What determines our blood pressure? It probably comes as no surprise that it has a lot to do with the heart—the power and frequency of its beat helps determine how forceful the blood flow will be. But the heart isn’t alone. Our blood pressure is also influenced by features of the blood vessels, the amount of salt in our blood, and even our kidneys. Linking all of these factors together is a gene known as angiotensinogen (AGT).
If you’ve ever played with a garden hose, you probably know how to convert normal, passive water flow into a laser-like torrent—just put your thumb over the hose nozzle. It’s a predictable outcome because the same amount of water is being pushed through the hose, regardless of how wide the opening is. If you place your thumb over the opening, you reduce the amount of free space for water flow. As a result, the water pressure increases. This concept also applies to blood pressure.
Blood pressure can change over time
Like water flowing through a hose, the force of blood flow can be affected by the amount of available space in the blood vessels. Small muscles wrapped around blood vessels can constrict, causing the volume of the vessels to decrease and blood pressure to rise. This is important because increased blood pressure allows our body to rapidly transport blood and its contents—like oxygen, sugar, and other nutrients—to various parts of the body. During exercise, a person’s muscles need much more oxygen and sugar than they normally do. To accommodate this, the person’s blood pressure will rise. However, high blood pressure comes at a cost: Increased force from blood flow can damage blood vessels. For this reason, it’s important that our body keep a tight control on blood pressure. This is where AGT comes into play.
AGT is a gene that tells our body how to make the angiotensinogen protein. This protein is made in the liver and helps control blood pressure in many ways1,2. When the body needs to increase blood pressure, it will produce angiotensinogen and a protein known as renin. Renin will then break a small part of the angiotensinogen protein off. That little fragment will go on to be modified slightly by another protein (known as ACE), at which point it can alter blood pressure. In blood vessels, the modified angiotensinogen fragment promotes constriction of the muscles surrounding blood vessels, which leads to increased blood pressure1. It also has an indirect effect on our kidneys.
Kidneys function as a filtration system for our body. Excess water, salt, potassium, and other molecules in our blood are passed through them, and what we don’t need is excreted. In this role, the kidneys can control how much water is removed from the blood, which is a function that can be used when we need higher blood pressure. The modified angiotensinogen protein fragment can indirectly cause the kidney to reabsorb water and salt, which has chemical properties that help control the flow of the water. That water re-enters the blood flow and increases the blood volume. With more blood trying to flow through the same space, blood pressure increases1-3.
Variants in AGT may relate to blood pressure
For the most part, a person’s blood pressure stays within a consistent range, but that range may vary from person to person2-4. Research into why some people are predisposed to having high or low blood pressure has shown that changes in the DNA may be an important factor. One such change occurs in the AGT gene. By looking at many people’s DNA sequences along with their blood pressure, scientists have seen that a variant in the AGT gene may result in an elevated blood pressure relative to people without the variant2,5. Exactly how this change in the DNA affects the angiotensinogen protein is unclear, but some evidence indicates that the change could increase the amount of angiotensinogen that a person’s body makes2,5.
Decades of research has shown us that blood pressure is a complex trait that can be influenced by a person’s environment, habits, and genetics4. There are likely many genes that play a role in determining a person’s average blood pressure, one of which is AGT.
- “AGT Gene – Genetics Home Reference – NIH.” U.S. National Library of Medicine, National Institutes of Health, ghr.nlm.nih.gov/gene/AGT#normalfunction.
- Takeuchi, Fumihiko, et al. “Reevaluation of the Association of Seven Candidate Genes with Blood Pressure and Hypertension: a Replication Study and Meta-Analysis with a Larger Sample Size.” Hypertension Research, vol. 35, no. 8, 2012, pp. 825–831., doi:10.1038/hr.2012.43.
- Ehret, Georg B., and Mark J. Caulfield. “Genes for Blood Pressure: An Opportunity to Understand Hypertension.” European Heart Journal 34.13 (2013): 951–961. PMC. Web. 1 Oct. 2018.
- Zhao, Qi et al. “Progress and Future Aspects in Genetics of Human Hypertension.” Current hypertension reports 15.6 (2013): 676–686. PMC. Web. 1 Oct. 2018.
- Watkins, W. Scott et al. “Genotype – Phenotype Analysis of Angiotensinogen Polymorphisms and Essential Hypertension: The Importance of Haplotypes.” Journal of hypertension 28.1 (2010): 65–75. PMC. Web. 2 Oct. 2018.