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).
Figure 3.13 Overview of the RAAS
Source: OpenStax (2013) Anatomy and Physiology. Rice University. Available at: https://openstax.org/books/anatomy-and-physiology/pages/1-introduction
Biochemical steps in the RAAS
The RAAS is triggered whenever there is a drop in blood pressure and follows a set series of events, which are highlighted below.
When BP falls, the kidneys release an enzyme termed renin (Chapter 11).
Renin rapidly converts angiotensinogen into the protein angiotensin-I.
Angiotensin-1 is inert and has no biological activity; it circulates freely in the blood until it reaches the lungs.
Within the lung tissue are located the angiotensin-converting enzymes (ACEs). These convert the inert angiotensin-I into its biologically active form angiotensin-II.
Angiotensin-II binds to receptors on smooth muscle cells in the tunica media (muscle layer) of arteries to initiate vasoconstriction. The process of vasoconstriction increases peripheral resistance (PR), helping to restore BP (remember, this mechanism was triggered by a drop in BP).
Angiotensin-II stimulates the release of aldosterone from the adrenal cortex.
Aldosterone promotes sodium retention by the kidneys, increasing plasma sodium levels. Sodium attracts water from the tissues into the blood (water follows sodium) by osmosis, increasing blood volume and pressure.
Angiotensin-II stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary gland. As described previously, ADH increases blood volume by reducing urine output while simultaneously inducing vasoconstriction.
The end result of the RAAS is that blood pressure is restored and maintained.
Now you have completed this chapter, attempt the multiple-choice questions in Activity 3.5 to assess your knowledge.
Activity 3.5 Multiple-choice questions
1 Which of the following layers of the heart is composed predominantly of branched cardiac muscle fibres?a) The endocardiumb) The epicardiumc) The myocardiumd) The visceral pericardium
2 The bicuspid (mitral valve) is locateda) Between the left atrium and left ventricleb) Between the right atrium and right ventriclec) At the origin of the pulmonary arteriesd) At the origin of the aorta
3 During which phase of the cardiac cycle does 70 per cent of the atrial blood volume pass into the ventricles?a) Isovolumetric contractionb) Passive ventricular fillingc) Ejectiond) Atrial systole
4 Which of the following resting heart rates would be referred to as tachycardia?a) 90 bpmb) 45 bpmc) 112 bpmd) 75 bpm
5 Which of the following areas of the cardiac conductive system acts as the heart’s natural pacemaker?a) The
