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Published on: June 27, 2022
Hydrogen sulphide is involved in testosterone vascular effect
Mariarosaria Bucci1, Vincenzo Mirone, Annarita Di Lorenzo
1Dipartimento di Farmacologia Sperimentale, Universita' di Napoli Federico II, Napoli, Italia.
European Urology
|May 31, 2008
Summary
Testosterone rapidly relaxes blood vessels through a non-genomic pathway. This study reveals that hydrogen sulfide (H₂S) mediates this testosterone-induced vasodilation by increasing its production.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Biochemistry
Background:
- Testosterone (T) causes rapid vascular relaxation via non-genomic mechanisms.
- The precise mediators of testosterone-induced vasodilation remain debated.
Purpose of the Study:
- To investigate the involvement of the hydrogen sulfide (H₂S) pathway in testosterone's vascular effects.
- To elucidate the role of H₂S as a mediator in testosterone-induced vasodilation.
Main Methods:
- Thoracic aortas from male Wistar rats were used for in vitro studies.
- Vascular reactivity was measured using isometric force transducers.
- Hydrogen sulfide (H₂S) production was quantified, and enzyme activity (CBS, CSE) and protein levels were assessed.
Main Results:
- Testosterone significantly increased H₂S production from L-cysteine.
- Testosterone induced concentration-dependent vasodilation, inhibited by CSE inhibitors (PGG, BCA) and glibenclamide.
- Enzyme expression (CBS/CSE) remained unchanged, indicating modulation of enzymatic activity.
Conclusions:
- Testosterone's vasodilatory effect involves hydrogen sulfide (H₂S), a novel gaseous mediator.
- Testosterone modulates H₂S levels by enhancing the enzymatic conversion of L-cysteine.
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