11-Deoxycorticosterone-induced hypertension, glomerulosclerosis and renal arterial and arteriolar lesions.
Glomerulosclerosis and vascular lesions occurring in rats receiving 11-deoxycorticosterone and salt-loading have been studied in order to examine their relationship. The glomerular lesion started as focal segmental sclerosis. The globally sclerosed glomeruli were enlarged in size, demonstrating that these showed no evidence of ischemic atrophy. Advanced glomerulosclerosis occurred independent of preglomerular arteriolar pathologic lesion. No meaningful structural changes were observed in the arterial system. In conclusion, DOC-salt-induced glomerulosclerosis started as segmental lesion, occurred independent of structural alterations in the preglomerular arterioles, and took place without evidence of intrarenal arterial stenosis. Further studies are necessary to clarify about the role of hemodynamic stress-related injury to glomerular microcirculatory system as a major cause for DOC-Salt-induced glomerulosclerosis.
Shimamura
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Department of Pathology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854.
D000818:Animals; D003900:Desoxycorticosterone; D005921:Glomerulonephritis / Q000209:etiology*; D005923:Glomerulosclerosis, Focal Segmental / Q000209:etiology* / Q000473:pathology; D006973:Hypertension / Q000139:chemically induced / Q000150:complications*; D007668:Kidney / Q000098:blood supply / Q000473:pathology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride / Q000494:pharmacology
D003900:Desoxycorticosterone; D012965:Sodium Chloride