Minimally　modified　low　density　lipoprotein　(mmLDL)　is　a　risk　factor　for　cardiovascular　diseases.　However,　no　studies　examining　the　effect　of　mmLDL　on　vascular　smooth　muscle　receptors　have　been　released.　The　current　study　investigated　the　effect　of　mmLDL　on　the　mesenteric　artery　at　adrenoceptor　and　the　molecular　mechanisms.　Mice　were　divided　into　the　normal　saline　(NS),　mmLDL,　and　mmLDL　+　U0126　groups.　In　the　mmLDL　+　U0126　group,　the　animals　were　subjected　to　an　intravenous　tail　injection　of　mmLDL　and　an　intraperitoneal　injection　of　U0126.　Vascular　tension　caused　by　noradrenaline　(NA)　in　mesenteric　arteries　was　measured　with　a　sensitive　myograph　system.　The　serum　levels　of　oxLDL,　TNF-alpha,　and　IL-1　beta　were　detected　using　enzyme　linked　immunosorbent　assays.　The　expressions　of　the　at　adrenoceptor,　the　alpha(2)　adrenoceptor,　INF-alpha,　IL-1　beta,　and　pERK1/2　were　detected　using　real-time　polymerase　chain　reactions　and　Western　blot　analysis.　Compared　with　the　NS　group,　the　mmLDL　group　exhibited　a　noticeably　enhanced　NA　shrinkage　dose-response　curve　and　a　significantly　increased　E-max　value　(P　＜　0.01).　Prazosin　(alpha(1)　adrenoceptor　antagonist)　caused　a　noticeable　right　shift　of　the　dose-response　curve.　U0126　inhibited　the　increases　in　the　serum　levels　and　vessel　wall　expression　of　IL-1　beta　and　TNF-alpha　and　enhanced　the　NA　shrinkage　dose-response　curve　caused　by　mmLDL,　as　observed　by　a　significantly　decreased　E-max　value　(P　＜　0.01).　It　inhibited　the　increased　at　adrenoceptor　expression　caused　by　mmLDL.　The　serum　levels　of　IL-1　beta　and　TNF-alpha　demonstrated　a　positive　correlation　with　the　NA-induced　maximum　shrinkage　percentage.　U0126　inhibited　the　mmLDL-induced　increase　in　the　pERK1/2　protein　level　in　the　vessel　wall.　In　conclusion,　mmLDL　increased　the　serum　levels　of　IL-1　beta　and　TNF-alpha　in　vivo　by　activating　the　ERK1/2　pathway,　which　resulted　in　alpha(1)　receptor-mediated　vasoconstriction　and　an　increase　in　the　expression　of　alpha(1)　adrenoceptor.　The　results　of　this　study　may　provide　new　ideas　for　the　prevention　and　cure　of　cardiovascular　diseases　in　the　future.　(C)　2015　Elsevier　Inc.　All　rights　reserved.