ISSN:1420-4096    

DOI:10.1159/000172798

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

To investigate the relation between renin content in each juxtaglomerular apparatus and reduction of plasma renin activity (PRA) with aging, the PRA and microdissected superficial or juxtamedullary single nephron renin content (SNRC) were determined in 5 young (3–6 months) and 5 aged (13–18 months) rats fed on a normal salt diet. The mean value of the PRA in the aged group was significantly lower than that of the young group. A highly significant correlation was found between the RPA and mean values of the superficial SNRC. The mean values of both the superficial and deep SNRC in the aged rats were significantly lower than those of the corresponding zones in the young rats. It is suggested that decreased synthesis of renin in each juxtaglomerular apparatus is an important factor in the decreased PRA observed with ag

ISSN:1420-4096    

DOI:10.1159/000172799

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

These experiments were designed to compare the natriuretic ability of old (age 22–24 months) and young (4–6 months) rats after volume expansion. No difference in extracellular fluid volume was noted as estimated by inulin space; old 18.8 ± 0.6% and young 18.2 ± 0.7% of body weight. Standard clearance techniques were utilized in unanesthetized animals. The fraction of infused sodium excreted during and after expansion with isotonic saline equal to 7% BW was statistically lower in the old group 53 ± 2 vs. 68 ± 3% (p < 0.01). Similar measurements were made during the infusion of whole blood equal to 2.3% BW. Again the old rats excreted a significantly lower fraction of the infused Na, 55 + 10 vs. young 112 ± 12%. These differences do not appear to be explained by changes in glomerular filtration rate, blood pressure, hematocrit or serum protein concentration. We conclude that aged rats have an impaired ability to excrete sodium with volume expansion but the mechanism for this defect is yet to be de

ISSN:1420-4096    

DOI:10.1159/000172800

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

The mechanisms of the abnormal renal tubular handling of sodium and water in hypothyroidism are still unexplained. Since prostaglandins (PG) have been shown to diminish the tubular reabsorption of both sodium and water, this study was undertaken to examine the possibility that the tubular abnormalities observed in hypothyroidism are prostaglandin mediated. Renal clearance studies were performed in rats before and after administration of two prostaglandin synthetase inhibitors. There was no significant difference in the PG-inhibitor induced absolute and percentage decrease of sodium and fluid excretion between the normal and hypothyroid rats during mild volume expansion. This indicates that prostaglandins are not responsible for the increased fractional sodium and water excretion in hypothyroid animals.

ISSN:1420-4096    

DOI:10.1159/000172801

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

In an effort to elucidate mechanisms by which glucocorticoids enhance urinary protein excretion, albumin and lysozyme excretion patterns were studied in normal rats which had been subjected to a variety of experimental protocols. On the basis of these studies the following conclusions were reached: (1) The acute administration of glucocorticoids produces an immediate increase of both glomerular nitration rate (GFR) and of urinary albumin and lysozyme excretion rates. (2) A delayed albuminuric response to glucocorticoids occurs 14–32 h after drug administration. This second period of albuminuria is quantitatively far more significant than the acute albuminuric response and it occurs at a time when GFR is not statistically different from control experimental animals. (3) Lysozyme excretion 14–32 h following glucocorticoid administration is normal, suggesting an intact tubular protein reabsorption mechanism at the time of maximal albuminuria. (4) The delayed albuminuric period cannot be acutely reproduced by infusion of 5 ml of serum harvested from dexamethasone pretreated albuminuric rats. (5) Dietary Na intake (and presumed activity of the renin/angiotensin axis) does not appear to influence the magnitude of the glucocorticoid-induced albuminuric reaction. Further work is needed to more fully delineate the pharmacologic pathway by which glucocorticoids affect urinary protein excretion and to ascertain whether this response differs between the normal and pathologic kid

ISSN:1420-4096    

DOI:10.1159/000172802

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

This investigation describes the evolution of functional and morphological changes in the kidney of female spontaneously hypertensive rats (SHR; 5–90 weeks) and control animals of the same genetic strain, Wistar-Kyoto (WKY). Systolic blood pressure in SHR was 162.0 ± (SD) 14.1 mm Hg up to 45 weeks, then increased to 189.4 ± (SD) 16.6 mm Hg (50–90 weeks). Blood pressure in WKY controls remained constant (117.8 ± 13.6 mm Hg, 5–100 weeks). Protein excretion in the SHR was higher than controls (1.5 ± 0.5 mg/24 h x 100 g BW, 5–100 weeks) from week 30 on. At 90 weeks, excretion rose to 26.1 ± 9.8 mg/24 h x 100 g BW and is predominately an albuminuria. After 70 weeks superficial tubular fluid albumin concentration in the SHR is significantly increased (p < 0.001) over controls. Microscopic changes were evident in glomeruli, tubules, interstitium and arterial vessels at 72–90 weeks and demonstrated an increasing gradient of severity from outer to inner cortex. Glomeruli show sclerosis, fibrinoid necrosis and pericapsular fibrosis. Glomeruli studied with a polyanionic stain revealed a marked decrease in staining affinity of deep, compared to superficial glomeruli. The arterial lesions consisted of thickening of the intima and hyperplasia of the media. WKY kidneys were unremarkable. The selectivity of renal injury and proteinuria in the female SHR is similar to that in the male SHR. However, the evolution of these changes is delayed and may be related to a lower blood pressure until 5

ISSN:1420-4096    

DOI:10.1159/000172803

出版商:S. Karger AG    

年代:1981

数据来源: Karger