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. 2011 May 1;14(9):1625–1635. doi: 10.1089/ars.2010.3279

FIG. 1.

FIG. 1.

Angeli's salt induces vasodilatation and smooth muscle cell hyperpolarization. (A) Typical trace illustrating the dilatation in response to Angeli's salt. A mesenteric artery mounted in a pressure myograph was preconstricted with phenylephrine (PE, 0.8 μM, 73% tone), and Angeli's salt (AS, 30 μM) added to the bath during the period indicated by the bar. ACh (1 μM) was added at the end. Following 5 min exposure to AS, almost complete vasodilatation was achieved, and over a longer period of time the degree of vasodilatation was reduced, perhaps resulting from decomposition of AS. Note that vasomotion was observed in these experiments, and was consistently augmented by Angeli's salt. The NO scavenger carboxy-PTIO (200 μM) was present throughout. Maximum and minimum outer diameters were 320 and 110 μm. (B) Typical trace showing hyperpolarization to AS in an artery. Smooth muscle cell membrane potential (Em) was recorded using sharp microelectrodes in a mesenteric artery mounted in a wire myograph. Both AS (10 and 30 μM) and ACh (1 μM) evoked hyperpolarization from resting membrane potential. The microelectrode was manually pulled out of the cell at the asterisk. Data are summarized in (C), n = 6–7 from three arteries; *p < 0.05 vs control. The NO scavenger carboxy-PTIO (200 μM) was present throughout all experiments. (D) Typical trace showing hyperpolarization to AS in a single smooth muscle cell. Perforated patch-clamp recording in current-clamp mode of membrane potential in a mesenteric artery smooth muscle cell in the presence of the NO scavenger HXC (100 μM). The arrow indicates where 10 μM AS's was applied, resulting in a significant hyperpolarization. Data are summarized in (E), n = 5 cells from four animals; *p < 0.05 vs control.