pressure is particularly important for changes in posture or when engaging in strenuous physical activities. The baroreceptor responses highlighted below are classic examples of homeostatic negative feedback (Chapter 2) where deviations from normal systolic and diastolic BP are resisted and BP is normalised.
Many things can cause a drop in BP but a common cause is suddenly standing up (Figure 3.11).
Figure 3.11 Neural responses to decreased BP
In the situation in Figure 3.11, gravity will pull arterial blood downwards (arteries have no valves), leading to a significant drop in BP. If BP is not restored rapidly, there is a risk of reducing cerebral blood flow, potentially leading to dizziness and fainting (syncope). This phenomenon is termed postural hypotension or orthostatic intolerance and becomes more common with age. An understanding of postural hypotension is essential for nurses, so to develop your understanding further read through Janet’s case study before attempting Activity 3.4.
Case study: Janet – postural hypotension
Janet is a 71-year-old woman who has recently returned home following a long 10-day stay in hospital recovering from a severe bout of pneumonia. Janet has hypertension which has for many years been treated successfully using a combined beta blocker and diuretic. When Janet stood up to make herself a cup of tea she promptly fainted, hitting her head on a coffee table as she fell. Fortunately, her partner was with her and able to drive her quickly to A&E for stitches and a full assessment.
As a nurse, you should be able to link your knowledge of human anatomy and physiology to patient histories.
Activity 3.4 Evidence-based practice and research
From what you have learnt in this chapter, describe what is likely to have caused Janet’s faint. Could this be related to her recent hospital stay or blood pressure medication?
You should now have a good understanding of the nature of postural hypotension and the risk of falls associated with this condition. Although postural hypotension becomes more common in older people, high blood pressure affects a much greater proportion of the population.
Increased BP may occur as a result of disease (e.g. atherosclerosis), stress or simply through increased sodium (salt) consumption (Figure 3.12). Hormonal mechanisms tend to be more effective in reducing elevated BP; however, neural mechanisms also play a more immediate role.
Figure 3.12 Neural responses to increased BP
In addition to the rapid neural adjustments to BP that are required as a result of postural changes, it is essential that BP is controlled and maintained over the longer term. It is here that hormonal mechanisms play the dominant role.
Hormonal control of blood pressure
Hormones are chemical signals which are transported to their sites of action in the blood (Chapter 5). A multitude of hormones are involved in regulating blood pressure and there is much synergy (working together) between these and also much interplay between the hormonal mechanisms and neural mechanisms described above.
Antidiuretic hormone (ADH)
Also known as vasopressin, ADH is a neuropeptide hormone (small protein produced by nerve cells) that is synthesised in the hypothalamus. Once produced, ADH is transported along the axons of hypothalamic neurones to be stored in the posterior pituitary gland. There are several potential triggers that stimulate the release of ADH, including a decrease in BP as detected by the aortic arch and carotid sinus baroreceptors, an increase in blood concentration as detected by hypothalamic osmoreceptors (receptors that measure the osmotic potential of the blood) and the presence of angiotensin-II from the rennin angiotensin aldosterone mechanism (see section on RAAS below).
Physiological actions of ADH
The term antidiuretic hormone is applied to this hormone since its major effect is to reduce urine output by the kidneys, leading to the production of dark, concentrated urine (Chapter 11). When BP is low this is an ideal strategy, since by reducing urine production more water remains in the blood, boosting plasma volume and increasing BP. ADH further increases BP by stimulating arterial vasoconstriction.
Conversely, when the aortic arch and carotid sinus baroreceptors detect an increase in BP the release of ADH from the posterior pituitary is reduced or stopped. This leads to the production of a large volume of dilute urine, effectively allowing the body to ‘dump’ blood volume in the form of dilute urine to reduce BP. Simultaneously, reduced levels of ADH will reduce arterial vasoconstriction to further reduce BP.
Atrial natriuretic peptide (ANP)
This hormone is produced by the atria of the heart in response to increased blood volume. If blood volume increases, the atria are subjected to increased stretch, with the atrial myocytes (muscle cells) releasing ANP at concentrations proportional to the degree of stretch. ANP is a powerful natural diuretic peptide and stimulates the kidneys to produce a large amount of dilute urine to normalise the total blood volume. ANP and ADH can be seen to be antagonistic to each other in terms of regulating blood volume and blood pressure. The physiology of these hormones and their effects on the kidney are discussed in greater detail in Chapter 11.
Adrenaline (epinephrine)
Adrenaline is produced by the central portion of the adrenal glands (adrenal medulla) and is the body’s major fight-or-flight hormone. Adrenaline is released during periods of excitement or fear and functions primarily to prepare the body for immediate action. Adrenaline is a catecholamine hormone which, when released into the blood, has powerful physiological effects, many of which are mediated through activation of the sympathetic nervous system (Chapter 5). Here we focus on its influence on BP.
Cardiovascular effects of adrenaline
Adrenaline increases the heart rate and cardiac output by binding to beta (β) adrenergic receptors at the pacemaker (SAN). The drugs termed β blockers block adrenaline and noradrenaline from binding, thereby slowing the heart rate and reducing cardiac output and BP. Until recently β blockers such as atenolol were frequently prescribed to treat hypertension, but their use in treating this condition has now been largely superseded by ACE inhibitors (see below).
Adrenaline promotes vasoconstriction of blood vessels in the skin and gut: during periods of adrenaline release, the skin may take on an ashen appearance and many people complain of a feeling of butterflies in the stomach, which is thought to correspond to vasoconstriction in the gut. Simultaneously, adrenaline promotes vasodilation of blood vessels in the lungs and muscles, ensuring that blood is diverted to the key areas required for a fight-or-flight response.
The net result of increased cardiac output and changes in vascular tone mediated through adrenaline is a sudden increase in BP.
The renin angiotensin aldosterone system (RAAS)
The RAAS is the most important hormonal mechanism for maintaining blood pressure over the long term. It is a cascade mechanism that involves several major organs working together. At the centre of this cascade is the inert plasma protein angiotensinogen, which is continually produced by the liver and found as a normal component of the blood (Figure 3.13).