Apoptosis Occurs in Endothelial Cells during Hypertension-Induced Microvascular Rarefaction

摘要: Disappearance of microvessels (microvascular rarefaction) during hypertension is a process that exacerbates the hypertensive condition. The cellular by which vessels disappear not known. In present study, we investigate pathogenic role cell death, specifically apoptosis, in hypertension-induced microvascular rarefaction. An established rodent one kidney/one clip (1K1C) Goldblatt model was used. Histological and ultrastructural characteristics apoptosis necrosis were used to define incidence two types death. new method situ end-labeling DNA fragmentation known occur analyzed, expression an apoptosis-related gene, clusterin, identified using Northern blots hybridization. Microvessels skeletal muscle compared 1K1C animals (n = 3 per time point) control 6) at experimental times after surgery up (1, 2, 4 days 1, 6 weeks). Loss verified. Endothelial necrosis, more frequent than controls. Apoptosis endothelial cells found most often within 1 week surgery. Clusterin mRNA transcripts increased above levels all treatments, but localized cells. this instance, clusterin may be epiphenomenon, directly related presence apoptosis. results demonstrate for development rarefaction hypertension. significance novel finding these now direct site-specific anti-apoptosis therapy treatment structural rarefaction, unaffected conventional anti-hypertensive therapies.