FIG. 6.

HNO induces spreading dilatation responses in pressurized rat mesenteric arteries. (A) Using a third pipette, one branch at an arterial bifurcation (Br 1) was cannulated, through which perfusate containing an agonist and fluorescent marker was infused. (B) Simultaneous traces of outer diameter in response to luminal infusion of 30 μM Angeli's salt (AS) and 0.1 μM carboxyfluorescein into Branch 1 (Br 1). The arrowheads in (A) indicate the positions of diameter and fluorescence measurement in Br 1 and upstream from the bifurcation into the Feed artery (0–2.0 mm). Phenylephrine (0.5 μM) was present in the superfusion solution, resulting in 79% of maximum tone and synchronized vasomotion along the entire arterial segment. AS was infused during the period indicated by the bar (0–360 s) and clearly evoked spreading dilatation that decayed with distance from the bifurcation, but was associated with continued synchronized vasomotion (compare to Fig. 1A). (C) Summary data showing local (Br 1) and spreading dilatation (0–2.0 mm) to luminal perfusion of 30 μM AS into Br 1 (n = 3). The data are normalized to ∼ 80% dilatation at 0 mm. The local and spreading dilatation were markedly reduced in the presence of either 45 mM K⁺ (n = 1) or TEA (1 mM) and 4-AP (150 μM) (n = 2), and these data were combined (K⁺, n = 3). (D) Summary data showing local (Br 1) and spreading dilatation (0–2.0 mm) to luminal perfusion of ACh (10 μM) into Br 1. Responses were obtained in the absence (Control) and presence of apamin (50 nM) and TRAM-34 (1 μM, A + T) (n = 4), and were normalized to ∼ 80% dilatation at 0 mm. The local and spreading dilatation were markedly reduced by the additional presence of either L-cysteine (3 mM, A + T + L-cys, n = 4), or the NOS inhibitor L-NAME (100 μM, A + T + L-N, n = 4).