Experimental Renal Hypertension Research Articles

Renal blood flow in experimental renal hypertension: Cororan, A. C., and page, I. H.: Am. J. Physiol. 135: 361, 1942

Renal blood flow in experimental renal hypertension: Cororan, A. C., and page, I. H.: Am. J. Physiol. 135: 361, 1942

Effects on Arterial Hypertension of Heat-inactivated Tyrosinase Preparations.

Recent studies of the mechanisms involved in the production of experimental renal hypertension show that several humoral agents may be involved. Following the hypothesis that phenolic amines may be involved in renal hypertension, Schroeder and Adams1 found tyrosinase preparations from mushrooms to be effective in lowering the blood pressures of hypertensive animals. Their studies were extended to the effects of tyrosinase preparations on arterial hypertension in man and reported results in 17 patients, with significant falls in blood pressures in 13 of these following daily administration of unspecified amounts of their tyrosinase preparations. Some phenolic substance was considered to be altered by the injected enzyme to account for the lowered blood pressures observed.The present experiments were carried out with mushroom tyro-sinase preparations made by modifications of the purification procedures of Keilin and Mann.3 The valuation of the enzymic activity was made upon a catechol-hydroquinone substrate...

The effect of renin on experimental renal hypertension in the dog: Wakerlin, G. E., and Johnson, C. A.: J.A.M.A. 117: 416, 1941

The effect of renin on experimental renal hypertension in the dog: Wakerlin, G. E., and Johnson, C. A.: J.A.M.A. 117: 416, 1941

EXPERIMENTAL HYPERTENSION AND THE NEUROHYPOPHYSIS

THE PARTICIPATION OF THE HYPOPHYSIS in a causative or sustaining role in any form of clinical or experimental hypertension is in dispute (1). It is generally held that the hypophysis plays no direct part in the production of expert mental hypertension of the Goldblatt type (2–7). There is evidence, however, that the hypophysis may contribute to conditions favoring the existence of a hypertension by its effects upon other endocrine glands such as the adrenal cortex, or upon the responsiveness of the blood vessel musculature to pressor substances derived from ischaemic kidneys. Animals which are otherwise normal may show lowered blood pressures after hypophysectomy (2, 8, 9). Page and Sweet (2) and Page (8) have shown that hypophysectomy in dogs with experimental renal hypertension may cause definite decline in blood pressure. However, hypophysectomy will not always prevent the onset of a hypertension when the renal arteries are compressed subsequent to the hypophysectomy (2, 10).

THE EFFECT OF RENIN ON EXPERIMENTAL RENAL HYPERTENSION IN THE DOG

Of the numerous methods reportedly available for producing hypertension in animals¹(table 1), the most satisfactory is that of constriction of the renal arteries reported by Goldblatt²in his now classic experiment. During the past several years, moreover, there has accumulated growing evidence of similarity between experimental renal (Goldblatt) hypertension in the dog and essential hypertension as found in the great majority of patients so diagnosed³(table 2). Although a therapeutic agent which is effective in experimental renal hypertension may prove ineffective in essential hypertension, and vice versa, any new therapy proposed for essential hypertension should first receive an adequate trial in experimental renal hypertension. As a consequence, a number of attempts have been made to reduce the blood pressures of renal hypertensive dogs. Only a few of these efforts have met with some degree of success. Thus Davis and Barker⁴reported that potassium thiocyanate reduced

THE VASOCONSTRICTOR ACTION OF PLASMA FROM HYPERTENSIVE PATIENTS AND DOGS

1. Plasma from the renal vein, femoral artery or vein of normal dogs and plasma from the femoral artery, femoral and antecubital veins of man cause little or no vasoconstriction when added in small amounts to blood from a bilaterally nephrectomized dog used as perfusing medium in an isolated rabbit's ear. 2. Plasma from the femoral vessels and antecubital vein of patients with essential hypertension, malignant hypertension, and chronic nephritic hypertension causes marked vasoconstriction under the same circumstances. The plasma of dogs made hypertensive either by constriction of the parenchyma by the scar of silk perinephritis or by constriction of the renal artery by a clamp also causes pronounced vasoconstriction. 3. Plasma from the renal vein of normal dogs produces little or no vasoconstriction, but that of hypertensive dogs elicits vasoconstriction but usually not so marked as that elicited by plasma collected from peripheral vessels. A sample of renal venous plasma from one hypertensive patient caused severe vasoconstriction, not quite so intense as that produced by the peripheral vein plasma. 4. Since renin is liberated into the renal vein in large amounts in hypertensive dogs and reacts with renin-activator to produce angiotonin and since the conditions of the experiment are such as to enhance greatly the sensitivity of the ear preparation to angiotonin, it is believed that the vasoconstriction is the result of the presence of angiotonin in the peripheral blood. 5. Since vasoconstriction occurs under the same experimental conditions with plasma from both hypertensive patients and dogs, this is considered cogent evidence in favor of the view that the chemical mediator of both is similar and is possibly angiotonin. 6. A method is presented which is believed will distinguish between plasma from patients with normal blood pressure and that from those with hypertension, and between plasma from normal dogs and that from dogs with experimental renal hypertension.

The increased sensitivity of arterial muscle in the prehypertensive phase of experimental renal hypertension: Ogden, Eric, Brown, Lewis T., and Page, Ernest W.: Am. J. Physiol. 129: 560, 1940

The increased sensitivity of arterial muscle in the prehypertensive phase of experimental renal hypertension: Ogden, Eric, Brown, Lewis T., and Page, Ernest W.: Am. J. Physiol. 129: 560, 1940

Antiserum for Renin.

Conclusions1. The rabbit is able to produce an antiserum which counteracts the pressor effect of dog renin. 2. The antiserum for dog renin appears to diminish the pressor response to rabbit renin.3. This antiserum has no effect on the pressor action of pituitrin.4. The dog appears able to produce an antiserum to hog renin. 5. The active principle of the antiserums (antirenin) is most likely a non-precipitating antibody or possibly an antihormone. 6. Studies are now in progress to determine the value of antirenin in the therapy of experimental renal hypertension and also in the elucidation of the possible pathogenetic role of renin in this form of hypertension.

Pulmonary arterial pressure in experimental renal hypertension: Katz, L.N., and Steinitz, F.S.: Am. J. Physiol. 128: 433, 1940

Pulmonary arterial pressure in experimental renal hypertension: Katz, L.N., and Steinitz, F.S.: Am. J. Physiol. 128: 433, 1940

CLINICAL PICTURES ASSOCIATED WITH INCREASED BLOOD PRESSURE: A STUDY OF 100 PATIENTS

Article1 October 1939CLINICAL PICTURES ASSOCIATED WITH INCREASED BLOOD PRESSURE: A STUDY OF 100 PATIENTSJ. R. WILLIAMS JR., T. R. HARRISONJ. R. WILLIAMS JR.Search for more papers by this author, T. R. HARRISONSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-13-4-650 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONUntil comparatively recently hypertension has been divided into the "renal" type (including glomerular nephritis and a few rarer disorders of the kidneys) and the "essential" type, the latter term being employed to indicate a rise in blood pressure not due to renal disease. Many clinicians have tended to accept essential hypertension as an entity due to a single but unknown cause. This concept is no longer tenable for two reasons. In the first place the demonstration by Goldblatt and his coworkers1that animals with experimental renal hypertension may present a clinical picture similar in all respects to that of...Bibliography1. GOLDBLATTLYNCHHANZALSUMMERVILLE HJRFWW: Studies on experimental hypertension; production of persistent elevation of systolic blood pressure by means of renal ischemia, Jr. Exper. Med., 1934, lix, 347. CrossrefGoogle Scholar2. FISHBERG AM: Hypertension and nephritis, 1931, Lea & Febiger, Philadelphia, p. 668. Google Scholar3. AYMAN D: Personality type of patients with arteriolar essential hypertension, Am. Jr. Med. Sci., 1933, clxxxvi, 213. Google Scholar4. LEVINEERNSTENE SAAC: Observations on arterial blood pressure during attacks of angina pectoris, Am. Heart Jr., 1933, viii, 323. CrossrefGoogle Scholar5. ALAMSMIRK MFH: Observations in man upon blood pressure raising reflex arising from voluntary muscles, Jr. Physiol., 1937, lxxxix, 372. CrossrefGoogle Scholar6. CUSHING HW: Papers relating to the pituitary body, hypothalamus and parasympathetic nervous system, 1932, Thomas & Co., Springfield. Google Scholar7. PETERS JP: Nature of toxemias of pregnancy, Jr. Am. Med. Assoc., 1938, cx, 329. CrossrefGoogle Scholar8. LONGCOPE WT: Chronic bilateral pyelonephritis: its origin and its association with hypertension, ANN. INT. MED., 1937, xi, 149. LinkGoogle Scholar9. RYTAND DA: Pathogenesis of arterial hypertension in coarctation of the aorta, Proc. Soc. Exper. Biol. and Med., 1938, x, 11. Google Scholar10. SCHROEDERSTEELE HAJM: Abnormalities of the urinary tract in "essential hypertension," Proc. Soc. Exper. Biol. and Med., 1938, xxxix, 107. CrossrefGoogle Scholar11. HARRISON TR: Failure of the circulation, 2nd Ed., 1939, The Williams and Wilkins Co., Baltimore, pp. 396. Google Scholar12. PRINZMETALOPPENHEIMER MET: Rôle of arteries in peripheral resistance to hypertension, Proc. Soc. Exper. Biol. and Med., 1937, xxxvi, 675. CrossrefGoogle Scholar13. BRAUN L: Experimentelle Untersuchungen über Blutdruck und Niere, Wien. klin. Wchnschr., 1933, xlvi, 225 and 1471; Also ibid., 1934, xlvii, 65 and 131. Google Scholar14. GOLDBLATT H: Studies on experimental hypertension; pathogenesis of experimental hypertension due to renal ischemia, ANN. INT. MED., 1937, xi, 69. LinkGoogle Scholar15. BLALOCKLEVY ASE: Studies on etiology of renal hypertension, Ann. Surg., 1937 cvi, 826. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Nashville, Tennessee*Read at the New Orleans meeting of the American College of Physicians March 28, 1939.From the Department of Medicine, Vanderbilt University, Nashville, Tennessee.This work was aided by grants from the Josiah Macy Jr. Foundation, the Rockefeller Foundation, and from Mr. Joe Werthan, Nashville, Tennessee. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byHypertensive Vascular Disease: Its Clinical Course, Differential Diagnosis, Pathogenesis and TreatmentUrologic disease as a cause of hypertensionUrologic hypertension as an entityUnilateral Renal Disease and Renal Vascular Changes in Relation to Hypertension in ManEssential Hypertension, its Nature and Etiology.Hypertension in diphtheria 1 October 1939Volume 13, Issue 4Page: 650-670KeywordsBlood pressureHypertensionKidneysNephritisRenal diseases Issue Published: 1 October 1939 PDF downloadLoading ...

Production of a Sustained Neurogenic Hypertension of Renal Origin

Several methods have been devised for producing experimentally a renal ischemia hypertension. That of Goldblatt, Lynch, Hanzal and Summerville1 is most frequently used. These methods have all involved the use of a foreign material such as a clamp and have produced blood pressure changes that are not reversible without removing the foreign material or the involved kidney.It has therefore been difficult to apply these technics to experimental studies analysing the value of various methods of surgical treatment of hypertension in man. It has also been difficult to evaluate the possible importance of a primary nervous factor or a primary vascular disease factor in attempting to correlate experimental renal ischemia hypertension with essential hypertension in man.A technic has been devised to determine in dogs whether an over-activity of the renal vasoconstrictor splanchnic nerves can produce hypertension. The technic consists of sympathectomizing all of the animal except the origin and the distribution of the...

The Adrenals in Experimental Hypertension

In preliminary experiments by Goldblatt, bilateral adrenalectomy in dogs appeared to interfere with the development or maintenance of the hypertension which follows experimental production of renal ischemia. Similar results were obtained by Blalock and Levy and by Page. On the other hand, Collins and Wood concluded that, “It is unlikely that the adrenal cortex is involved specifically in the etiology of experimental renal hypertension other than in the sense that the cortex is important in the maintenance of blood pressure in normal as well as in hypertensive states.” Our experiments show that this form of experimental hypertension can exist in the complete absence of the adrenal glands, in untreated animals. Seven dogs were subjected to complete bilateral adrenalectomy in addition to constriction of the main renal arteries by means of Goldblatt clamps. Four of these animals were treated by administration of salt (sodium chloride and citrate, occasionally also bicarbonate) alone or in addition to a commercial extract of adrenal cortex. In 3 experiments no treatment whatever was employed and the use of salt for seasoning food was avoided. All the blood pressure observations were made by the carotid loop (Van Leersum) method. The cuff was adjusted by the same observer in every case and not less than 12 readings were recorded each time. Following excision of the second adrenal, in hypertensive dogs, a decided fall of blood pressure sometimes occurs within a day. We have observed a similar fall of pressure in some hypertensive animals after operations other than adrenalectomy. Our experience has shown that return to hypertensive levels of pressure can occur in such adrenalectomized dogs without administration of salt or adrenal extract. The rise in pressure, therefore, cannot be attributed, with confidence, to treatment when given.

Reduction of Experimental Renal Hypertension by Pexis of Spleen or Omentum to the Kidney

The effect of the pexis between kidney and the spleen or omentum upon the blood pressure of dogs rendered hypertensive by Goldblatt's1 method of renal constriction has been studied in this laboratory since 1936. Sixty-five dogs have been employed in the development of 2 suitable technics for establishing organ pexis to such ischemic kidneys. Seven animals survived the various surgical procedures for producing carotid loop,2 hypertension1 and the union of the organs.Only 2 died as the result of the latter operation. Fifty-six dogs died or were discarded because of hemorrhage from the carotid loop employed for blood pressure determination, anesthetic deaths, uremia from infarction of the kidneys, distemper, and operative infection. Postoperative shock was insignificant following the pexis which was performed one to 3 months after the hypertension was established. Control operations in which the omentum and spleen were manipulated did not result in a significant prolonged fall in blood pressure.The blood pre...

Acute arterial lesions in rabbits with experimental renal hypertension: Wilson, C., and Pickering, G. W.: Clin. Sc. 3: 343, 1938

Acute arterial lesions in rabbits with experimental renal hypertension: Wilson, C., and Pickering, G. W.: Clin. Sc. 3: 343, 1938

UNUSUAL HYPERTENSIVE RENAL DISEASE

The problem of the precise nature of the relationship between renal disease and arterial hypertension has been brought nearer to a satisfactory solution by the work of Goldblatt and his associates.1The purpose of the present discussion is twofold: (1) to report unique clinical analogies to experimental renal hypertension and (2) to illustrate other types of somewhat unusual organic kidney disease associated with hypertension. It is hoped that this paper will stimulate the publication of more extended clinical studies on the subject of renal hypertension. Conclusions drawn from animal experiments or even from excellent pathologic studies on hypertensive patients2involve some danger of oversimplification of the problems of human hypertension. ACUTE HYPERTENSION DUE TO THROMBO-ARTERITIS OBLITERANS OF SMALL RENAL ARTERIES Case 1.—History.— F. M., a man aged 40, was admitted in January 1933 complaining of headaches, pains in the legs, loss of weight and intermittent hiccup

Failure to Demonstrate Pressor Properties in Extracts of Blood from Hypertensives

The theory that hypertension may be due to the accumulation of a humoral pressor substance or substances of renal origin has been supported by the finding of increased concentrations of pressor material in kidneys from patients with various hypertensive diseases and from dogs with experimental renal hypertension, Against this hypothesis is the failure to find increased pressor properties in the blood of subjects with hypertension. Recent chemical studies indicated that the pressor principle in rabbits'kidneys is related to the globulins. This work suggested the possibility of concentrating the hypothetical pressor substance in blood by similar chemical procedures. The present report is concerned with the vasomotor properties of extracts of human and of dog's blood containing protein fractions prepared in the following way. Approximately 100 cc of freshly drawn blood was defibrinated and centrifuged. The serum was drawn off and half saturated with ammonium sulfate, and the resulting precipitate dialyzed against tap water until free of sulphate. The dialysate was then dried in a Florsdorf-Mudd apparatus and taken up in a small volume of saline. The final solution was tested by intravenous injection into small unanesthetized dogs with Van Leersum (carotid) loops, and the effect on the blood pressure noted. Observations were made on the blood of 5 patients with persistent hypertension, and 3 dogs with hypertension due to renal ischemia. In no instance was a well-defined pressor response noted. The failure to find the renal pressor material in the blood stream may be due to a number of possible causes, such as inefficient extraction, insufficient amount of the pressor substance in the blood stream, or differences between the chemical properties of renal pressor substance in man and rabbits. It is also possible that ultimately the pressor substance may prove to have no relation to hypertension.

Effect of Total Sympathectomy on Experimental Renal Hypertension in Dogs.

SummaryIn one dog with sustained hypertension established by application of Goldblatt clamps to both renal arteries, total sympathectomy produced a moderate drop in the blood pressure, which, however, has remained well above the control level. In another dog, previously sympathectomized, hypertension could be produced by bilateral application of Goldblatt clamps.

STUDIES ON EXPERIMENTAL HYPERTENSION

Excision of the thoracic portion of the splanchnic nerves and the lower four dorsal sympathetic ganglia on both sides failed to prevent the development of persistent hypertension which, in dogs, follows the production of renal ischemia by partial clamping of the renal arteries (1). In dogs with this type of experimental renal hypertension existent for varying lengths of time (up to about 4 years), excision of the splanchnic nerves and the lower four dorsal sympathetic ganglia failed to effect any degree of permanent lowering of the blood pressure. For the dog, at least, these results tend to minimize the importance of the splanchnic vasomotor mechanism in the pathogenesis of renal hypertension. This is in agreement with the conclusions of Prinzmetal and Wilson (6) and of Pickering (7) about the part played by the vasomotor system in human hypertension. It is also in agreement with the work of Page (8), and of Collins (9), who showed that in dogs excision of the extrinsic renal nerves alone does not prevent experimental hypertension due to renal ischemia. Although the results of this investigation fail to give experimental support for the operation that is being practised on human beings with hypertension, yet they do not necessarily controvert the reports of beneficial effects in some cases of human hypertension. Further study of the effects on man is necessary before the results of this operation can be adequately evaluated.

Effect of Transfusion of Blood From Dogs with Experimental Renal Hypertension into Normal Dogs.

Ischemia of the dog's kidney, produced by constriction of the renal arteries, results in a chronic hypertension (Goldblatt, Lynch, Hanzal and Summerville1). Destruction of the nerves to the kidney does not prevent the development of this hypertension (Page,2 Collins3). Hence it may be supposed that we are dealing with a chemical mechanism. A number of workers (Prinzmetal and Friedman4; Harrison, Blalock and Mason5; Govaerts and Dicker6) have reported that extracts from the kidneys of dogs with such experimental renal hypertension exert a greater pressor effect than similar extracts from normal kidneys. This finding leads one to believe that the hypertension is due to the liberation of pressor substances into the blood stream from the ischemic kidney. The theory would be greatly supported if increased amounts of pressor substance could be demonstrated in the blood. Dicker7 in fact reports that the blood of such dogs contains a hypertensive substance, while that of normal dogs does not. However, Page8 could...

The effect of renal denervation on the blood pressure in experimental renal hypertension: Arnott, W. M., and Kellar, R. J.: J. Path. & Bact. 42: 141, 1936

The effect of renal denervation on the blood pressure in experimental renal hypertension: Arnott, W. M., and Kellar, R. J.: J. Path. & Bact. 42: 141, 1936