Effect of Hydrogen Sulfide on Sympathoinhibition in Obese Pithed Rats and Participation of K ⁺ Channel

Figures

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  Figure 1. Timeline of sympathetic stimulation, stimulation with exogenous noradrenaline, and drug administration.

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  Figure 2. Experimental design. Solid line: electrical stimulation. Dotted line: exogenous noradrenaline.

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  Figure 3. Original recordings of NaHS-induced sympathoinhibition in lean and obese rats. Original recordings show the vasopressor responses induced by selective electrical stimulation of the vasopressor sympathetic outflow at the frequencies of 0.03, 0.1, 0.3, 1.0, 3.0, and 10 Hz in the absence (a) or the presence (b, c) of i.v. infusion of 310 μg/kg·min NaHS in lean (b) and obese (c) rats. Also, no significant changes in heart rate were observed during the electrical stimulation.

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  Figure 4. Effect of continuous i.v. infusion of PBS and NaHS on the vasopressor responses induced by sympathetic stimulation in lean (a, b) and obese (c–e) rats or exogenous noradrenaline in obese rats (f–h). Each point represents the mean ± S.E.M of 6 animals. ⁣∗, p < 0.05 vs. “lean” or “obese,” respectively.

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  Figure 5. Original recordings of K+ channel blockers in obese rats. Original recordings show the vasopressor responses induced by selective electrical stimulation of the vasopressor sympathetic outflow at the frequencies of 0.03, 0.1, 0.3, 1.0, 3.0, and 10 Hz in the presence of i.v. administration of (a) TEA (16.5 mg/kg), (b) 4-AP (5 mg/kg), (c) BaCl2 (65 μg/kg), and (d) glibenclamide (10 mg/kg).

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  Figure 6. Effect of (a) TEA (16.5 mg/kg), (b) 4-AP (5 mg/kg), (c) BaCl2 (65 μg/kg), and (d) glibenclamide (10 mg/kg) over the vasopressor responses induced by electrical stimulation of the sympathetic tone in obese rats. Each point represents the mean ± S.E.M of 6 animals. ⁣∗, p < 0.05 vs. obese.

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  Figure 7. Original recordings of the effect of K+ channel blockers and NaHS i.v. continuous infusion in obese rats. Original recordings show the vasopressor responses induced by selective electrical stimulation of the vasopressor sympathetic outflow at the frequencies of 0.03, 0.1, 0.3, 1.0, 3.0, and 10 Hz in the presence of i.v. administration of (a) TEA (16.5 mg/kg), (b) 4-AP (5 mg/kg), (c) BaCl2 (65 μg/kg), and (d) glibenclamide (10 mg/kg) and the continuous i.v. infusion of NaHS (310 μg/kg·min).

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  Figure 8. Effect of (a) TEA (16.5 mg/kg), (b) 4-AP (5 mg/kg), (c) BaCl2 (65 μg/kg), and (d) glibenclamide (10 mg/kg) over the sympathoinhibition induced by NaHS infusion (310 μg/kg·min). Each point represents the mean ± S.E.M of 6 animals. ⁣∗, p < 0.05 vs. obese.

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  Figure 9. Effect of (a) glibenclamide vehicle (control), (b) glibenclamide (10 mg/kg), and (c) glibenclamide (10 mg/kg) + NaHS infusion (310 μg/kg·min) on the vasopressor responses induced by electrical stimulation in lean rats. Effect of (d) glibenclamide vehicle (control), (e) glibenclamide (10 mg/kg), and (f) glibenclamide (10 mg/kg) + NaHS infusion (310 μg/kg·min) on the vasopressor responses induced by exogenous noradrenaline in obese rats. Each point represents the mean ± S.E.M of 6 animals.