Experimental Renal Hypertension Research Articles

Pathogenesis of polyarteritis nodosa in hypertensive rats.

The pathogenesis of the vascular lesions of polyarteritis nodosa found in young rats with experimental renal hypertension is described. The panarteritic lesion was a product of the combination of renal injury and feeding sodium chloride. It began with a fibrinoid necrosis of the intima and media which was followed by an extensive inflammatory reaction with subsequent fibrosis of all layers of the vessel wall.

Mean Circulatory Filling Pressure Measured Immediately After Cessation of Heart Pumping

Mean Circulatory Filling Pressure Measured Immediately After Cessation of Heart Pumping

ADRENALECTOMY FOR SEVERE HYPERTENSIVE VASCULAR DISEASE

The role of the adrenal in human hypertension has not been clearly defined. That it plays a part in maintenance of normal blood pressure and may play a part in production of hypertension is suggested by some experimental and clinical evidence. Goldblatt found that total adrenalectomy interfered with experimental renal hypertension unless adequate supportive and substitution therapy was given. He assumed that the adrenal glands might play an accessory role. The primary mechanism of nephrogenic hypertension seems to be renal anoxia, with liberation of renin, interaction of renin and a substrate or activator, and formation of a pressor substance (named angiotonin by Page and hypertensin by Houssay). The depressor effect of adrenalectomy in the Goldblatt experiments probably resulted from development of a deficiency state that in turn caused alteration of the peripheral vascular resistance so that maintained increase of blood pressure could not occur. Clinical evidence of a relationship between

ASSOCIATION OF POLYURIA AND ALBUMINURIA WITH HYPERTENSION OF UNILATERAL RENAL ORIGIN

EXPERIMENTAL renal hypertension in animals is associated with polyuria, albuminuria, and sometimes edema. These manifestations may be evident whether the hypertension results from manipulation of both kidneys or of one kidney. In the latter event the function of the normal kidney is apparently altered. Since 1937, when Butler 4 reported the cure of a hypertensive child by nephrectomy, it has been known that unilateral kidney disease can cause reversible hypertension in humans. The review by Smith 29 in 1948 emphasized the difficulty of distinguishing these cases preoperatively. Perera and Haelig 24 have recently described one type of clinical history which, when present, can help in so distinguishing them. There have been many analyses of the underlying diseases of the affected kidney, but little emphasis has been placed on the effects of this type of process other than the elevation of arterial pressure, although such effects are well known in experimental

Protection against hypertension, arteriolonecrosis and death by hog renal extracts in experimental malignant hypertension.

Since hog renin is effective in the treatment and prophylaxis of chronic experimental renal hypertension in the dog, probably through antirenin, a study was made of the prophylactic effect of crude and semipurified hog renins from cortex and from whole kidney on the hypertension, arteriolonecrosis, and course of experimental renal malignant hypertension in the dog. In the absence of medullary protein, protection against the hypertension was found to be well correlated with the antirenin titer. More importantly, the nonrenin fraction of crude hog renin from cortex significantly protected against the arteriolonecrotic lesions and death.

Development of experimental renal hypertension in the dog following reduction of renal artery pulse pressure without reducing mean pressure.

ArticleDevelopment of Experimental Renal Hypertension in the Dog Following Reduction of Renal Artery Pulse Pressure Without Reducing Mean PressureEdward W. Hawthorne, Sheridan L. C. Perry, and William G. PogueEdward W. HawthorneFrom the Department of Physiology, College of Medicine, Howard University, Washington, D. C., Sheridan L. C. PerryFrom the Department of Physiology, College of Medicine, Howard University, Washington, D. C., and William G. PogueFrom the Department of Physiology, College of Medicine, Howard University, Washington, D. C.Published Online:01 Sep 1953https://doi.org/10.1152/ajplegacy.1953.174.3.393MoreSectionsPDF (596 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByInfluence of pulsatile perfusion upon renin release from the isolated perfused rat kidneyPflügers Archiv European Journal of Physiology, Vol. 415, No. 6Radiation Nephritis Clinical manifestations and pathophysiologic mechanismsUrology, Vol. 27, No. 5Renin secretion in the chronically perfused pulseless calf. Evidence for failure of stimulation by decreased pulse pressure.Circulation Research, Vol. 45, No. 1A Centrifugal Pump for Circulatory AssistanceTHE ROLE OF IMPEDANCE PLETHYSMOGRAPHY IN THE EVALUATION OF RENAL VASCULAR HYPERTENSIONAnnals of the New York Academy of Sciences, Vol. 170, No. 2 InternationalClinical Evaluation of the Phonorenogram for the Diagnosis of Occlusive Renal Artery DiseaseJournal of Urology, Vol. 101, No. 4Physiologie und Pathologie des Renin/Angiotensin-SystemsControl of Aldosterone SecretionDie renal-vasculäre HypertoniePathophysiologie des Kreislaufs und der großen GefäßeRecent advances in hypertensionThe American Journal of Medicine, Vol. 39, No. 4Pseudoxanthoma Elasticum and HypertensionNew England Journal of Medicine, Vol. 271, No. 23EditorialCirculation, Vol. 30, No. 1Die Hypertonie bei einseitigen NierenerkrankungenStudies on Segmental Renal Ischemia in the Etiology of HypertensionJournal of Urology, Vol. 91, No. 1Experimental Pyelonephritis: The Influence of Reduced Pulse Pressure on Susceptibility of the Dog Kidney to InfectionJournal of Urology, Vol. 86, No. 5HypertonieHypertonieFunctional distention of the kidney in perinephritic hypertensionAmerican Heart Journal, Vol. 58, No. 4Renin und Hypertensin, physiologische oder pathologische Wirkstoffe?Klinische Wochenschrift, Vol. 36, No. 15Conference on the Role of the Renal Pressor System in Maintenance of Experimental Renal HypertensionCirculation, Vol. 17, No. 4Cardiac Output in Rats During the Development of Cardiac HypertrophyCirculation Research, Vol. 6, No. 2 More from this issue > Volume 174Issue 3September 1953Pages 393-396 Copyright & PermissionsCopyright © 1953 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1953.174.3.393PubMed13092261History Received 28 April 1953 Published online 1 September 1953 Published in print 1 September 1953 Metrics

Treatment and prophylaxis of experimental renal hypertension with renin.

Abstract Chronic experimental renal hypertension in dogs has been successfully treated with crude and semipurified hog renins and chronic experimental renal hypertension in dogs has been prevented by prophylaxis with crude and semipurified hog renins. These therapeutic and prophylactic effects are well-correlated with the antirenin titer. This evidence for antirenin (or an antibody to a protein closely related to renin) as the mechanism of the antihypertensive effects of hog renins constitutes support for the affirmative of the long-standing controversy regarding the primary role of renin (or some closely related protein) in the pathogenesis of experimental renal hypertension. Hog renal medulla contains a factor which interferes with the antihypertensive effects of hog renin in experimental renal hypertension in the dog by a mechanism presently unknown. Renotoxic and renal protective factors have been found to occur in fractions of renal extracts. Toxicity consists in increased and protection in decreased incidence of uremia after constriction of the renal arteries. After further preliminary experiments in animals, the possible pathogenetic role of the kidney in essential hypertension will be studied by passive immunization of patients with purified antirenin to human renin.

Pantothenic acid deficiency in experimental renal hypertension in dogs.

Pantothenic acid deficiency in experimental renal hypertension in dogs.

Factors involved in the production of acute arterial lesions in rabbits with experimental renal hypertension.

The Journal of Pathology and BacteriologyVolume 65, Issue 2 p. 441-450 Article Factors involved in the production of acute arterial lesions in rabbits with experimental renal hypertension H. A. Fleming, H. A. Fleming Department of Medicine, University of Otago, Dunedin, New Zealand Working under a grant from the Medical Research Council of New Zealand.Search for more papers by this author H. A. Fleming, H. A. Fleming Department of Medicine, University of Otago, Dunedin, New Zealand Working under a grant from the Medical Research Council of New Zealand.Search for more papers by this author First published: April 1953 https://doi.org/10.1002/path.1700650216Citations: 6 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 Citing Literature Volume65, Issue2April 1953Pages 441-450 RelatedInformation

Comparative effectiveness of several new hypotensive agents as determined by their action in experimental renal hypertension and in the human patient

Comparative effectiveness of several new hypotensive agents as determined by their action in experimental renal hypertension and in the human patient

Amines in experimental hypertensions.

A sympathomimetic amine, Paredrine, was shown to be a good antihypertensive agent in experimental renal, experimental neurogenic and spontaneous hypertensions in the dog. Other closely related amines failed to possess antihypertensive activity. Paredrine did not prevent the development of experimental renal hypertension. This amine was also without chronic effect on the blood pressure of normotensive dogs.

Obstruction of the common bile duct in experimental renal hypertension in dogs.

The frequency of arterial hypertension in subchronic atrophy of the liver is very low in relation to what might be expected according to the age-distribution of the patients. The hypothesis was established that a severely damaged liver function may prevent the development of arterial hypertension, or may obviate an already existing hypertension, and that a normal or only slightly inhenced liver function is a necessary condition for the development of hypertension.Summarizing, it can be said about the results of our experiments that 6 hypertensive dogs (with experimental, rend hypertension according to Goldblatt's method!) -4 having had hypertension of short duration, 2 having had a more prolonged hypertension -displayed a gradual fall of the blood pressure towards or down to the normal, pre-operative values after obstruction of the common bile duct had been established. These blood pressure falls were observed in clogs in good health, which were sufficiently fed.In one dog biliary cirrhosis with ascites a...

The intrarenal pressure during experimental renal hypertension.

The intrarenal interstitial pressure was measured during the course of experimental renal hypertension in dogs. In perinephritic hypertension, produced by wrapping the kidney in a cellophane bag, the intrarenal pressure rose slowly from the normal value of 25 mm. Hg to a final level of about 60 mm. Hg. Strong pressure pulsations were observed in the renal parenchyma during this type of hypertension. In the hypertension following partial occlusion of the renal artery, the intrarenal pressure remained approximately normal, except in malignant hypertension when it tended to decline to about 9 mm. Hg. The hypertension of perinephritis is interpreted as a consequence of renal ischemia, the high intrarenal pressure, produced by the constricting fibrotic hull, acting to reduce the effective perfusion pressure of the kidney. The two experimental hypertensions herein examined are considered as examples of influent resistance hypertensions and effluent resistance hypertensions, the former being due to renal arterial or arteriolar resistance and the latter due to renal venous resistance, specifically at the arcuate-interlobar junction. The application of this concept to renal hypertensive disease in man is discussed.

Effect of adrenalectomy in experimental renal hypertension in the dog.

ArticleEffect of Adrenalectomy on Experimental Renal Hypertension in the DogWade Williams, Charles Whisnant, and William T. Fitts JR.Wade WilliamsFrom the Harrison Department of Surgical Research, University of Pennsylvania Schools of Medicine, and the Robinette Foundation for the Study and Treatment of Cardiovascular Disease, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, Charles WhisnantFrom the Harrison Department of Surgical Research, University of Pennsylvania Schools of Medicine, and the Robinette Foundation for the Study and Treatment of Cardiovascular Disease, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, and William T. Fitts JR.From the Harrison Department of Surgical Research, University of Pennsylvania Schools of Medicine, and the Robinette Foundation for the Study and Treatment of Cardiovascular Disease, Hospital of the University of Pennsylvania, Philadelphia, PennsylvaniaPublished Online:01 Jul 1952https://doi.org/10.1152/ajplegacy.1952.170.1.57MoreSectionsPDF (479 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Volume 170Issue 1July 1952Pages 57-60 Copyright & PermissionsCopyright © 1952 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1952.170.1.57PubMed12985863History Received 20 January 1952 Published online 1 July 1952 Published in print 1 July 1952 Metrics

Congenital coarctation of the abdominal aorta with resultant renal hypertension.

ESTABLISHMENT of experimental hypertension by compression of one or both renal arteries with a metal clamp1directed attention to lesions of main renal arteries as causes of hypertension in man. Some investigators2believed that they could demonstrate at autopsy a high incidence of arteriosclerotic narrowing in fixed preparations of renal arteries from hypertensive patients. However, Lisa and associates3could not show a relation between the level of arterial pressure during life and the caliber of the renal arteries in fresh preparations. Yuille4reviewed the relation between lesions of main renal arteries and hypertensive disease and discounted the participation of renal arteriosclerosis in the genesis of this condition. He pointed out that the lesions of large vessels were commonly associated with intrarenal arteriolar sclerosis and that both were presumably results and not causes of hypertensive disease. Had the arterial lesions been primary, then, as in experimental renal hypertension in rats,5arteriolar

Role of adrenal in pathogenesis of experimental renal hypertension as determined by a study of the bilaterally adrenalectomized nephrectomized dog.

ArticleRole of Adrenal in Pathogenesis of Experimental Renal Hypertension as Determined by a Study of the Bilaterally Adrenalectomized Nephrectomized DogLouis B. Turner, and Arthur GrollmanLouis B. TurnerFrom the Department of Experimental Medicine, Southwestern Medical School University of Texas, Dallas, Texas, and Arthur GrollmanFrom the Department of Experimental Medicine, Southwestern Medical School University of Texas, Dallas, TexasPublished Online:31 Oct 1951https://doi.org/10.1152/ajplegacy.1951.167.2.462MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Volume 167Issue 2October 1951Pages 462-472 Copyright & PermissionsCopyright © 1951 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1951.167.2.462PubMed14894674History Received 6 July 1951 Published online 31 October 1951 Published in print 31 October 1951 Metrics

Effects of caloric restriction, salt restriction, and role of pituitary and adrenal glands in experimental renal hypertension.

ArticleEffects of Caloric Restriction, Salt Restriction, and Role of Pituitary and Adrenal Glands in Experimental Renal HypertensionPhilip Handler, and Frederick BernheimPhilip HandlerFrom the Departments of Biochemistry and Nutrition and of Physiology and Pharmacology, Duke University School of Medicine, Durham, North Carolina, and Frederick BernheimFrom the Departments of Biochemistry and Nutrition and of Physiology and Pharmacology, Duke University School of Medicine, Durham, North CarolinaPublished Online:01 Sep 1951https://doi.org/10.1152/ajplegacy.1951.166.3.528MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Volume 166Issue 3September 1951Pages 528-537 Copyright & PermissionsCopyright © 1951 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1951.166.3.528PubMed14885439History Received 22 February 1951 Published online 1 September 1951 Published in print 1 September 1951 Metrics

EFFET DE L’ACIDE ASCORBIQUE SUR L’HYPERTENSION EXPÉRIMENTAL

In previously reported observations, we have shown that (a) ascorbic acid, given in large doses, had a hypotensive effect on normal blood pressure, (b) the initial hypotension, due to sudden exposure to cold, was prevented by large doses of ascorbic acid, (c) the hypertension encountered upon long exposures to cold was lowered by ascorbic acid. The present paper confirms the last result and also shows that actually ascorbic acid has a hypotensive action on experimental hypertension obtained by the two following ways: (1) excess of sodium chloride in drinking water and (2) renal compression. The hypertension and adrenal hypertrophy caused by a long exposure to cold regress when the animals are brought back to normal temperature. In its initial phase, the experimental renal hypertension is lowered by ascorbic acid but not in its chronic phase.

Renal anoxia syndrome: a review and report of 22 cases.

Excerpt Azotemia from nonrenal disease states has received much attention in the literature in recent years. Such azotemia has been described in a multitude of conditions— medical, surgical, obstet...

The nature and significance of changes in adrenal cytology, weight, and cortical/medullary ratio in experimental renal hypertension and clinical hypertension.

There is a direct proportionality between the degree of adrenal and that of cardiac enlargement in experimental renal hypertension. This is evidence for the participation of the adrenal to an extent dependent on the severity of the hypertension as reflected in the degree of cardiac hypertrophy. The greater part of the weight increase of the adrenal is due to growth of the cortex. However, the relative degree of medullary growth exceeds that of cortical growth. There is evidence of medullary hyperplasia, but the cortical growth may be due to cell hypertrophy alone. In view of the known relationship between prolonged skeletal muscle work and the size of the adrenals, in which there is likewise a relatively greater growth of the medulla, the possibility that adrenal growth in experimental renal hypertension is a consequence of the metabolic demand of increased heart muscle work must be considered. The hyperplastic, hypertrophic medulla of the renal hypertensive rat is presumed to be producing increased amounts of a hormone whose action is not known. The adrenal medulla is not necessary for the development of moderate renal hypertension though this does not exclude the possibility that it may be involved somehow in the maintainance of the hypertensive state. Large, periodic-Schiff-positive, hyaline droplets are found in the cytoplasm of adrenal cortical cells with nuclear evidence of active function. There is some evidence that these indicate hypophyseal stimulation. Similar particles are found in the medulla, suggesting an interrelationship between the two parts of the adrenal. The close resemblance of changes in adrenal weight, nuclear/cytoplasmic ratio, and nuclear and cytoplasmic structure, indicates that similar physiological and morphological controlling mechanisms are involved in the pathogenesis and maintainance of experimental renal hypertension and clinical essential hypertension.