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Oxidized LDL reduces NO-mediated and endothelium-derived hyperpolarizing factor-mediated dilations. We studied, in hamster skeletal muscle resistance arteries (213+/-8 micrometer n=51), whether an altered vascular smooth muscle (VSM) response, particularly sensitization of the VSM contractile apparatus to Ca(2+), is involved in this oxLDL effect. Methods and Results-VSM or endothelial [Ca(2+)](i) and vascular diameter were measured in response to norepinephrine (0.3 micromol/L), sodium nitroprusside (10 micromol/L), C-type natriuretic peptide (1 to 100 nmol/L), papaverine (0.1 to 10 micromol/L), or the endothelial agonist acetylcholine (ACh, 0.01 to 1 micromol/L). OxLDL significantly increased resting VSM [Ca(2+)](i) (11+/-3%), decreased diameter (8+/-2%), and enhanced norepinephrine-induced constrictions. Dilations to sodium nitroprusside and C-type natriuretic peptide were significantly reduced (by 10+/-2% and 35+/-6%), whereas dose-response curves for papaverine and ACh were shifted to the right, despite unchanged increases in endothelial Ca(2+) after ACh. OxLDL significantly shifted the Ca(2+)-diameter relation to the left, as assessed by stepwise increasing extracellular Ca(2+) (0 to 3 mmol/L) in depolarized skeletal muscle resistance arteries. This sensitization to Ca(2+) by oxLDL was abolished after inhibition of Rho (C3 transferase) or Rho kinase (Y27632).

circulation

Oxidized LDL Increases the Sensitivity of the Contractile Apparatus in Isolated Resistance Arteries for Ca <sup>2+</sup> via a Rho- and Rho Kinase–Dependent Mechanism

Oxidized LDL Increases the Sensitivity of the Contractile Apparatus in Isolated Resistance Arteries for Ca 2+ via a Rho- and Rho Kinase–Dependent Mechanism

Oxidized LDL Increases the Sensitivity of the Contractile Apparatus in Isolated Resistance Arteries for Ca ²⁺ via a Rho- and Rho Kinase–Dependent Mechanism