History of hypertension

From Wikipedia, the free encyclopedia
Jump to: navigation, search

The modern history of hypertension begins with the understanding of the cardiovascular system with the work of physician William Harvey (1578–1657), who described the circulation of blood in his book "De motu cordis". The English clergyman Stephen Hales made the first published measurement of blood pressure in 1733.[1][2] Descriptions of hypertension as a disease came among others from Thomas Young in 1808 and especially Richard Bright in 1836.[1] The first report of elevated blood pressure in a person without evidence of kidney disease was made by Frederick Akbar Mahomed (1849–1884).[3] However hypertension as a clinical entity really came into being in 1896 with the invention of the cuff-based sphygmomanometer by Scipione Riva-Rocci in 1896.[4] This allowed blood pressure to be measured in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is ausculated with a stethoscope while the sphygmomanometer cuff is deflated.[2]

The term essential hypertension ('Essentielle Hypertonie') was coined by Eberhard Frank in 1911 to describe elevated blood pressure for which no cause could be found.[5] In 1928, the term malignant hypertension was coined by physicians from the Mayo Clinic to describe a syndrome of very high blood pressure, severe retinopathy and adequate kidney function which usually resulted in death within a year from strokes, heart failure or kidney failure.[6] A prominent individual with severe hypertension was Franklin D. Roosevelt.[7] However, while the menace of severe or malignant hypertension was well recognised, the risks of more moderate elevations of blood pressure were uncertain and the benefits of treatment doubtful. Consequently, hypertension was often classified into "malignant" and "benign". In 1931, John Hay, Professor of Medicine at Liverpool University, wrote that "there is some truth in the saying that the greatest danger to a man with a high blood pressure lies in its discovery, because then some fool is certain to try and reduce it".[8][9] This view was echoed by the eminent US cardiologist Paul Dudley White in 1937, who suggested that "hypertension may be an important compensatory mechanism which should not be tampered with, even if we were certain that we could control it".[10] Charles Friedberg's 1949 classic textbook "Diseases of the Heart",[11] stated that "people with 'mild benign' hypertension ... [defined as blood pressures up to levels of 210/100 mm Hg] ... need not be treated".[9] However the tide of medical opinion was turning: it was increasingly recognised in the 1950s that "benign" hypertension was not harmless.[12] Over the next decade increasing evidence accumulated from actuarial reports[2][13] and longitudinal studies, such as the Framingham Heart Study,[14] that "benign" hypertension increased death and cardiovascular disease, and that these risks increased in a graded manner with increasing blood pressure across the whole spectrum of population blood pressures. Subsequently, the National Institutes of Health also sponsored other population studies, which additionally showed that African Americans had a higher burden of hypertension and its complications.[15]

Historically the treatment for what was called the "hard pulse disease" consisted in reducing the quantity of blood by blood letting or the application of leeches.[1] This was advocated by The Yellow Emperor of China, Cornelius Celsus, Galen, and Hippocrates.[1]


In the 19th and 20th centuries, before effective pharmacological treatment for hypertension became possible, three treatment modalities were used, all with numerous side-effects: strict sodium restriction (for example the rice diet[1]), sympathectomy (surgical ablation of parts of the sympathetic nervous system), and pyrogen therapy (injection of substances that caused a fever, indirectly reducing blood pressure).[1][15] The first chemical for hypertension, sodium thiocyanate, was used in 1900 but had many side effects and was unpopular.[1] Several other agents were developed after the Second World War, the most popular and reasonably effective of which were tetramethylammonium chloride and its derivative hexamethonium, hydralazine and reserpine (derived from the medicinal plant Rauwolfia serpentina).

A major breakthrough was achieved with the discovery of the first well-tolerated orally available diuretics, the first of which was chlorothiazide,[1] which was derived from the antibiotic sulfanilamide and became available in 1958.[1][16]

A randomized controlled trial sponsored by the Veterans Administration comparing hydrochlorothiazide plus reserpine plus hydralazine versus placebo had to be stopped early because those not receiving treatment developed many more complications and it was deemed unethical to withhold treatment from them. The study continued in people with lower blood pressures and showed that treatment even in people with mild hypertension more than halved the risk of cardiovascular death.[9] w[17] In 1975, the Lasker Special Public Health Award was awarded to the team that developed chlorothiazide.[15] The results of these studies prompted public health campaigns to increase public awareness of hypertension and promoted the measurement and treatment of high blood pressure. These measures appear to have contributed at least in part to the observed 50% fall in stroke and ischemic heart disease between 1972 and 1994.[15]

Soon more drugs became available to treat hypertension. The British physician James W. Black developed beta blockers in the early 1960s;[18] these were initially used for angina, but turned out to lower blood pressure. Black received the 1976 Lasker Award and in 1988 the Nobel Prize in Physiology or Medicine for his discovery.[15] The next class of antihypertensives to be discovered were calcium channel blockers. The first member was verapamil, a derivative of papaverine that was initially thought to be a beta blocker and used for angina, but then turned out to have a different mode of action and was shown to lower blood pressure.[15] The renin-angiotensin system was known to play an important role in blood pressure regulation, and angiotensin converting enzyme (ACE) inhibitors were developed through rational drug design. In 1977 captopril, an orally active agent, was described;[19] this led to the development of a number of other ACE inhibitors.[15] More recently angiotensin receptor blockers and renin inhibitors have also been introduced as antihypertensive agents.[20][21]


  1. ^ a b c d e f g h i Esunge PM (October 1991). "From blood pressure to hypertension: the history of research". J R Soc Med. 84 (10): 621. PMC 1295564Freely accessible. PMID 1744849. 
  2. ^ a b c Kotchen TA (October 2011). "Historical trends and milestones in hypertension research: a model of the process of translational research". Hypertension. 58 (4): 522–38. PMID 21859967. doi:10.1161/HYPERTENSIONAHA.111.177766. 
  3. ^ Swales JD, ed. (1995). Manual of hypertension. Oxford: Blackwell Science. pp. xiii. ISBN 0-86542-861-1. 
  4. ^ Postel-Vinay N, ed. (1996). A century of arterial hypertension 1896–1996. Chichester: Wiley. p. 213. ISBN 0-471-96788-2. 
  5. ^ Paul I. Korner Professor of Medicine Monash University (Emeritus) and Director of the (11 May 2007). Essential Hypertension and Its Causes : Neural and Non-Neural Mechanisms: Neural and Non-Neural Mechanisms. Oxford University Press, USA. pp. 4–. ISBN 978-0-19-535740-0. 
  6. ^ Keith NM, Wagener HP, Kernohan JW (1928). "The syndrome of malignant hypertension". Arch. Intern. Med. 41 (2): 141–188. doi:10.1001/archinte.1928.00130140003001. 
  7. ^ Bruenn HG (1970). "Clinical notes on the illness and death of president Franklin D. Roosevelt". Annals of Internal Medicine. 72 (4): 579–591. PMID 4908628. doi:10.7326/0003-4819-72-4-579. 
  8. ^ Hay JH (1931). "A British Medical Association Lecture on THE SIGNIFICANCE OF A RAISED BLOOD PRESSURE". Br. Med. J. 2 (3679): 43–47. PMC 2314188Freely accessible. PMID 20776269. doi:10.1136/bmj.2.3679.43. 
  9. ^ a b c Moser M (August 2006). "Historical perspectives on the management of hypertension". J. Clin. Hypertens. (Greenwich). 8 (8 Suppl 2): 15–20; quiz 39. PMID 16894244. doi:10.1111/j.1524-6175.2006.05836.x. 
  10. ^ White PD (1937). Heart Disease (2nd ed.). New York, NY: MacMillan Co. p. 326. 
  11. ^ Friedberg CK (1949). Diseases of the Heart. Philadelphia, PA: WB Saunders Co. 
  12. ^ Pickering GW (1952). "The natural history of hypertension". Br. Med. Bull. 8 (4): 305–9. PMID 12987687. 
  13. ^ Society of Actuaries Committee on Mortality (1960). Build and blood pressure study, 1959. Chicago, IL: Society of Actuaries. 
  14. ^ "Section 30: Some characteristics related to the incidence of cardiovascular disease and death: 18 year follow-up". The Framingham Study; DHEW Publication No. (NIH) 74-599. Bethesda, MD: National Heart and Lung Institute. 1974. 
  15. ^ a b c d e f g Dustan HP, Roccella EJ, Garrison HH (September 1996). "Controlling hypertension. A research success story". Arch. Intern. Med. 156 (17): 1926–35. PMID 8823146. doi:10.1001/archinte.156.17.1926. 
  16. ^ Novello FC, Sprague JM (1957). "Benzothiadiazine dioxides as novel diuretics". J. Am. Chem. Soc. 79 (8): 2028. doi:10.1021/ja01565a079. 
  17. ^ Freis ED (1974). "The Veterans Administration Cooperative Study on Antihypertensive Agents. Implications for Stroke Prevention" (PDF). Stroke. 5 (1): 76–77. PMID 4811316. doi:10.1161/01.STR.5.1.76. 
  18. ^ Black JW, Crowther AF, Shanks RG, Smith LH, Dornhorst AC (May 1964). "A new adrenergic beta receptor antagonist". Lancet. 1 (7342): 1080–1. PMID 14132613. doi:10.1016/S0140-6736(64)91275-9. 
  19. ^ Ondetti MA, Rubin B, Cushman DW (April 1977). "Design of specific inhibitors of angiotensin-converting enzyme: new class of orally active antihypertensive agents". Science. 196 (4288): 441–4. PMID 191908. doi:10.1126/science.191908. 
  20. ^ Wexler RR, Greenlee WJ, Irvin JD, et al. (February 1996). "Nonpeptide angiotensin II receptor antagonists: the next generation in antihypertensive therapy". J. Med. Chem. 39 (3): 625–56. PMID 8576904. doi:10.1021/jm9504722. 
  21. ^ Jensen C, Herold P, Brunner HR (May 2008). "Aliskiren: the first renin inhibitor for clinical treatment". Nature Reviews Drug Discovery. 7 (5): 399–410. PMID 18340340. doi:10.1038/nrd2550.