H₂S causes contraction and relaxation of major arteries of the rabbit

Cardiovascular disease (CVD) caused by atherosclerosis remains a worldwide burden. Hydrogen sulfide is a promising new therapeutic avenue for the treatment of CVD, however reports show exogenous H₂S has both vasodilator and vasoconstrictor effects depending on organ examined, and in vitro studies in animal models which are not resistant to developing atherosclerosis are limited. We sought to determine if rabbit arteries constricted or dilated to hydrogen sulfide.

The aorta, carotid, renal and iliac arteries were harvested from New Zealand White rabbits (n=4) and subjected to a concentration response curve to the fast H₂S releaser NaHS. In addition, a bolus dose of NaHS was used to determine if further dilation was achievable after maximum dilation to acetylcholine similar to nitric oxide donors. Further, NaHS was used to determine if H₂S could impair homocysteine induced endothelial dysfunction.

Blood vessels relaxed poorly to NaHS and contracted at higher doses. A bolus dose of NaHS relaxed then contracted the aorta, however a bolus dose of NaHS after maximal relaxation to acetylcholine caused marked contraction. NaHS did not prevent homocysteine induced vascular dysfunction.

NaHS at low doses caused minor relaxation of rabbit blood vessels, indicating a possible therapeutic benefit for low dose H₂S in the cellular milieu.