Figure 1
Figure 1. HHcy impaired endothelium-dependent and EDHF-mediated vascular relaxation in SMAs of Tg-hCBS Cbs mice. SMAs were isolated from Tg-hCBS Cbs mice. (A) Plasma total Hcy levels. (B-C) Vascular contractile responses to KCl (120mM) and to cumulative additions of PE. (D) Endothelium-independent relaxation. SMAs were precontracted with PE (1μM) and examined for relaxation to cumulative additions of SNP. (E) Endothelium-dependent relaxation. SMAs were precontracted with PE and examined for relaxation to ACH. (F) NO-independent relaxation. SMAs were pretreated with the NOS inhibitor L-NAME (100μM), precontracted with PE, and examined for relaxation to ACH. (G) PGI2-independent relaxation. SMAs were pretreated with the nonselective COX inhibitor INDO (10μM), precontracted with PE, and examined for relaxation to ACH. (H) PGI2-mediated relaxation. SMAs were pretreated with the NOS inhibitor L-NAME (100μM) and the nonselective KCa blocker TEA (1mM), precontracted with PE, and examined for relaxation to ACH. (I) NO-mediated endothelium-dependent relaxation. SMAs were pretreated with the nonselective COX inhibitor INDO (10μM) and the nonselective KCa blocker TEA, precontracted with PE, and examined for relaxation to ACH. (J) EDHF-mediated endothelium-dependent relaxation. SMAs were pretreated with INDO and the NOS inhibitor L-NAME, precontracted with PE, and examined for relaxation to ACH. Values are means ± SEM (n = 5-7 mice, 2 vessel segments/mouse). *P < .05 compared with control mice. CT indicates the control group.

HHcy impaired endothelium-dependent and EDHF-mediated vascular relaxation in SMAs of Tg-hCBS Cbs mice. SMAs were isolated from Tg-hCBS Cbs mice. (A) Plasma total Hcy levels. (B-C) Vascular contractile responses to KCl (120mM) and to cumulative additions of PE. (D) Endothelium-independent relaxation. SMAs were precontracted with PE (1μM) and examined for relaxation to cumulative additions of SNP. (E) Endothelium-dependent relaxation. SMAs were precontracted with PE and examined for relaxation to ACH. (F) NO-independent relaxation. SMAs were pretreated with the NOS inhibitor L-NAME (100μM), precontracted with PE, and examined for relaxation to ACH. (G) PGI2-independent relaxation. SMAs were pretreated with the nonselective COX inhibitor INDO (10μM), precontracted with PE, and examined for relaxation to ACH. (H) PGI2-mediated relaxation. SMAs were pretreated with the NOS inhibitor L-NAME (100μM) and the nonselective KCa blocker TEA (1mM), precontracted with PE, and examined for relaxation to ACH. (I) NO-mediated endothelium-dependent relaxation. SMAs were pretreated with the nonselective COX inhibitor INDO (10μM) and the nonselective KCa blocker TEA, precontracted with PE, and examined for relaxation to ACH. (J) EDHF-mediated endothelium-dependent relaxation. SMAs were pretreated with INDO and the NOS inhibitor L-NAME, precontracted with PE, and examined for relaxation to ACH. Values are means ± SEM (n = 5-7 mice, 2 vessel segments/mouse). *P < .05 compared with control mice. CT indicates the control group.

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