Fig. 3.
Isolated mouse coronary arterioles dilated in a concentration-dependent manner to ACh. ACh-induced vasodilation was blunted in coronary arterioles from Leprdb mice (n = 7). A lower (200 μg·kg−1·day−1, n = 7 animals) and a higher (400 μg·kg−1·day−1, n = 4 animals) dose of neutralizing antibodies to MCP-1 restored nitric oxide-mediated coronary arteriolar dilation to ACh in Leprdb mice in a similar manner (A). Flow-induced vasodilation (B) was impaired in Leprdb mice coronary arterioles (n = 6 animals) compared with m Leprdb (n = 6 animals), but it was restored with neutralizing antibodies to MCP-1 (400 μg·kg−1·day−1, n = 5 animals). ΔP, difference in pressure. Sodium nitroprusside-induced, endothelium-independent vasodilation (C) was identical in m Leprdb, Leprdb, and Leprdb treated with anti-MCP-1 (400 μg·kg−1·day−1). *P < 0.05 vs. m Leprdb; #P < 0.05 vs. Leprdb.