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L J RATHER

Publications and source records attributed to L J RATHER.

At least 37 records · Page 2Linked to original sources
PubMed1951

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.

Adrenal Glands↗
PubMed1950

The pathogenesis of hypertension induced by renal constriction.

Blood pressures were determined on forty-two young male albino rats and a basal level established. The rats were then divided into four groups and subjected to one of the following operations: (a) unilateral nephrectomy with exposure and handling of the opposite kidney; (b) unilateral nephrectomy and constriction of the remaining kidney with a silk figure-of-eight ligature; (c) unilateral renal constriction with a silk figure-of-eight ligature, the other kidney being left intact after exposure and handling; (d) unilateral nephrectomy and removal of the poles of the contralateral kidney (three-quarters nephrectomy). The animals were followed for 50 days, during which blood pressures were measured on twenty occasions, then killed by exsanguination under ether anesthesia. The organs were weighed according to a standardized procedure and studied histologically. Individual determinations of serum creatinine and of the hematocrit levels were made. Mean lines and frequency distributions of blood pressure were subjected to statistical analysis. A definitely significant increase in blood pressure developed in the group subjected to operation (b) within 4 days postoperative. In none of the other groups did hypertension develop. Analysis of the individual renal weights and creatinine levels indicates the independence of the development of hypertension from the total mass of functioning renal tissue. Nor is it dependent on the prevention of renal hypertrophy or the presence of fibrous perinephritis. The effect is probably due to the production of a disturbance of hemodynamics or tissue tension with the liberation of a pressor substance by the injured kidney.

Animals↗
PubMed1950

Renin protein uria in the rat; evidence that renin does not interfere with the tubular resorption of purified human hemoglobin or bovine albumin.

The intraperitoneal injection of renin together with purified human hemoglobin or bovine albumin increases the weight of the kidneys and increases the number of athrocytosed particles of protein in the cells of the proximal convoluted tubules. In the case of bovine albumin administration there is a threefold increase in protein excretion in those rats given renin as compared with those given bovine albumin alone. A possible explanation of these effects is given.

Albumins↗