McKenna's Pharmacology for Nursing, 2e

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P A R T 8  Drugs acting on the cardiovascular system

Hypertension When a person’s blood pressure is above normal limits for a sustained period, a diagnosis of hypertension is made (Table 43.1). In New Zealand, heart disease that includes hypertension accounted for 30% of all deaths in the 2006 census. Ma– ori people were the main ethnic group highly represented for cardiovascular death. In Australia, the Australian Bureau of Statistics (2014) reported in 2012–13 that 20% of the Indigenous popu- lation over the age of 55 years had hypertension. Ninety percent of the people with hypertension have what is called essential hypertension , or hypertension with no known cause. People with essential hyperten- sion usually have elevated total peripheral resistance. Their organs are being perfused effectively, and they usually display no symptoms. A few people develop secondary hypertension, or high blood pressure result- ing from a known cause. For instance, a tumour in the adrenal medulla called a phaeochromocytoma can cause hypertension related to the release of large amounts of noradrenaline from tumour cells, which resolves after the tumour is removed. The underlying danger of hypertension of any type is the prolonged force on the vessels of the vascular system. The muscles in the arterial system eventually thicken, leading to a loss of responsiveness in the system. The left ventricle thickens because the muscle must constantly work hard to expel blood at a greater force. The thick- ening of the heart muscle and the increased pressure that

Low blood pressure or poor oxygenation of a nephron causes the release of renin from the juxta­ glomerular cells, a group of cells that monitor blood pressure and flow into the glomerulus. Renin is released into the bloodstream and arrives in the liver to convert the compound angiotensinogen (produced in the liver) to angiotensin I. Angiotensin I travels in the bloodstream to the lungs, where the metabolic cells of the alveoli use angiotensin-converting enzyme (ACE) to convert angio­ tensin I to angiotensin II. Angiotensin II reacts with specific angiotensin II receptor sites on blood vessels to cause intense vasoconstriction. This effect raises the total peripheral resistance and the blood pressure, restoring blood flow to the kidneys and decreasing the release of renin. Angiotensin II, probably after conversion to angio- tensin III, also stimulates the adrenal cortex to release aldosterone. Aldosterone acts on the nephrons to cause the retention of sodium and water. This effect increases blood volume, which should also contribute to increas- ing blood pressure. The sodium-rich blood stimulates the osmoreceptors in the hypothalamus to cause the release of antidiuretic hormone (ADH), which in turn causes retention of water in the nephrons, further increasing the blood volume. This increase in blood volume increases the blood pressure, which should increase blood flow to the kidneys. This should lead to a decrease in the release of renin, thus causing the compensatory mechanisms to stop (Figure 43.2).

2 Liver produces

3 Activation of angiotensin I to angiotensin II occurs in the pulmonary capillary bed by a converting enzyme.

angiotensinogen.

Renin reacts with angiotensinogen to form angiotensin I

Angiotensin I

Angiotensin II

Juxtaglomerular cells

Glomerulus

Efferent arteriole

Decreased perfusion pressure in the afferent arteriole stimulates secretion of renin by the juxtaglomerular cells.

1

Arteriole

Angiotensin II receptors

ADH release and water retention to blood volume. Sodium retention

4

Angiotensin II: a powerful vasoconstrictor

Afferent arteriole

5

6

Aldosterone causes increased sodium and water reabsorption by the tubules of the kidney. Result is increased blood volume.

Angiotensin II becomes angiotensin III which causes the release of aldosterone from the adrenal cortex.

FIGURE 43.2  The renin–angiotensin–aldosterone system.