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One of the proteins present in the blood is called angiotensinogen. This is a short protein produced by the liver and is inactive; it just circulates in the blood. However, when renin acts on angiotensinogen it converts it into another shorter protein called angiotensin I. As angiotensin I passes through the lungs it is converted into angiotensin II by an enzyme called angiotensin converting enzyme (ACE). Angiotensin II is a powerful vascular vasoconstrictor; this will increase peripheral resistance which will in turn increase blood pressure. In addition to increasing BP by direct vasoconstriction angiotensin II also stimulates the secretion of aldosterone from the adrenal cortex. This will increasethe amount of sodium reabsorbed from the renal tubules and so increase levels of sodium in the blood. As mentioned, increased levels of sodium increases the osmotic potential of the blood and so it attracts more water. This means more water is retained in the plasma increasing blood volumes. These increased volumes will increase venous return and so blood pressure. Conversely, lower amounts of angiotensin II will reduce aldosterone secretion leading to more sodium excretion. This will lower sodium levels in the blood leading to lowered blood volumes and so lower BP. If the systemic blood pressure is increased the pressure in the afferent arteriole will also be increased. This will be detected by the JGA cells which will respond by reducing renin secretion. When less renin is present in the blood, more angeotensionogen will remain in inactive form. This renin-angiotensin-aldosterone mechanism allows the kidneys to regulate their own blood flow to an extent. When an organ regulates itself in this way it is called autoregulation. If for any reason the kidneys over-secrete renin blood pressure will be raised. An abnormally high BP is termed hypertension. Renin excess probably explains most cases of chronic hypertension. You may have come across ACE inhibiting drugs; these inhibit ACE (angiotensin converting enzyme) and so inhibit the conversion of angiotensin I into angiotensin II. If there is less angiotensin II there will be less vasoconstriction and less secretion of aldosterone and so blood pressure will be lowered.

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