Receptors for sympathetic neurotransmitters activate at least 80% of contractile tone in mouse femoral arteries in vivo.

(A) Upper panel: 5 (a–e) successive transverse line-scan images of a femoral artery in vivo. Artery diameter was obtained as the distance between the two peaks in fluorescence intensity, representing the fluorescence within the walls of the artery. Artery diameter was measured only during the final 10 seconds of a 10 min duration control period or exposure to an antagonist. There is thus a 10 minute gap between each image (a–e) and between each corresponding diameter trace in the lower panel. Lower panel: Artery diameter under each condition (a–e). (a) Control, represents artery in basal state of anesthetized animal. (b–e) Arterial diameter upon on cumulative exposure to RS79948 (0.1 µM) (b), Prazosin (0.1 µM) (c), Suramin (0.5 mM)+BIBP3226 (1 µM) and (e). 0[Ca²⁺]. (B) Average data from 6 arteries. Fractional diameter is the measured diameter divided by the passive diameter for each artery, measured in the presence of 0[Ca²⁺] solution. In the combined presence of α₁-, α₂- adrenoceptor, NPY₁ and P_2X receptor blockers, active vascular tone was reduced to less than 20% of the control level. As shown later, α₁-adrenoceptors are not fully blocked at the concentration of prazosin used (0.1 µM), and thus the tone activated by noradrenaline is greater than shown here. Significance of difference from previous drug treatment, ^*P<0.05, ^**P<0.01, ^***P<0.001 (ANOVA followed by Newman-Keuls multiple comparison test).