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HYPERTENSION – ORIGINS
https://t.me/med1917
Garabed Eknoyan, MD
CHAPTER 43
QUESTIONS
1. When did hypertension enter medical nosography as a disease?
It all started in antiquity with the recognition of the pulse as a sign of life, death, and disease. The Mesopotamian
epic of Gilgamesh (c. 2600 BCE) records the lament of its protagonist, Gilgamesh, at the death of his best friend,
Enkidu, “I touch his heart but it does not beat at all.” How he touched the heart is not stated. That the pulse was
synchronous wherever felt on the body and coincided with the heartbeat is recorded in ancient Egyptian medical
texts of about 1500 BCE. Variations in the frequency and force of the pulse in the course of diseases was studied
and refined in ancient Chinese medicine, where the diagnosis and site of disease was made by palpation of the
pulse. Whereas examination of the pulse (sphygmós) was used and recorded in Greek medicine, its physiologic
study was hampered by the concept of the circulation promulgated by Galen (130–210) that blood is made in
the liver, from whence it flows to and fro in the vasculature, and that “vital spirits” are added to it in its course
through the heart, an erroneous view that prevailed for fifteen centuries until the discovery of the circulation in
1628 by William Harvey (1578–1657). Harvey showed that blood circulates and that ventricular systole provides
the force that drives it through the arteries and causes their pulsation. It is from these foundations that the force
of the blood pressure which had been assessed from the pulse came to be identified as a clinical condition that
deserved better scrutiny in the 18th century.
That an arterial pulse that is hard to compress is an omen of poor health has been recognized since antiquity. Its association with shortened life and lesions of the brain, heart, and the kidneys began to be studied in the
19th century, after the report that a hard pulse was associated with ventricular hypertrophy in patients with kidney
disease by Richard Bright (1789–1858) in 1836. However, it was only with measurement of the blood pressure by
sphygmography (writing of the pulse, from the Greek for pulse, sphygmós and from Latin for writing, graphia) that
quantification rather than mere qualitative description of the arterial pulse began to be studied in the 20th century.
The epidemiologic data that accrued thereafter documented the clinical relevance of elevated blood pressure and
identified hypertension as a disease rather than a mere sign of disease.
2. How did the measurement of blood pressure evolve?
The actual measurement of arterial blood pressure can be traced to an English clergyman, the Reverend Stephen
Hales (1677–1761) who, in 1733, reported on the “force of the blood” from the height of a blood column connected to the femoral artery of horses and dogs. It would be another century before the French physicist Jean
Poiseuille (1797–1869) introduced a mercury manometer for the measurement of the force of the blood in 1828,
thereby reducing the awkwardness of the height of the column (9 feet) used to measure the arterial pressure
directly. Shortly thereafter, in 1847, the German physiologist Carl Ludwig (1816–95) added a float to the mercury
manometer connected to an arm which inscribed the pressure on a rotating drum (kymograph), thereby providing
a permanent record of studies on pulse pressure, rate, and rhythm.
The clinical determination of blood pressure had to wait for the development of noninvasive methods of
measurement. Several attempts at doing that with a mercury manometer applied to the radial artery were tried.
The turning point came in 1896 when the Italian pediatrician Scipione Riva-Rocci (1863–1937) developed a clinically useful sphygmomanometer (sphygmós from Greek for pulse; manométre from French for measuring instrument) which connected a mercury manometer to a wrap-around inflatable cuff applied around the upper arm and
inflated to occlude the pulse palpated in the radial artery. That allowed for the estimation of systolic pressure. The
accuracy of the procedure was increased in 1901 when the width of the inflatable cuff was increased from 5 to 13
centimeters by the German physician Heinrich von Recklinghausen (1867–1942).
The next breakthrough in the clinical assessment of blood pressure was introduced in 1905 by a Russian
surgeon from St. Petersburg, Nikolai Korotkov (1874–1920) who described the sounds heard through a stethoscope over the brachial artery below the inflatable cuff during its deflation. He reported the auscultated sounds
from their initial tapping to their disappearance in a one-page article. For all the fame that Korotkov achieved, he
had no interest in hypertension. His quest was that of a surgeon in evaluating the blood supply to the extremities
of patients with vascular disease before surgery. Another surgeon who actually popularized the clinical measurement of blood pressure using the stethoscope was the American neurosurgeon Harvey Cushing (1869–1939), who
visited Riva-Ricci in Turin in 1901 and on his return introduced the procedure in the United States. The clinical
utility of the procedure was then promoted by the physiologist Walter Cannon (1871–1945) who went on to use it
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HYPERTENSION – ORIGINS 229
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in his studies of shock. By 1912, the regular measurement of the blood pressure of patients admitted to the Mas-
sachusetts General Hospital was required and soon became an established routine in clinical practice.
It was this marriage of the stethoscope to the sphygmomanometer adopted in clinical practice early in the
20th century that generated the data base that would lead to the identification of hypertension as a disease. The
1925 report of the Actuarial Society of America was the first landmark report on the detrimental effects of elevated
blood pressure on survival based on data derived from office blood pressure recordings. It made a transformative
statement which convinced the medical profession of the ill effects of hypertension that had been long suggested
from its tactile description as hard pulse pressure.
3. How were the effects of hypertension on organs recognized?
A hard-wiry radial pulse had long been associated with concerns of poor health. But it was the association of
albuminuria, dropsy, and kidney disease in 1827 by Richard Bright that would open the door to its investigation.
Actually, it was Bright’s subsequent report in 1836 of the association of ventricular hypertrophy with the fullness
of a hard pulse in patients with kidney disease which launched the studies that would eventuate in identifying the
systemic effects of hypertension as a disease rather than merely a sign of disease.
Most of the studies that followed were based on pathological observations of the vasculature in general, and
that of the kidney in particular. A contemporary of Bright, the London physician George Johnson (1818–96) was
the first to argue that it was the increased resistance of the narrowed vasculature which necessitated an increase
in blood pressure to overcome their resistance. Stated otherwise, a rise in blood pressure was essential to maintain blood supply to organs. This concept was strengthened by the studies of two other London physicians, William
Gull (1816–90) and his junior colleague Henry Sutton (1837–91), who, in 1872, described “arterio-capillary
fibrosis” and “hyaline-fibrinoid” changes in arterioles throughout the body of patients with ventricular hypertrophy,
with and without kidney disease. They proposed that these generalized vascular changes accounted for the renal
disease and cardiac hypertrophy.
A primary role of high arterial pressure causing vascular sclerosis and ventricular hypertrophy had been
proposed in 1856 by a founder of experimental pathology in Germany, Ludwig Taube (1818–76). Actually, a fibrous
hardening and medial muscular hypertrophy of the arteries had been reported earlier by the French pathologist
Jean Lobstein (1777–1835) as “arteriosclerosis” in 1833, but they were not linked to blood pressure or kidney
disease until then.
The first clinical evidence of these pathological observations was presented by Frederick Mahomed
(1849–84) working at Guy’s Hospital in London who, in 1874, started using a modified Poiseuille manometer to
measure the blood pressure of his patients. In 1879, Mahomed reported what he termed the “pre-albuminuric
stage of Bright’s disease,” wherein the blood pressure was elevated in the absence of evident kidney disease.
He went on to propose that high blood pressure itself, in the absence of Bright’s disease, could give rise to the
vascular lesions described by Gull and Sutton.
The clinical findings of Mahomed were supported by the Cambridge professor of medicine T. Clifford Allbutt
(1836–1925) who, in a series of reports, argued that renal disease was not necessary for the presence of elevated
blood pressure, which in 1896 he termed “hyperpiesis” as a manifestation of the primary malady he dubbed
“hyperpiesia,” rather than one merely secondary to kidney disease. Based on detailed studies of cases of severe
hypertension (up to 250/140 mm Hg) the first professor of medicine at Johns Hopkins, Theodor Janeway (1872–
1917), proposed in 1904 naming the disease “hypertensive cardiovascular disease,” specifically to differentiate
it from that associated with Bright’s disease. Actually, the term hypertension had been introduced in 1889 by the
French cardiologist Henri Huchard (1814–1910) in his report that elevated blood pressure can occur independent
of nephritis. It was revived in 1911 as essential hypertension (“essentielle Hypertonie”) by the German physician
from Wiesbaden Emil Frank, and came to prevail over those proposed by Allbutt and Janeway. Although characterizing hypertension as “essential” gained clinical acceptance, it has been and continues to be questioned by basic
scientists who prefer its definition as “primary” or “idiopathic.”
Subsequently, the German clinician Fanz Volhard (1872–1950), in cooperation with his pathology associate
Theodor Fahr (1877–1945), went on to differentiate essential hypertension into the so-called red or benign (gut-
tartig) hypertension from that of white or malignant (bösartig) hypertension. The classification of hypertension with
particular emphasis on the retinal changes in differentiating benign from malignant hypertension was reported
from the Mayo Clinic by Norman Keith (1885–1976) in 1927. The following meticulous clinical studies of hypertensive subjects by George Pickering (1904–80) from Oxford University ultimately established hypertension as a
quantitative disease of graded severity that appeared to be related to the level of blood pressure.
4. How did the treatment of hypertension evolve?
The data available early in the 20th century on the detrimental effects of hypertension was derived from cases
of severe or malignant hypertension (>180/110 mm Hg). As a result, the treatment of hypertension continued
to be debated and even recommended not to be lowered. As late as 1937, the eminent cardiologist Paul Dudley
White (1886–1973) declared that “hypertension may be an important compensatory mechanism which should
not be tampered with, even if we were certain that we could control it.” The effectiveness and wisdom of treating
hypertension would continue to be questioned well into the 1950s. The classic example of this conundrum is
230 MISCELLENIA
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that of President Franklin Roosevelt (1882–1945) who succumbed to a massive intracranial hemorrhage due to
malignant hypertension that had been treated with rest, massage, and sedatives.
In the absence of effective antihypertensive drugs, surgical procedures such as bilateral thoraco-lumbar
sympathectomy and nephrectomy of unilateral atrophic kidneys came into vogue in the 1940s. Both approaches
proved to be only temporally effective, definitely ineffective in the long run, and were abandoned by the 1960s as
new antihypertensives became available.
The antihypertensive properties of most drugs introduced then were discovered accidentally. Sulfanilamide,
introduced as an antimicrobial, was found to have diuretic properties that led to the synthesis of chlorothiazide
(Diuril) in 1958. Methyldopa, developed for the treatment of carcinoid syndrome, was introduced as an antihypertensive (Aldomet) in 1960. Clonidine, developed for the treatment of allergic rhinitis, caused drowsiness due to
hypotension and was approved as an antihypertensive (Catapres) in 1966. The beta-blocker propranolol (Inderal),
introduced for the treatment of angina, was found to lower blood pressure and was approved as an antihypertensive in 1964. Similarly, the calcium channel blocker nifedipine (Adalat), introduced for the treatment of angina,
was approved for the treatment of hypertension in 1969.
The availability of potentially effective antihypertensives corresponded to that of the entry of randomized
clinical trials in medicine in 1952, and the study of antihypertensives proved to be one of the first beneficiaries of
these early ventures into evidence-based medicine in the 1960s. The first multicenter double-blind randomized
trial designed for the treatment of hypertension was the Veterans Administration Cooperative Study on Antihypertensive Agents begun in 1964 at the initiative of Edward Fries (1912–2005). This placebo-controlled study used
the three antihypertensive drugs available then, the vasodilator hydralazine, the adrenergic suppressor reserpine,
and the diuretic chlorothiazide. The results showed a major salutary effect on severe hypertension and a favorable
outcome of those with milder hypertension.
The series of landmark studies that followed clearly established the efficacy of antihypertensive drug
therapy. The increasing recognition of hypertension as a common and serious public health problem that is
potentially preventable led to the establishment of the National High Blood Pressure Education Program in 1972,
a forerunner of programs that followed under the auspices of the National Heart Lung and Blood Institute (NHLBI).
Notable amongst those was the establishment of the Joint National Committee (JNC) on Detection and Treatment
of High Blood Pressure which published the first set of guidelines for the treatment of hypertension in 1977. Since
then, the definition of hypertension and the target level for its treatment have been a downward moving target,
with lower targets recommended for diabetics and those with kidney disease.
KEY POINTS
1. Blood pressure was assessed from the hardness of the pulse until 1896 when the sphygmomanometer was
introduced.
2. Hypertension as a disease, rather than a sign of disease, was established in the late 1920s from epidemiologic
data collected by insurance companies.
The treatment of hypertension was questioned until the 1950s. The first randomized clinical trial to establish the
3.
effectiveness of hypertension treatment was published in 1967.
4. The antihypertensive effects of drugs introduced initially were accidentally discovered. The first drugs specifically
developed for treatment of hypertension were the angiotensin-converting enzyme inhibitors introduced in the
1980s.
BiBliography
Bedford DE. The ancient art of feeling the pulse. Br Heart J. 1951;13:423–436.
Cameron JS. Villain and victim: the kidney and high blood pressure in the 19th century. J R Coll Physicians London. 1999;33:382–394.
Eknoyan G. On the contribution of studies on kidney in the recognition, conceptual evolution, and understanding of hypertension. Adv
Chronic Kid Dis. 2004;11:192–196.
Folkow B. Physiological aspects of primary hypertension. Physiol Rev. 1982;62:347–504.
Ruskin A. Classics in Arterial Hypertension. Springfield IL: Charles C. Thomas; 1956.
Wakerlin GE. From Bright toward light: the story of hypertension research. Circulation. 1962;26:1–6.
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