Effects of Sex Hormones on Vascular Reactivity in Boys With Hypospadias
Authors' conclusion
In healthy boys, testosterone and 17β-estradiol promote a vasoconstrictor phenotype, whereas in boys with hypospadias, these sex hormones reduce vasoconstriction, with androgens promoting vasorelaxation. Differences in baseline artery function may therefore be sex hormone-independent and the impact of early-life variations in androgen exposure on vascular function needs further study.
Study context
- Population
- Boys with hypospadias and healthy boys, median age 1.5 (range 1.2–2.7) years; small resistance arteries from excess foreskin tissue
- Participants
- 11 vs 12
- Comparison
- Sex hormones (17β-estradiol, dihydrotestosterone (DHT), testosterone) vs absence, in arteries from boys with hypospadias vs controls
- Casesn = 11
- Controlsn = 12reference
- Outcome
- Vascular reactivity (Emax) in the absence/presence of sex hormones
Methodological detailsex vivo wire myography
- Ex vivo wire myography
Main finding
As reported in the abstract
- Controls: contraction (Emax), basal vs after testosterone
- 83.74 vs 125.4, P < .0002
- Controls: contraction (Emax), basal vs after estradiol
- 83.74 vs 110.2, P = .02
- Controls: 17β-estradiol reduced vasorelaxation to acetylcholine (Emax)
- 10.6 vs 15.6, P < .0001
- Controls: 17β-estradiol reduced vasorelaxation to sodium nitroprusside (Emax)
- 14.6 vs 20.5, P < .0001
- Hypospadias: testosterone reduced contraction (Emax)
- 137.9 vs 107.2, P = .01
- Hypospadias: 17β-estradiol reduced contraction (Emax)
- 156.9 vs 23.6, P < .0001
- Cases: testosterone increased vasorelaxation to acetylcholine (Emax)
- 77.3 vs 51.7, P = .02
- Cases: DHT increased vasorelaxation to acetylcholine (Emax)
- vs 48.2, P = .0001
- Cases: testosterone increased vasorelaxation to sodium nitroprusside (Emax)
- 43.0 vs 39.5, P = .02
- Cases: DHT increased vasorelaxation to sodium nitroprusside (Emax)
- 39.6 vs 37.5, P = .04
Original publication
Effects of Sex Hormones on Vascular Reactivity in Boys With Hypospadias. J Clin Endocrinol Metab. Published 6 September 2023. doi:10.
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