title: H2S causes contraction and relaxation of major arteries of the rabbit.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  NaHS at low doses caused minor relaxation of rabbit blood vessels, indicating a possible therapeutic benefit for low dose H2S in the cellular milieu.
authors.affiliation: 2nd Department of Internal Medicine, Faculty of Medicine, Comenius University and University Hospital, Bratislava, Slovakia.
authors.forename: Martin
authors.initials: M
authors.lastname: Caprnda
authors.affiliation: The Centre for Chronic Disease, College of Health & Biomedicine, Victoria University, Melbourne, Werribee Campus, Victoria, Australia.
authors.forename: Tawar
authors.initials: T
authors.lastname: Qaradakhi
authors.affiliation: School of Health and Biomedical Sciences, RMIT University, Bundoora West, Victoria, Australia.
authors.forename: Joanne L
authors.initials: JL
authors.lastname: Hart
authors.affiliation: Department of Endocrinology, Bogomolets National Medical University, Kyiv, Ukraine.
authors.forename: Nazarii
authors.initials: N
authors.lastname: Kobyliak
authors.affiliation: Department of Chemical Drugs, Faculty of Pharmacy, University of Veterinary and Pharmaceutical Sciences, Brno, Czechia.
authors.forename: Radka
authors.initials: R
authors.lastname: Opatrilova
authors.affiliation: Department of Chemical Drugs, Faculty of Pharmacy, University of Veterinary and Pharmaceutical Sciences, Brno, Czechia. Electronic address: kruzliakpeter@gmail.com.
authors.forename: Peter
authors.initials: P
authors.lastname: Kruzliak
authors.affiliation: The Centre for Chronic Disease, College of Health & Biomedicine, Victoria University, Melbourne, Werribee Campus, Victoria, Australia.
authors.forename: Anthony
authors.initials: A
authors.lastname: Zulli
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000187:drug effects*; D050197:Atherosclerosis / Q000188:drug therapy; D006710:Homocysteine / Q000494:pharmacology; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D020030:Nitric Oxide Donors / Q000494:pharmacology; D011817:Rabbits; D013440:Sulfides; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D020030:Nitric Oxide Donors; D013440:Sulfides; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D006710:Homocysteine; C025451:sodium bisulfide; D000109:Acetylcholine; D006862:Hydrogen Sulfide
keywords: Aorta; Blood vessels; Carotid artery; Contraction; H(2)S; Renal artery