title: Testosterone induces dilation of canine coronary conductance and resistance arteries in vivo.
abstract: BACKGROUND
  Although estrogens have been shown to be vasoactive hormones, the vascular effects of testosterone are not well defined. Like estrogen, testosterone causes relaxation of isolated rabbit coronary arterial segments. We examined the vasodilator effects of testosterone in vivo in the coronary circulation and the potential mechanisms of its actions.
  
  
  RESULTS
  Using simultaneous intravascular two-dimensional and Doppler ultrasound, we examined the effect of intracoronary testosterone in coronary conductance and resistance arteries in 10 anesthetized dogs (5 male, 5 female). We also assessed the contribution of NO, prostaglandins, ATP-sensitive K+ channels, and classic estrogen receptors to testosterone-induced vasodilation. Testosterone induced a significant increase in cross-sectional area, average coronary peak flow velocity, and calculated volumetric coronary blood flow at the 0.1 and 1 mumol/L concentrations. This effect was independent of sex. Pretreatment with N omega-nitro-L-arginine methyl ester to block NO synthesis decreased testosterone-induced increase in cross-sectional area, average coronary peak flow velocity, and coronary blood flow. Pretreatment with glybenclamide to assess the role of ATP-sensitive K+ channels did not influence testosterone-induced dilation in epicardial arteries but did attenuate its effect in the microcirculation. Pretreatment with indomethacin or the classic estrogen-receptor antagonist ICI 182,780 did not alter testosterone-induced changes.
  
  
  CONCLUSIONS
  Short-term administration of testosterone induces a sex-independent vasodilation in coronary conductance and resistance arteries in vivo. Acute testosterone-induced coronary vasodilation of epicardial and resistance vessels is mediated in part by endothelium-derived NO. ATP-sensitive K+ channels appear to play a role in the vasodilatory effect of testosterone in resistance arteries.
authors.affiliation: Cardiovascular Research Institute, University of California at San Francisco 94143-0124, USA. chou@cardio.ucsf.edu
authors.forename: T M
authors.initials: TM
authors.lastname: Chou
authors.forename: K
authors.initials: K
authors.lastname: Sudhir
authors.forename: S J
authors.initials: SJ
authors.lastname: Hutchison
authors.forename: E
authors.initials: E
authors.lastname: Ko
authors.forename: T M
authors.initials: TM
authors.lastname: Amidon
authors.forename: P
authors.initials: P
authors.lastname: Collins
authors.forename: K
authors.initials: K
authors.lastname: Chatterjee
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects; D001783:Blood Flow Velocity / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects*; D004285:Dogs; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D004965:Estrogen Antagonists / Q000494:pharmacology; D005260:Female; D000077267:Fulvestrant; D005905:Glyburide / Q000494:pharmacology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D013739:Testosterone / Q000494:pharmacology*; D014655:Vascular Resistance; D014664:Vasodilation / Q000187:drug effects
chemical_list: D004791:Enzyme Inhibitors; D004965:Estrogen Antagonists; D000077267:Fulvestrant; D013739:Testosterone; D004958:Estradiol; D005905:Glyburide; D019331:NG-Nitroarginine Methyl Ester