The kidneys rule the vessels. They are all about the pressure. They thrive on it. If the kidney is not getting enough pressure, it releases renin. This enzyme uses the angiotensinogen from the liver to make Angiotensin I. Angiotensin I is then affected by Angiotensin Converting Enzyme (ACE) released by the lungs and kidney, an alliance to get the pressure to increase. ACE changes the Angiotensin I to Angiotensin II, and this chemical knows how to get things done. It affects a cascade of events that result in higher pressure and perfusion of the kidneys.

It switches the system to sympathetic mode. This increases cardiac output and decreases perfusion of non-essential organs. Sympathetic stimulation of the adrenal glands releases aldosterone to increase water retention, sodium absorption, and potassium excretion. It causes the arterioles to contract, thereby increasing the vascular resistance and blood pressure. Lastly, it stimulates the pituitary gland to release antidiuretic hormone (ADH). This hormone increases water retention. Since the vascular system is like a closed pumping system, more water in the pipes makes the pressure higher. Think of it like putting your thumb over the end of a running garden hose. The water that escapes through the more narrow opening is thinner, but faster, due to higher pressure.

If a patient has chronic hypo-perfusion to the kidneys due to arteriosclerosis, then they will have chronic hypertension as a result of the kidney constantly demanding more pressure. This pressure is not kidney specific, unfortunately, and puts the patient at risk of stroke, heart attack, and vascular damage. There are many other causes of renal hypo-perfusion, this is just one common example.

The medications that affect this system mostly affect the enzymes and hormones released due to the kidney’s distress signal of renin release. There are four kinds: beta blockers, ACE inhibitors, Angiotensin Receptive Blockers (ARBs), and direct renin inhibitors. The last three types of medications do exactly what their names imply. The ACE inhibitors are only good at stopping one piece of the cascade, so ARBs are often prescribed in conjunction to complete the block. Beta blockers decrease renin release, decrease the sympathetic response, thereby decreasing aldosterone release from the adrenal glands.

A side effect that patients should be warned about is cough. This can decrease medication compliance. Since aldosterone affects potassium excretion, blocking it artifically can cause potassium levels to become elevated, so caution patients to avoid salt substitutes. They should also be aware of the warning signs/symptoms of hyperkalemia such as irregular heart beat, paresthesia, fatigue, and shortness of breath.

This complex system is wonderful for keeping the organs alive and functioning in moments of trauma and crisis. When the system is fooled by a disease process, understanding the basic physiology can help the nurse make critical thinking decisions about the care and teaching of this patient population.