Hypertension: The Silent Killer

Hypertension, often called a silent killer, affects approximately 75 million adults in the United States today and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease (1). Hypertension is a chronic medical condition that is defined by elevated pressure in the arteries of the body. If left undetected, this asymptomatic disorder silently damages blood vessels in various parts of the body, including the heart, brain, and kidney (3).

History of Hypertension

The origins of this disease trace back to early 2600 B.C., when the ancient Chinese could only detect hypertension by the quality of one’s pulse and often referred to hypertension as the “hard pulse disease” (4). During this time period, the treatment of high blood pressure included bleeding through the use of leeches. It wasn’t until 1733 that English Reverend Stephan Hales discovered a method to directly measure blood pressure through tedious backyard experimentation on horses. The cumbersome device he invented measured approximately ten feet high. Schipione Riva-Rocci refined this design in 1896 and created a wraparound rubber cuff, known as a sphygmomanometer - this was the first portable device used to measure blood pressure (4). A few years later in 1905, Nikolai Korotkoff further developed the understanding of blood pressure by identifying systolic and diastolic sounds of the heart that he had heard with a stethoscope. These sounds, now referred to as “Korotkoff sounds”, are still a vital tool for the detection of high blood pressure(4). Despite these advances made in detecting high blood pressure, the etiology of the disease remained a mystery. At this time in the early 1900s, hypertension was thought of as a natural ad...

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...PB, and PLOD1 (17). These genes all affect hypertension by modifying the systolic and diastolic pressures in hypertension in unique ways. It was found that mutations in two of the five genes (AGTRAP and CLCN6) will decrease hypertension risk and mutations in the other three genes (NPPB, PLOD1, and MTHFR) will increase the risk for hypertension. Moreover, reanalysis of the human AGTRAP-PLOD1 locus showed that these findings could be highly implicated for treatment options in humans (17). This example of a GWAS study is one of many - further GWAS studies focused on understanding genetic components of hypertension will help to increase the current understanding of the pathology behind the disease (16). By having a thorough knowledge of the pathology, the opportunity arises for individualized treatment and novel therapeutic options for the prevention of hypertension.