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. 2013 Dec 13;306(4):H485–H495. doi: 10.1152/ajpheart.00557.2013

Fig. 1.

Fig. 1.

Cystamine blocks dithiothreitol (DTT)-dependent activation of endogenous transglutaminases and DTT-induced vasoconstriction but not depolarization-induced vasoconstriction. A: confocal images of rat cremaster arteriolar walls incubated with Alexa Fluor 488-cadaverine (green) and exposed for 4 h to vehicle control (left), 200 μM DTT (middle), or DTT in the presence of 1mM cystamine (right). Blue shows smooth muscle nuclei stained with 4′,6-diamidino-2-phenylindole (DAPI). B: mean fluorescence intensity of Alexa Fluor 488 cadaverine in control (n = 5), DTT (n = 7)-, and DTT + cystamine (n = 5)-treated arterioles. *P ≤ 0.05 vs. control or DTT + cystamine. C: percent control diameter of isolated arterioles exposed to incremental concentrations of DTT in the absence (n = 5) or presence (n = 5) of 1 mM cystamine. Diameters in the presence of cystamine at DTT 10−6.5 to 10−3.5 M were significantly greater than those with DTT alone (*P ≤ 0.05). D: internal diameter (μm) of isolated and pressurized (60 mmHg) arterioles before (tone) and after exposure to 80 mM KCl in the absence (n = 5) or presence (n = 5) of 1 mM cystamine. Data are means ± SE.