An enzyme released into the blood by cells of the kidney. Through a series of chemical reactions, renin converts angiotensinogen (a protein released into the blood by the liver) to angiotensin I. As blood passes through the lungs, angiotensin I is converted into angiotensin II, a highly potent vasoconstrictor (an agent that induces narrowing of the blood vessels). Angiotensin II stimulates the adrenal cortex to release aldosterone, a hormone that enhances sodium ion reabsorption by the kidneys. Sodium then moves into the blood, followed by water, and both blood volume and blood pressure rise.
Though renin itself has no effect on blood pressure, angiotensin II does. An excess of angiotensin II can lead to hypertension, or high blood pressure. The extra stress of hypertension on the heart can damage the lining of the arteries, and, if left untreated, can cause the arteries to narrow or become completely blocked.
Nearly 60% of people with Type 2 diabetes have hypertension, and people with both hypertension and diabetes face a high risk of cardiovascular disease. Fortunately, drugs such as angiotensin-converting enzyme (ACE) inhibitors and beta-blockers have been found to lower blood pressure. ACE inhibitors prevent the formation of angiotension II. This causes the arteries to dilate and, in effect, lowers blood pressure. Beta-blockers lower blood pressure by blocking the effects of adrenaline (also called epinephrine), a hormone that increases heart rate and contractility, and inhibiting renin secretion by the kidney.
Some studies have shown an association between increased renin activity and a cluster of cardiovascular disease risk factors called Syndrome X, or metabolic syndrome. These risk factors include insulin resistance (one of the major underlying problems in Type 2 diabetes), high triglycerides, low HDL (“good”) cholesterol, and some others.