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Angiotensin II: A Major Vasoconstrictor Of Blood Vessels
Becoming overweight and fat is associated with many metabolic disorders, but a common medical problem with obesity is high blood pressure. With increasing weight gain and increases in adipose tissue, the body tries to maintain a desirable bodyweight by increasing catecholamines or adrenaline to burn body fat. It’s well recognized that adrenaline or catecholamines not only increase fat mobilization, but will increase blood pressure through increased activation of the nervous system. Long-term activation of the sympathetic nervous system is thought to be one of the key mechanisms underlying obesity-associated hypertension.1 A powerful hormone that increases blood pressure by inducing vasoconstriction (i.e., narrowing of blood vessels. When blood vessels constrict, the flow of blood is restricted or slowed.) is angiotensin II (ANG II). Many people with high blood pressure are prescribed what’s called ACE inhibitors, which are medications that slow the activity of the enzymes, which decrease the production of ANG II. As a result, the blood vessels enlarge or dilate, and the blood pressure is reduced.
Angiotensin II: A Major Inhibitor Of Adipose Tissue Blood Supply
 It has recently been documented that ANG II is expressed also in both white and brown adipose cells.2, 3 In a recent study, injections of ANG II into subcutaneous adipose tissue led to an inhibition of fat mobilization in healthy volunteers.4 So what the hell is going on in adipose tissue that would inhibit fat mobilization? ANG II could be nicknamed the “python hormone” because it squeezes blood vessels, allowing less blood flow, which is bad news for burning body fat. When you want to increase fat burning, having a rich blood supply will facilitate lots of fats being mobilized from adipose tissue. It has been shown that when ANG II is infused into the forearm during exercise, it reduces blood supply to the forearm. Now, the results can be carried over to adipose tissue as well. This reduced fat-burning effect could be at least partly dependent on ANG II’s vasoconstricting ability (reducing blood supply) in abdominal subcutaneous adipose tissue.14, 15, 16
ANG II reduces adipose tissue blood flow in a dose-dependent manner (the more ANG II produced by adipose tissue, the lower the adipose tissue blood flow15). It’s interesting that adipose tissue blood flow has been reported to be lower in obese individuals, and weight reduction was followed by an increase in adipose tissue blood flow.5 Furthermore, weight loss by approximately 5 percent led to a reduction in ANG II in adipose tissue by 20 percent.6 Reducing ANG II with pharmacological blockade by ANG II inhibitors will not only reduce blood pressure in obese people, but it also increases blood flow in adipose tissue and causes weight loss.14 ANG II not only reduces blood supply to adipose tissue and inhibits fat burning, but may also stimulate fat-mass gain through the following mechanisms:
• ANG II causes stimulation of alpha2-adrenoceptors, which inhibit fat mobilization.9 The alpha2-receptors on fat cells are like the “Soup Nazi” character from the “Seinfeld” series. Once activated, they say: “No fat mobilization for you!” An increase in alpha receptors result in increased fat storage.
• ANG II also increases the activity of fat-storing enzymes (glycerol-3-phosphate dehydrogenase and fatty acid synthase).10
• ANG II causes insulin resistance in large fat cells and causes increased storage of lipids. Administration of ACE inhibitors (block ANG II production) has been shown to enhance insulin sensitivity and reduce fat mass.4
• ANG II levels are increased by plasma cortisol, smoking, high-fat diets and estrogen.
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Research and Review 
