Effects of H₂S on myogenic responses in rat cerebral arterioles.
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.


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.
Department of Physiology, Xuzhou Medical College, Xuzhou, Jiangsu, China.
Lei
L
Liu
Hong
H
Liu
Dong
D
Sun
Weili
W
Qiao
Youjian
Y
Qi
Hong
H
Sun
Changdong
C
Yan
D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D054022:Cerebrum / Q000098:blood supply*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D006862:Hydrogen Sulfide / Q000097:blood / Q000378:metabolism*; D054086:KATP Channels / Q000037:antagonists & inhibitors / Q000378:metabolism; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D026902:Potassium Channel Blockers / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013440:Sulfides / Q000378:metabolism / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D004791:Enzyme Inhibitors; D054086:KATP Channels; D026902:Potassium Channel Blockers; D013440:Sulfides; D014665:Vasodilator Agents; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; C025451:sodium bisulfide; D005905:Glyburide; D019331:NG-Nitroarginine Methyl Ester; D006862:Hydrogen Sulfide