Exact(1)
In mouse aorta, NO is the sole endothelial-derived mediator [ 26].
Similar(59)
Window L-type Ca2+ influx may underlie the reduced relaxing efficacy of NO in mouse aorta when the contraction is elicited mainly via L-type Ca2+ influx [ 30].
Recently, we showed that the relaxing efficacy of NO in mouse aorta was dependent on the contractile agonist, and more specifically, decreased when the contraction was mainly elicited via L-type Ca2+ influx as with elevated extracellular K+, but increased when Ca2+ influx was partially inhibited with L-type Ca2+ channel blockers [ 30].
TRP4 forms part of a store operated Ca2+ entry channel which is involved in the control of NO-dependent relaxation of the mouse aorta [ 8].
Furthermore, a recent investigation using high concentrations of 7-KC (205 μM) found no effect of ex vivo incubation on ACh-mediated relaxation of mouse aorta [36].
Endothelial cells were isolated from mouse aorta.
Interestingly, a severe aneurysm was observed in the aorta from an Ldlr-3KO mouse (aorta 6944; Figures S1 and S2).
Increased oxidative stress and ROS production, associated with decreased endothelial NO bioavailability, have been detected during the aging process in different vascular beds in various animal models including the rat aorta [ 37], coronary arteries [ 38], and mouse aorta [ 39].
Immunohistochemistry confirmed AR expression in intact mouse aorta and in cultured aortic EC and SMC.
Zhao et al. [ 22] showed that estrogen alters expression of miRNAs in the mouse aorta.
Figure S2: Aortic atherosclerosis in the APOE-null mouse aorta analyzed by RNA-seq.
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