Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels.

<p><b>A</b>: (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. <b>B</b>: Representative force myograph trace obtained from an ovx artery. <b>C and D</b>: Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their (<b>C</b>) change in tone and (<b>D</b>) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. <b>C</b>: Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). <b>D</b>: Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI₂) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.