Angiotensin I may have some minor activity, but angiotensin II is more potent. Angiotensin II has a variety of effects on the body:
Throughout the body, it is a potent vasoconstrictor.
In the kidneys, it constricts glomerular arterioles, having a greater effect on efferent arterioles than afferent. As with most other capillary beds in the body, the constriction of afferent arterioles increases the arteriolar resistance, raising systemic arterial blood pressure and decreasing the blood flow. However, the kidneys must continue to filter enough blood despite this drop in blood flow, necessitating mechanisms to keep glomerular blood pressure up. To do this, Angiotensin II constricts efferent arterioles, which forces blood to build up in the glomerulus, increasing glomerular pressure. The glomerular filtration rate (GFR) is thus maintained, and blood filtration can continue despite lowered overall kidney blood flow.
In the adrenal cortex, it acts to cause the release of aldosterone. Aldosterone acts on the tubules (i.e. the distal convoluted tubules and the cortical collecting ducts) in the kidneys, causing them to reabsorb more sodium and water from the urine. Potassium is secreted into the tubule in exchange for the sodium, which is reabsorbed. Aldosterone also acts on the central nervous system to increase a person's appetite for salt, and to make them feel thirsty.
Release of Anti Diuretic Hormone (ADH) -- also called vasopressin -- ADH is made in the hypothalamus. ADH is stored and released from the pituitary gland.
These effects directly act to increase the amount of fluid in the blood, making up for a loss in volume, and to increase blood pressure.
A new drug called Aliskiren is being released in 2007 which directly inhibits renin.
Other uses of ACE
Interestingly, ACE cleaves a number of other peptides, and in this capacity is an important regulator of the kinin-kallikrein system.
Fetal renin-angiotensin system
In the fetus, the renin-angiotensin system is predominantly a sodium-losing system, as angiotensin II has little or no effect on aldosterone levels. Renin levels are high in the fetus, while angiotensin II levels are significantly lower — this is due to the limited pulmonary blood flow, preventing ACE (found predominantly in the pulmonary circulation) from having its maximum effect.