. The release of angiotensin and aldosterone contribute to water retention as does the release of renin and anti-diuretic hormone

Peripheral Chemoreceptors

These small bodies occur near to the aortic and carotid barorecepters. Although they primarily control respiration they also have a small effect on vasomotor regions. They principally measure O₂ and CO₂ tension as well as blood pH. When stimulated they act to potentiate the action of the baroreceptors (when blood pressure is low alongside hypoxia or hypercapnia). When the two sets of receptors are opposing each other it is the action of the baroreceptors that predominates.

Central Chemoreceptors

More important than the reaction of the peripheral chemoreceptors to changes in carbon dioxide tension are the chemosensitive regions of the medulla. A rise in arterial CO₂ tension stimulates these regions of the medulla and increases peripheral resistance (and hence increase arterial pressure).

Hypothalamus

The hypothalamus is involved with behavioural and emotional control of the cardiovascular system, such as the increase in heart rate associated with anticipation of exercise. When stimulated the anterior region leads to a fall in blood pressure. The posterolateral region however leading to a rise in blood pressure and tachycardia. The temperature regulating centre of the hypothalamus is also responsible for mediating vasoconstriction but is more concerned with diverting blood to and from the skin vessels in order to regulate the temperature.

Cerebrum

Stimulation of motor and pre-motor regions here may lead to a rise in blood pressure through vasoconstriction. However some vasodilatation responses may be produced as in blushing and fainting.

Pulmonary reflex

The vagus nerves are again involved in these effects. The inflation of the lungs through inspiration leads to systemic vasodilation and lowering of blood pressure. Were they to collapse there would be systemic vasoconstriction.

(c)1998 Nick Manville