| Abstrakt: |
Morphological changes induced in the juxtaglomerular cells by mercuric chloride (HgCl) were studied using light and electron microscopy. HgCl was injected subcutaneously into rats at 4 mg per kg body weight and groups of rats were sacrificed at 30 min, 1, 3, 6, and 24 h after injection. The juxtaglomerular granulation index (JGI) was calculated according to the method of Hartroft and Hartroft (1953). Superficial JGI (sJGI), deep JGI (dJGI) and total JGI (tJGI) were determined for each animal. The mean values of all three JGF's were higher in experimental than in control rats. There was an abrupt increase in dJGI and tJGI (P<0.05) at 30 min after injection. In experimental rats, the ratios of sJGI/dJGI were lower than control values and gradually decreased over the treatment period with the exception of 30 min. The ratios were as follows: 4.3 (control), 2.4 (30 min), 3.3 (1 h), 2.8 (3 h), 2.0 (6 h) and 1.2 (24 h). At 30 min after injection, no obvious ultrastructural changes were seen in the juxtaglomerular cells. Ultrastructural changes were observed at 1 h, suggestive of active formation of granules. By 6 h granules were present in smooth muscle cells of the afferent arteriole adjacent to the granulated cells. By 24 h, hypergranulation and hypertrophy of juxtaglomerular granulated cells were observed. Although the mechanism of the effect of HgCl-induced acute renal failure is not fully understood, this study further substantiates the following hypothesis for the initiation of acute renal failure. We propose that increased renin synthesis and subsequent activation of the renin-angiotensin system, via the mechanism of tubuloglomerular feedback, results in the renal functional disturbances characteristic of acute renal failure and is responsible for the initiation of HgCl-induced acute renal failure. The present study supports this hypothesis since increased renin-angiotensin system activity, as judged by JGI, was observed after HgCl administration. [ABSTRACT FROM AUTHOR] |
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