title: Estrogen improves acetylcholine-induced but not metabolic vasodilation in biological males.
abstract: We have previously shown that chronic estrogen therapy improves endothelium-dependent vasodilation in the resistance vessels of biological males. Whether this is nitric oxide (NO) mediated and whether estrogen improves metabolic vasodilation is unknown. Resting forearm blood flow (FBF), ACh-induced vasodilation, and functional hyperemic blood flow (exercise) were assessed before and after the inhibition of NO with N(G)-monomethyl-L-arginine (L-NMMA) in 15 male-to-female transsexuals prescribed estrogen and in 14 age-matched males. Resting FBF was similar in the two groups and was similarly (P = 0.44) but significantly reduced by 48% after infusion of L-NMMA (P < 0.0001). The ACh dose-response relationship was shifted upward and to the left in the transsexual compared with the male group (P < 0.01). After the inhibition of NO, however, the difference in the ACh dose-response curve between the two groups was abolished (P = 0.15). Peak functional hyperemic blood flow was similar for the two groups (P = 0.94). L-NMMA produced a significant (P < 0.01) but similar (P = 0.64) reduction in peak hyperemia in the two groups. The volume of blood repaid to the forearm 1 and 5 min after exercise was also reduced by L-NMMA (P < 0.0001); however, there were no differences between the two groups. This suggests that ACh-mediated NO-dependent vasodilation may be more sensitive to the effects of chronic estrogen than exercise-induced vasodilation. Long-term estrogen does not appear to improve exercise-induced metabolic vasodilation in biological males, despite the fact that NO contributes to this process.
authors.affiliation: Centre for Heart and Chest Research, Monash University and Monash Medical Centre, Melbourne, Australia 3168.
authors.forename: G
authors.initials: G
authors.lastname: New
authors.forename: S J
authors.initials: SJ
authors.lastname: Duffy
authors.forename: R W
authors.initials: RW
authors.lastname: Harper
authors.forename: I T
authors.initials: IT
authors.lastname: Meredith
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000328:Adult; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D004966:Estrogens, Conjugated (USP) / Q000494:pharmacology; D004997:Ethinyl Estradiol / Q000494:pharmacology; D015444:Exercise; D005542:Forearm / Q000098:blood supply; D006801:Humans; D006940:Hyperemia; D007262:Infusions, Intravenous; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D008875:Middle Aged; D005082:Physical Exertion; D012016:Reference Values; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology*; D014189:Transsexualism / Q000503:physiopathology*; D014280:Triglycerides / Q000097:blood; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D019323:omega-N-Methylarginine / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004967:Estrogens; D004966:Estrogens, Conjugated (USP); D017270:Lipoprotein(a); D014280:Triglycerides; D019323:omega-N-Methylarginine; D004997:Ethinyl Estradiol; D004958:Estradiol; D002784:Cholesterol; D000109:Acetylcholine