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AGT
SNP Table
Summary
The AGT gene encodes angiotensinogen, a protein that helps control blood pressure and inflammation. Variants of AGT may play a role in high blood pressure by increasing angiotensinogen production, as well as Crohn’s Disease. Diet and supplement modifications may counteract the effects of this variant by blocking an enzyme involved in the renin-angiotensin system [R].
Angiotensinogen is part of the renin-angiotensin system (RAS). This system regulates blood pressure and the balance of fluids and salts in the body [R].
This protein is transformed into other proteins, which can [R, R]:
- Narrow the blood vessels (vasoconstriction)
- Expand the blood vessels (vasodilation)
- Prevent the loss of water through the kidneys (antidiuresis)
- Prevent blood clotting (antithrombosis)
Mutations in AGT can cause [R]:
- Kidney problems
- High blood pressure
- Low blood pressure
Protein names
Found in These Blog Articles
GHR Function
The AGT gene provides instructions for making a protein called angiotensinogen. This protein is part of the renin-angiotensin system, which regulates blood pressure and the balance of fluids and salts in the body. In the first step of this process, angiotensinogen is converted to angiotensin I. Through an additional step, angiotensin I is converted to angiotensin II. Angiotensin II causes blood vessels to narrow (constrict), which results in increased blood pressure. This molecule also stimulates production of the hormone aldosterone, which triggers the absorption of salt and water by the kidneys. The increased amount of fluid in the body also increases blood pressure. Proper blood pressure during fetal growth, which delivers oxygen to the developing tissues, is required for normal development of the kidneys, particularly of structures called the proximal tubules, and other tissues. In addition, angiotensin II may play a more direct role in kidney development, perhaps by affecting growth factors involved in the development of kidney structures.
More Information
AGT and Blood Pressure
The AGT gene codes for angiotensinogen, the first player in the renin-angiotensin system (RAS). RAS involves multiple precursors and enzymes that ultimately function to raise blood pressure when blood pressure is low [R, R].
The resulting product of RAS is angiotensin II, which promotes blood vessel constriction. Angiotensin II can also boost aldosterone, a hormone that signals the kidneys to reabsorb sodium and water and excrete potassium. High water retention increases blood volume, putting more pressure on blood vessels [R].
Renin from kidneys converts angiotensinogen into angiotensin I. Next, the ACE enzyme converts angiotensin I to angiotensin II (AII), the bioactive form that narrows blood vessels. Besides this well-studied role, RAS and AII also contribute to wound healing, inflammation, and more [R, R].
A variant of AGT has been associated with high blood pressure. This variant may increase angiotensinogen production, thereby promoting the production of angiotensin II and aldosterone [R].
In an attempt to ameliorate high blood pressure (hypertension), scientists have formulated drugs that block RAS. Some of these medications inhibit angiotensin-converting enzyme (ACE), which would otherwise help convert precursor angiotensin I to angiotensin II [R].
The Role of Angiotensin in Crohn’s Disease
Crohn’s disease (CD) is a subtype of inflammatory bowel disease (IBD), an autoimmune condition caused by a mixture of genetic and environmental factors. It mostly affects the small intestine and involves ulcerations of all cell layers of the gut lining [R, R, R].
Angiotensin II and other RAS components function as gut cytokines and control inflammation, scarring, and wound healing. Crohn’s disease patients have increased levels of AII in the gut lining, compared with healthy controls or patients with ulcerative colitis (UC) [R, R].
AII contributes to granulomatous inflammation, which is common in the gut of CD but not UC patients. It may enhance gut scarring via TGF-beta1 and increase inflammatory cytokines such as TNF-alpha [R, R, R].
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