Susceptibility to apoptosis measured by MYC, BCL-2, and BAX expression in arterioles and capillaries of adult spontaneously hypertensive rats

Hypertension results in microvascular rarefaction or disappearance of micro vessels. In the present study, we investigated the pathogenic role of apopt osis in hypertension-induced rarefaction of heart arterioles and capillarie s of spontaneously hypertensive rats (SHR). Experiments were performed on h earts from 6-week-old, 16-week-old, and 30-week-old SHR (n = 30 rats) (SHR6 , SHR16, SHR30). We used as controls 6-week-old, 16-week-old, and 30-week-o ld normotensive rats (WKY) (n = 30 rats) (WKY6, WKY16, WKY30). We analyzed the expression of c-myc, bcl-2, and bar and in situ end-labeling DNA fragme ntation in vascular smooth muscle cells of arterioles and endothelial cells of arterioles and capillaries. Endothelial cells of capillaries and endoth elial and smooth muscle cells of arterioles of hypertensive animals (SHR) e xpress more Bar protein and Myc protein than their respective normotensive controls by margins that were statistically significant. The SHR30 group ex pressed the lowest levels of Bcl-2 protein by a margin that was statistical ly significantly different from WKY30. We did not find evidence of apoptosi s in arterioles or capillaries on the basis of in situ end-labeling. Howeve r, our results indicated that alterations in the expression of members of t he Bcl-2 family of proteins and Myc protein occurred in smooth muscle cells and endothelial cells of arterioles and capillaries of SHR. In conclusion, although evidence of apoptosis in arterioles and capillaries was not found by in situ end-labeling, our findings suggest that in hypertension they ma y have a higher susceptibility to apoptosis, and therefore rarefaction may be a consequence of apoptosis. (C) 1999 American Journal of Hypertension, L td.