The renin-angiotensin-aldosterone system (RAAS) plays a physiological role in regulating blood volume and systemic vascular resistance. The two together have an influence on cardiac output and arterial blood pressure. There are three important components to the RAAS; renin, angiotensin, and aldosterone.
Stimulation of renin from the juxtaglomerular cells (JG) is stimulated by sympathetic nerve activation through B1-adrenoceptors, renal hypotension or decreased sodium in the distal tubules of the kidney. A reduction in blood pressure in the afferent arterioles causes release of renin, and conversely increased arteriole pressure inhibits renin release. Specialized cells of the distal tubules; the macula densa sense the concentration of sodium and chloride ions in normal tubular fluid. When NaCl ions are elevated, renin is inhibited, and when there is a reduction in tubular NaCl the JG is stimulated to release renin. When arteriole pressure is reduced, there is a decreased GFR. The decreased GFR reduces NaCl in the distal tubule which is an important mechanism contributing to renin release.
Renin acts upon the substrate angiotensinogen the undergoes cleavage to form angiotensin I. The vascular endothelium has an enzyme; angiotensin converting enzyme (ACE), that cleaves angiotensin I to form angiotensin II. Angiotensin II carries out several important functions; it causes vasoconstriction resulting in systemic vascular resistance and increase in arterial pressure. It also stimulates sodium reabsorption that increases the sodium and water retention in the body. It acts on the adrenal cortex to release aldosterone. It stimulates the release of vasopressin otherwise known as antidiuretic hormone that increases fluid retention in the kidneys. It stimulates thirst because of the amount of sodium being reabsorbed. Lastly it stimulates cardiac hypertrophy.
The RAAS is not only regulated by internal inhibition and stimulation, but by natriuretic peptides (NPs) that are synthesized in the heart, brain and other organs. The physiological function of NPs is too decrease blood volume and systemic vascular resistance. NPs increase the glomerular filtration rate which causes increased sodium excretion (natriuresis) and increased fluid excretion (diuresis). They also inhibit renin release and decrease circulating levels of angiotensin II and aldosterone. This results in systemic vasodilation.