The Treatment of Essential Hypertension

Mosenthal, Herman O.

doi:10.1001/jama.1928.02700100010003

Cited by 5 publications

(3 citation statements)

References 4 publications

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“…This led to the discovery that hypertension was primarily a condition observed in the United States and in Europe, and was extremely rare in other parts of the world, including Africa, Asia, Oceania, Australia, and South America [13]. The observation that many cases of hypertension had no clinical evidence of kidney disease and was often asymptomatic led to the term 'benign' hypertension to characterize those individuals [14]. In this context, some authorities suggested that the rise in blood pressure might be necessary or 'essential' in order to provide blood supply to its destination sites through the thickened blood vessels [15].…”

Section: The Development Of Paradigmsmentioning

confidence: 99%

“…One of the best examples is caused by neurovascular compression of the brain stem, such as from an enlarged posterior inferior cerebellar artery [59]. This was probably one of the causes of hypertension in the series of case reports provided by Mosenthal [14] in a study performed in the 1920s. A decrease in vascular compliance, such as occurs with aging in larger blood vessels such as the aorta, may also contribute to the development of isolated systolic hypertension.…”

Section: Guyton and The Role Of The Kidney In Salt-sensitive Hypertenmentioning

confidence: 99%

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Pathogenesis of essential hypertension: historical paradigms and modern insights

Johnson

Feig

Nakagawa

et al. 2008

Journal of Hypertension

114

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Since its first identification in the late 1800s, a variety of etiologies for essential hypertension have been proposed. In this paper we review the primary proposed hypotheses in the context of both the time in which they were proposed as well as the subsequent studies performed over the years. From these various insights, we propose a current paradigm to explain the renal mechanisms underlying the hypertension epidemic today. Specifically, we propose that hypertension is initiated by agents that cause systemic and intrarenal vasoconstriction. Over time intrarenal injury develops with microvascular disease, interstitial T cell and macrophage recruitment with the induction of an autoimmune response, with local angiotensin II formation and oxidant generation. These changes maintain intrarenal vasoconstriction and hypoxia with a change in local vasoconstrictor-vasodilator balance favoring sodium retention. Both genetic and congenital (nephron number) mechanisms have profound influence on this pathway. As blood pressure rises, renal ischemia is ameliorated and sodium balance restored completely (in salt-resistant) or partially (in salt-sensitive) hypertension, but at the expense of a rightward shift in the pressure natriuresis curve and persistent hypertension.

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Section: The Development Of Paradigmsmentioning

confidence: 99%

Section: Guyton and The Role Of The Kidney In Salt-sensitive Hypertenmentioning

confidence: 99%

Pathogenesis of essential hypertension: historical paradigms and modern insights

Johnson

Feig

Nakagawa

et al. 2008

Journal of Hypertension

114

View full text Add to dashboard Cite

show abstract

“…A week-end every month, spent at home, practically in bed, is a good habit to follow. 35 Frequent vacations away from home and business relieve largely, for the time being, a great amount of nerve tension and the responsibility and worry every family man of necessity has. This regimen should be advised gradually, so as not to alarm the patient unnecessarily and make him feel that his whole future is to be that of an invalid.…”

Section: Prognosismentioning

confidence: 99%

The Present Conception of Essential Hypertension

Granger¹

1929

JAMA

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It is rather remarkable that the clinical study of blood pressure, a subject on which so much stress has been placed in recent years, should have had its inception only forty-eight years ago in the work of von Basch with the first sphygmomanometer, though Vierordt's 1 attempts to measure the compressibility of the pulse were made years before and Richard Bright scented the condition in his monograph on the disease bearing his name. In 1886 Flint2 mentioned the association between chronic interstitial nephritis, the resistance to the flow of blood through the small vessels, left ventricular hypertrophy, and increased arterial tension. The first contributions to the literature in this country dealing with observations on human blood pressure were made by Richard Cabot3 in 1903 and 1904. Instruments free from error for measuring the pressure were not in use until 1901,4 and the auscultatory method was described by Korotkow 5 in 1905.Since the common use of the sphygmomanometer, physicians have been observing a certain group of patients in increasing numbers who show hypertension unaccompanied by nephritis, hyperthyroidism, aortic insufficiency or any other condition usually associated with a rise in the blood pressure. To this type the name primary or essential hypertension has been given in this country, and also primary hypertensive cardiovascular disease by Janeway,1 who recognized the nonassociation of kidney disease with this type of hyper¬ tension. It corresponds to the latent angiosclerosis of von Basch, the hyperpiesis of Allbutt, the presclerosis of Huchard, and the benign essential hypertension of Volhard and Fahr.0 Essential hypertension is a pro¬ gressive disease, probably beginning in the second and third decades of life and ending usually from the third decade on, by cardiac failure, cerebral accidents or renal insufficiency: Fahr7 estimates that approximately 140,000 people die annually in the United States from hyperpiesia, and that about half these deaths are due to cardiac failure consequent to the hypertension. PROBABLE ETIOLOGYThere is no known etiology of this condition, but certain factors have been determined by clinical observa¬ tion and experimental work which undoubtedly have a marked influence on the incidence of this type of hyper¬ tension. The more important of these factors will be briefly discussed:1. Sclerosis of the arterioles of the medulla, dish¬ ing,3 in 1901, drew the conclusion from experimental work that an anemia of the vasomotor center in the medulla caused a systemic hypertension, and formulated the law that "an increase of the intracranial tension occasions a rise in the blood pressure, which tends to find a level slightly above that of the pressure exerted against the medulla." Anrep and Starling9 and Starling 10 found that vascular lesions in the medulla which impaired the blood supply can produce a com¬ pensatory rise in the systemic pressure, which rather tends to support the theory that anemia of the brain due to sclerosis of the vessels supplying the vasomotor cen¬ te...

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Nature of the Symptoms Associated With Essential Hypertension

Ayman¹,

Pratt²

1931

Arch Intern Med

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The Treatment of Essential Hypertension

Cited by 5 publications

References 4 publications

Pathogenesis of essential hypertension: historical paradigms and modern insights

Pathogenesis of essential hypertension: historical paradigms and modern insights

The Present Conception of Essential Hypertension

Nature of the Symptoms Associated With Essential Hypertension

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