Essential Hypertension In Man Research Articles

Congenital Malformation of the Renal Artery, a Cause of Hypertension

The causal relationship of renal pathology to arterial hypertension is not yet clearly defined. The classic experiments of Goldblatt (10) convincingly demonstrated that interference with the renal arterial blood flow through one or both kidneys in the experimental animal can result in sustained hypertension. Goldblatt (11, 12) presents formidable evidence to show that such experimental hypertension bears a striking similarity to essential hypertension in man and suggests that the mechanisms in the two may be identical. There is, however, a large body of opinion which is strongly opposed to this point of view. Indeed, Smith (24), Goldring (13), and Thompson and Smithwick (26) insist that, with the possible exception of pyelonephritic and pyonephrotic atrophy, urologic disease does not increase the incidence of hypertension, nor is renal disease more common in the hypertensive than in the normotensive population. Be that as it may, there is general agreement that there are at least certain forms of renal disease which definitely represent the exact human counterpart of the experimental renal hypertension of Goldblatt. Such cases are those in which, for one reason or another, there is a marked reduction, but not a complete suppression, of the arterial blood flow through one or both kidneys. While the actual mechanism is not definitely understood, it is generally assumed that a relatively ischemic kidney elaborates a pressor substance which acts as a humoral hypertensive agent. The occasional cases of unilateral renal disease in which removal of the diseased kidney alleviates or cures the hypertensive state, lend support to this theory. These cases comprise a very small but nevertheless an important segment of all cases of hypertension in man. The most obvious instances in this category are the lesions which reduce the renal blood flow directly by mechanical narrowing of the lumen of the main renal artery. Such mechanical narrowing may be caused by thrombosis, arteriosclerotic plaques, aneurysm, neoplasm, or congenital anomaly. Congenital malformation of the renal artery, producing hypertension by the Goldblatt mechanism, is undoubtedly a rare entity. Yet, it probably occurs more often than it is actually found or even suspected. Careful search of the literature reveals a remarkable paucity of reported examples, and none has appeared, as far as we could discover, in the roentgenologic literature. In 1954, Howard et al. (17), reporting on 6 hypertensive patients with unilateral renal disease, described a case (Case 3) of a thirty-nine-year-old man from whom a non-functioning left kidney was removed. Pathologic examination of the specimen disclosed that the main renal artery was absent and in its place several small arteries entered the hilus of the kidney.

Pathogenesis of spontaneous and pyelonephritic hypertension in the dog.

The upper limit of normotension in the trained, unanesthetized dog appears to be 145 (135-155) ± 7.5 mm. Hg mean femoral arterial pressure. The incidence of naturally occurring hypertension on the basis of this criterion was 0.9 per cent in 1000 dogs, 1 to 4 years of age. Six of the dogs had so-called spontaneous hypertension which may be similar to or the counterpart of essential hypertension in man. The other three had hypertension associated with chronic pyelonephritis. A renal, renin pathogenesis is indicated for both of these hypertensions by the antihypertensive effect produced by injections of hog renin with resulting antirenin and by passive transfer of high titre homologous antiserum containing antirenin to hog renin which also neutralizes dog renin.

Evidence for relationship between sodium (chloride) intake and human essential hypertension.

THERE are considerable data which indicate that the sodium ion is important or necessary for the development of certain types of experimental hypertension.* So far, to our knowledge, no evidence has been published to suggest that a similar relationship exists with so-called essential hypertension in man. A statistical analysis of the data to be presented in this paper, however, indicates that there is a significant correlation between sodium chloride intake and the development of hypertension in man. While the effects of sodium and chloride could not be separated in this study, all the experimental evidence indicates that the sodium ion alone is important, and our interest has centered solely about that ion. For some years one of us has been intrigued by the lack of significant numbers of persons with hypertension among truly primitive human races. Recently Bays and Scrimshaw 7 have suggested that this may not be uniformly so.

Cortical ablations in dogs with chronic neurogenic hypertension.

MANY CLINICIANS believe that psychosomatic factors are important in the pathogenesis of essential hypertension in man. If so, it is likely that zones of the cerebral cortex constitute, at least in part, the neuroanatomic substrate responsible for the introduction of these factors into the physiologic processes concerned with regulation of the blood pressure. Indeed, Fulton 1 has stated that perhaps the most significant disclosure of the past few years in the field of scientific medicine has been the recognition of certain cortical regions as being integral parts of the autonomic nervous system because that revelation has afforded a sound physiologic background for psychosomatic aspects of medicine. There have been isolated reports of persistent falls in the blood pressure of hypertensive patients subsequent to various psychosurgical procedures.* Although this was not the usual result of such operations,† no deliberate effort was made to remove or undercut cortical regions demonstrated at

The role of the sympathetic nervous system in essential hypertension in man.

The role of the sympathetic nervous system in essential hypertension in man.

THEORY OF ESSENTIAL HYPERTENSION IN MAN

Transactions of the New York Academy of SciencesVolume 11, Issue 2 Series II p. 49-50 THEORY OF ESSENTIAL HYPERTENSION IN MAN EDMUND JACOBSON, EDMUND JACOBSON Laboratory for Clinical Physiology, Chicago Illinois. This paper, illustrated by lantern slides, was presented at the meeting of the Section on October 18, 1948.Search for more papers by this author EDMUND JACOBSON, EDMUND JACOBSON Laboratory for Clinical Physiology, Chicago Illinois. This paper, illustrated by lantern slides, was presented at the meeting of the Section on October 18, 1948.Search for more papers by this author First published: December 1948 https://doi.org/10.1111/j.2164-0947.1948.tb00958.xCitations: 2 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume11, Issue2 Series IIDecember 1948Pages 49-50 RelatedInformation

THE RENAL PATHOLOGY OF NUTRITIONAL HYPERTENSION IN RATS

Rats subsisting on a diet partially deficient in the heat-stable fractions of the vitamin B complex are known to experience a rise in blood pressure. The present study shows that after prolonged administration of this dietary, abnormal structural changes occur in the kidneys. The surface of this organ becomes finely granular. The afferent arterioles show degenerative changes, consisting of irregular subendothelial hyaline deposits which encroach on the lumen. The interlobular arteries undergo the same change, plus degeneration of the media; the lumen of these vessels is likewise compromised. Resultant, small, streak-like areas of ischemic atrophy occur in both cortex and medulla, with necrosis of the epithelial lining of the uriniferous tubules. The glomeruli are reduced in size, the number of their component loops decreased, their pattern simplified, and the capillary basement membrane thickened. In addition to these changes, kidneys from animals on a more profoundly deficient diet display numerous areas of hemorrhagic infiltration in the cortical and subcapsular regions. The possible identity of these lesions with those seen in essential hypertension in man is discussed.

UNILATERAL RENAL TUBERCULOSIS ASSOCIATED WITH HYPERTENSION

Case Reports1 August 1941UNILATERAL RENAL TUBERCULOSIS ASSOCIATED WITH HYPERTENSIONG. GILL RICHARDS, M.D., F.A.C.P.G. GILL RICHARDS, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-15-2-324 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptBecause Goldblatt1 could, by removing the ischemic kidney in his experimental hypertensive dogs, cause a fall of blood pressure to normal, the possible clinical application of his results to cases of essential hypertension in man aroused considerable interest, particularly among internists and urologists. The following report deals with a case of unilateral renal tuberculosis with hypertension and the satisfactory result which has continued for 11 months after nephrectomy.CASE REPORTL. P., a married white male, aged 37 years, was admitted to the Latter-Day Saints Hospital on January 10, 1940, complaining of occipital headaches of extreme degree, fatigue, shortness of...Bibliography1. GOLDBLATT H: Studies on experimental hypertension due to renal ischemia, ANN. INT. MED., 1937, xi, 69-103. LinkGoogle Scholar2. BUTLER AM: Chronic pyelonephritis and arterial hypertension, Jr. Clin. Invest., 1937, xvi, 889-897. CrossrefGoogle Scholar3. BARNEYSUBY JDHI: Unilateral renal disease with arterial hypertension, New England Jr. Med., 1939, ccxx, 744-746. CrossrefGoogle Scholar4. CRABTREE EG: Hypertension in destructive infected unilateral lesions of the kidney, Trans. Am. Assoc. Genito-Urin. Surgeons, 1938, xxxi, 299-319. Google Scholar5. LEADBETTERBURLAND WFCE: Hypertension in unilateral renal disease, Jr. Urol., 1938, xxxix, 611-626. CrossrefGoogle Scholar6. BOYDLEWIS CHLG: Nephrectomy for arterial hypertension, Jr. Urol., 1938, xxxix, 627-635. CrossrefGoogle Scholar7. BARKERWALTERS NWW: Hypertension and chronic pyelonephritis: results of nephrectomy, Jr. Am. Med. Assoc., 1940, cxv, 912-916. CrossrefGoogle Scholar8. FITZ R: Hypertension, Mississippi Doctor, 1940, xvii, 531-541. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Salt Lake City, Utah*Received for publication December 27, 1940. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAtypical causes of curable renovascular hypertension: A reviewRenal hypertension secondary to renal tuberculosisAmelioration of Asthma and Hypertension after Nephrectomy for Renal TuberculosisUnilateral Nephrectomy in Hypertensive DiseaseHypertension in Unilateral Renal Disease 1 August 1941Volume 15, Issue 2Page: 324-328KeywordsBlood pressureFallsFatigueHypertensionKidneysNephrectomy ePublished: 1 December 2008 Issue Published: 1 August 1941 PDF downloadLoading ...

EXPERIMENTAL HYPERTENSION

In healthy dogs and monkeys (macaques) persistent elevation of the systolic and the diastolic pressure, with or without a decrease of renal excretory function, followed permanent partial constriction of the main renal arteries. 1 The eyes of these hypertensive animals have been studied during a period of more than five years. A preliminary report 2 and an interim report 3 have been made. These dogs exhibited two definite types of hypertension: a benign phase, without a decrease of renal excretory function, and an acute malignant phase, with very high blood pressure and severe damage of the renal excretory function. These two phases correspond to the benign and malignant phases of essential hypertension in man. The acute malignant phase of hypertension occurred, or was produced, in dogs already hypertensive, owing to constriction of the main renal arteries when the arteries were reconstricted to a great degree, or in healthy dogs in

EXPERIMENTAL ATHEROSCLEROSIS AND BLOOD PRESSURE IN THE RABBIT

1. Van Leersum's range for the normal blood pressure in the rabbit, as recorded by his method, is confirmed. 2. Van Leersum's conclusion concerning the influence of a liver diet on the blood pressure of the rabbit is not substantiated by his data, since the fluctuations of blood pressure he obtained do not surpass his own recorded figures for normal animals. 3. Fluctuations of systolic blood pressure beyond the "normal" range are not necessary for the production of experimental atherosclerosis of the aorta in rabbits. Inversely, egg yolk feeding experiments in rabbits in which atherosclerosis of varying degree, even extreme, is obtained, are not accompanied by an elevation of blood pressure outside the "normal" range. 4. The fluctuations of blood pressure observed during experimental atherosclerosis do not simulate the condition of essential hypertension in man.