Читать книгу Understanding Anatomy and Physiology in Nursing - John Knight - Страница 134

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.