The renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood pressure and fluid balance. It plays a critical role in cardiovascular physiology by controlling the volume of fluids in the body and systemic vascular resistance.
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RAAS activation begins with the release of renin from the kidneys in response to low blood pressure or low sodium levels.
Renin converts angiotensinogen, produced by the liver, into angiotensin I, which is then converted into angiotensin II primarily by the enzyme ACE (angiotensin-converting enzyme).
Angiotensin II has multiple effects: it causes vasoconstriction, stimulates aldosterone secretion from the adrenal cortex, and promotes sodium reabsorption in the kidneys.
Aldosterone increases sodium and water reabsorption while promoting potassium excretion, leading to increased blood volume and blood pressure.
Pharmacological drugs targeting RAAS include ACE inhibitors, angiotensin II receptor blockers (ARBs), and aldosterone antagonists, used to manage conditions such as hypertension and heart failure.
Review Questions
What triggers the release of renin from the kidneys?
Describe how angiotensin I is converted to angiotensin II.
What are the primary physiological effects of angiotensin II?
Medications that block aldosterone receptors, reducing sodium reabsorption and lowering blood pressure.
Angiotensin II Receptor Blockers (ARBs): Drugs that block the action of angiotensin II at its receptor sites, leading to vasodilation and reduced blood pressure.
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