The natural course of malignant hypertension

Milliez, P; Tcherdakoff, P; Samarcq, P; Rey, L. P.

doi:10.1007/978-3-642-49899-2_13

Cited by 7 publications

(1 citation statement)

References 37 publications

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“…In the former, glucocorticoids induce breakdown of proteins and nucleic acids, decrease protein synthesis and enhance amino acid release, whereas, in the latter, in addition to lipolysis of white fat deposits, glucocorticoids increase the ability of lipolytic agents to activate triglyceride lipolysis and also potentiate the lipolytic effects of other hormones. It is interesting to note that profound body weight loss is one of the main features of human malignant hypertension in which 10, 20 and even 34 kg may be lost in a short time (Keith, Wagener and Kernohan, 1928;Kincaid-Smith, McMichael and Murphy, 1958;Milliez et al, 1960). An explanation for this phenomenon has not yet been found.…”

Section: Discussionmentioning

confidence: 99%

Differing patterns of altered glucocorticoid secretion in experimental malignant and benign hypertension. Influences upon the lymphoid system and on arterial connective tissue metabolism

Chatelain

Bumpus

Chernicky

et al. 1983

The Journal of Pathology

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Alterations in plasma glucocorticoid levels and in the evolution of the thymus gland were studied in groups of malignant (MHY) and benign (BHY) hypertensive rats sacrificed at 6, 9, 12 and 24 days after aortic ligation between the renal arteries. Although the degree of blood pressure elevation was similar in MHY and BHY animals, MHYs were characterised by severe weight loss, increased plasma renin activity and elevated blood urea nitrogen. MHY animals sacrificed at day 6 showed markedly increased plasma corticosterone (PC) levels (PC: 604 ± 3·9 μg/dl) accompanied by severe thymus atrophy (123 ± 19 mg). In 6‐day BHY animals elevated plasma corticosterone and thymus atrophy were also present but were not as marked as in MHY (BHY: PC: 38·8 ± 4·6 μg/dl, thymus wt: 244 ± 33 mg). Values from BHYs were, however, significantly different from sham‐operated (Sham‐op) controls (Sham‐op: PC: 22·6 ± 1·4 μg/dl; thymus wt: 631 ± 32 mg). In BHY animals sacrificed at day 9, plasma corticosterone had returned to baseline levels. From this time period onward, in BHY animals normal plasma corticosterone was accompanied by a steady recovery of the thymus gland, generalised lymphoid proliferation, and by the proliferation of collagen and elastin (measured by the in‐vitro incorporation of 14C‐l‐proline into both proteins) in the intima‐media and adventitia of the thoracic aorta. Contrary to the normalisation of plasma corticosterone and thymus recovery observed in BHYs, corticosterone remained chronically elevated in MHYs and thymus atrophy was present throughout the entire evolution oif the disease. In MHYs, the arterial connective tissue proliferation was repressed and the synthesis of collagen and elastin was similar to normotensive controls. A. Statistically significant decrease in collagen concentration was present in both intima‐media and adventitia of MHYs when compared to either BHMs or normotensive controls. Impaired vascular hypertrophy in MHYs coexisted with marked alterations in the lymphoid system. In the thymus severe atrophy, thymocyte depletion and a reverse corticomedullary pattern were observed. When the thymocytes remaining in the organ were challenged with the T cell mitogen concanavalin A they showed an impaired proliferative response. In the blood a significant reduction in circulating lymphocytes and marked neutrophilia were observed. These findings suggest that increased glucocrticoid secretion marks important modifications in cells and tissues involved in the production of necrotising arterial lesions during the evolution of malignant hypertension.

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Section: Discussionmentioning

confidence: 99%

Differing patterns of altered glucocorticoid secretion in experimental malignant and benign hypertension. Influences upon the lymphoid system and on arterial connective tissue metabolism

Chatelain

Bumpus

Chernicky

et al. 1983

The Journal of Pathology

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Indications for Pretransplant Nephrectomy

Rosenberg

Azcárate

Fleischmann³

et al. 1973

Arch Surg

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Acute arterial fibrinoid deposition and ischaemic parenchymal damage of the kidney. Pathogenic factors in the development of malignant hypertension

Chatelain

Dardik

Shainoff

1983

The Journal of Pathology

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The development and evolution of hypertensive vascular lesions affecting the arterial supply of (a) the kidney and (b) organs other than the kidney were studied in rats developing either malignant (MHY) or benign (BHY) hypertension 3, 6, 9 and 12 days after aortic ligation between the renal arteries. Vascular disease evolved into two distinct patterns which suggested acute renal damage to be the determinant for the development of either the malignant or benign form of hypertension. Three days after aortic ligation MHY and BHY animals showed widespread fibrinoid deposition in vascular territories above the aortic ligature. However, in MHYs these lesions were much more severe and, in the kidney, they were accompanied by the development of focal parenchymal atrophy, microinfarcts and hyalin droplet degeneration of cells of the Bowman capsule. The degree of renal damage correlated with elevations in blood urea nitrogen (BUN) and plasma creatinine; however, there was no correlation with rises in blood pressure, plasma renin activity (PRA), aldosterone or corticosterone which were similarly elevated in 3-day MHY and 3-day BHY animals. Between 6 and 12 days a marked clearance of fibrinoid took place in all organ beds of BHYs, but in the non-renal vasculature of MHY animals fibrinoid remained prominent and served as the central core for necrotising arterial lesions. In the kidney of MHYs some reduction in the fibrinoid content was observed, but the parenchymal damage perpetuating from the earlier stages had exacerbated leading to collagen deposition and a marked increase in the collagen concentration of the renal cortex. These features were accompanied by further elevations in PRA and corticosteroids and a progressive deterioration of renal function. By contrast, in 12-day BHY animals, despite sustained hypertension, PRA and corticosteroids were falling from their previously higher levels and normal renal function was maintained. These studies warrant inference that extensive parenchymal damage of the kidney due in part to severe arterial fibrinoid deposition is one of the initial events in the development of malignant hypertension.

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The natural course of malignant hypertension

Cited by 7 publications

References 37 publications

Differing patterns of altered glucocorticoid secretion in experimental malignant and benign hypertension. Influences upon the lymphoid system and on arterial connective tissue metabolism

Differing patterns of altered glucocorticoid secretion in experimental malignant and benign hypertension. Influences upon the lymphoid system and on arterial connective tissue metabolism

Indications for Pretransplant Nephrectomy

Acute arterial fibrinoid deposition and ischaemic parenchymal damage of the kidney. Pathogenic factors in the development of malignant hypertension

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