Basement membrane of hypothalamus and cortex capillaries from normotensive and spontaneously hypertensive rats with streptozotocin-induced diabetes

Basement membrane of hypothalamus and cortex capillaries from normotensive and spontaneously hypertensive rats with streptozotocin-induced diabetes

U. Junker;C. Jaggi;G. Bestetti;G. L. Rossi;U. Junker;C. Jaggi;G. Bestetti;G. L. Rossi;
acta neuropathologica 1970 Vol. 65 pp. 202-208
192
junker1970actabasement

Abstract

Basement membrane (BM) thickness of hypothalamic arcuate nucleus capillaries was measured in normotensive (WKY) and hypertensive (SHR) rats 4 and 8 months after streptozotocin or saline injection. Three groups were studied: controls (C), diabetics (D), and animals with impaired glucose tolerance (L). For comparison, BM thickness of cortical capillaries of an occipital, and a frontal area was measured in three different layers starting from the pial surface. Independently from strain, hypothalamic capillary BM was thicker in older than in younger animals. At both 4 and 8 months, BM thickness was lowest in C, highest in D, and intermediate (between C and D) in L. Hypertension combined with diabetes did not further increase BM thickness. In both C and D no difference was found between the two cortical areas. The BM thickness of C increased from the superficial to the deep layer. In C hypertension induced BM thickening in the superficial frontal and the deep occipital layer. In the intermediate and the deep layer of the frontal area BM was thicker in WKY-D than in WKY-C. In every layer BM was thicker in SHR-D than in corresponding controls. Hypertension combined with diabetes enhanced BM thickening in the intermediate and the deep layer of the frontal and in the intermediate layer of the occipital area. Degenerative changes occurred in hypothalamic and cortical pericytes. These changes were more frequent in hypertensive than in normotensive animals. In conclusion, a microangiopathy characterized by BM thickening and pericytic degeneration occurs in the brain of diabetic animals. Its intensity and enhancement by a concomitant hypertension vary from hypothalamus to cortex.

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