Scientific Reports (Nov 2024)

Systemic alpha-1 adrenergic receptor inhibition reduces sperm damage in adult and aging spontaneously hypertensive rats

  • Nicolle R. Machado,
  • Mika A. Miyazaki,
  • Thayná D. Oliveira,
  • Karina T. Dias,
  • Lucas G. Colli,
  • Larissa B. Belardin,
  • Ricardo P. Bertolla,
  • Stephen F. Rodrigues

DOI
https://doi.org/10.1038/s41598-024-77661-7
Journal volume & issue
Vol. 14, no. 1
pp. 1 – 13

Abstract

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Abstract Decreased sperm quality has been reported in men with different clinical conditions, including aging and hypertension. In the male reproductive tract, it has been suggested that the α1-adrenergic receptor influences fertility and spermatogenesis, and important functions are also attributed to the renin–angiotensin axis, such as regulation of steroidogenesis, spermatogenesis, and sperm function. Previously, our group demonstrated impaired testicular vasomotion via α1-adrenergic receptor activation and increased hypoxia-related proteins in the testes of spontaneously hypertensive rats (SHRs) compared to Wistar normotensive rats. In this study, we aimed to investigate the effect of hypertension and inhibition of systemic α1-adrenergic receptor or angiotensin II AT1 receptor on sperm quality, sperm functional characteristics, and testicular microcirculation in rats from three different ages: young (8–10-week-old), adult (20–24-week-old) and older adult (60–66-week-old). We observed higher blood pressure in SHRs of all ages compared to age-matched Wistar rats. Lower blood pressure was observed either in prazosin or losartan-treated adult or aged SHRs. Additionally, lower sperm concentration, impaired motility and higher acrosome damage were demonstrated in SHRs. Prazosin treatment alleviated the effects of hypertension on sperm concentration and motility but not acrosome damage. Higher vasomotion was noticed in testicular blood vessels of adult and aged SHRs compared to Wistar rats. Thus, impaired sperm quality was observed in SHRs of different ages and was improved by sub-chronically blocking the α1-adrenergic receptor.

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