Results. : In steroid-treated eyes ECM (plaques) accumulated under the endothelium of the inner wall of the outflow loops. On electron microscopy, this material contained fine fibrils that labeled for type VI collagen. Plaques were also seen in the contralateral controls of the treated animals but here they were significantly less in amount. In the untreated Braford controls and in untreated calf eyes, plaques were nearly absent. In the TM cells of the treated eyes there was a loss of glycogen from the cytoplasm and an increase in basement membrane-like material. These changes were not seen in contralateral eyes or eyes of untreated animals.
CBG seems to be expressed in numerous cells within the human heart, most of them MC targets. Our results with RT-PCR indicate intrinsic biosynthesis of the binding globulin. This is in contrast to previous studies, which described the lack of CBG expression in rat heart [ 16 ]. This discrepancy may be due to species differences or to differences in immunocytochemical methods. Cardiac CBG found in human heart may be identical with or be rather similar to liver CBG, judging from the equal sizes of both amplification products. Another steroid binding protein, sex hormone binding globulin (SHBG) has previously been shown to occur in human myocardium [ 13 ]. Extra hepatic expression of steroid binding globulins has been observed in numerous organs including prostate, testis, and throughout the brain, for review see [ 14 ]. Although the functional importance of cardiac CBG is yet to be determined, it seems likely that CBG is involved in adrenal steroid actions on the heart, perhaps in part independent from nuclear GR. GR immunoreactivity was found only in scattered myocardial cells while MR expression was abundant. It has been suggested that most cardiac effects of GCs are mediated through the MR [ 17 ]. Chronic high levels of GCs seem to act in heart mainly as MR antagonists [ 18 ] perhaps accounting for tissue damage known to occur in heart upon chronic stress [ 19 ].