BACKGROUND: The potential biological significance of hydrogen sulfide (H₂S) has attracted growing interests in recent years, but its role in the myogenic response of rat cerebral arterioles has not been explored. METHODS AND RESULTS: Rats were injected with NaHS (an H₂S donor, 2-200 µmol·kg⁻¹·day⁻¹, i.p.) or saline for 3 weeks. MBP was measured with a tail-cuff method. Cerebral arterioles were isolated and cannulated in an organ bath system, and vessel diameters were measured with an image-shearing device. Changes in diameter in response to stepwise increases in intravascular pressure (20-120 mmHg) were investigated under no-flow conditions. After the treatments, plasma H₂S increased and MBP decreased significantly. NaHS reduced the myogenic response in a dose-dependent manner. This effect was markedly attenuated by glibenclamide, a K(ATP) channel blocker. Blockade of nitric oxide (NO) production with NG-nitro-L-arginine methyl ester (L-NAME, a NO synthase inhibitor) enhanced, whereas removal of the endothelium abolished the inhibitory role of NaHS on the myogenic response. CONCLUSIONS: For the first time it has been demonstrated that H₂S decreases the myogenic response of cerebral arterioles in vivo, and this effect is endothelium-dependent and partially mediated by K(ATP) channels.
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Liu et al. (2012) studied this question.
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