RAASaktivitás

RAASaktivitás refers to the activity of the renin-angiotensin-aldosterone system, a hormonal cascade that helps regulate blood pressure, extracellular fluid volume, and electrolyte balance. It is principally driven by the kidneys, which release renin in response to reduced renal perfusion, sympathetic activation, or low sodium chloride delivery to the distal tubule.

In the cascade, renin cleaves angiotensinogen from the liver to angiotensin I; angiotensin-converting enzyme (primarily in pulmonary endothelium) converts it to angiotensin II, a potent vasoconstrictor. Angiotensin II stimulates aldosterone release from the adrenal cortex, promoting sodium and water reabsorption and potassium excretion, increasing blood pressure and volume. It also induces thirst and antidiuretic hormone release, reinforcing fluid retention.

Regulation of RAASaktivitás is largely controlled by negative feedback. Elevated blood pressure and improved renal perfusion suppress renin release; macula densa cells, baroreceptors, and sympathetic nerves modulate renin secretion depending on sodium chloride delivery and volume status.

Clinically, RAAS activity is assessed by measurements such as plasma renin activity or concentration and aldosterone levels, often in combination with other tests. Dysregulation contributes to hypertension, heart failure, chronic kidney disease, and diabetic nephropathy. Pharmacologic inhibitors targeting this system include ACE inhibitors, angiotensin II receptor blockers (ARBs), direct renin inhibitors, and mineralocorticoid receptor antagonists such as spironolactone and eplerenone, used to reduce cardiovascular and renal risk.

A local or tissue RAAS operates in organs like the heart, kidney, and brain, influencing organ function independently of circulating RAAS. In various conditions, angiotensin II–dependent pathways are targeted therapeutically to mitigate cardiovascular risk.