title: Testosterone Replacement Therapy Prevents Alterations of Coronary Vascular Reactivity Caused by Hormone Deficiency Induced by Castration.
abstract: The present study aimed to determine the effects of chronic treatment with different doses of testosterone on endothelium-dependent coronary vascular reactivity in male rats. Adult male rats were divided into four experimental groups: control (SHAM), castrated (CAST), castrated and immediately treated subcutaneously with a physiological dose (0.5 mg/kg/day, PHYSIO group) or supraphysiological dose (2.5 mg/kg/day, SUPRA group) of testosterone for 15 days. Systolic blood pressure (SBP) was assessed at the end of treatment through tail plethysmography. After euthanasia, the heart was removed and coronary vascular reactivity was assessed using the Langendorff retrograde perfusion technique. A dose-response curve for bradykinin (BK) was constructed, followed by inhibition with 100 μM L-NAME, 2.8 μM indomethacin (INDO), L-NAME + INDO, or L-NAME + INDO + 0.75 μM clotrimazole (CLOT). We observed significant endothelium-dependent, BK-induced coronary vasodilation, which was abolished in the castrated group and restored in the PHYSIO and SUPRA groups. Furthermore, castration modulated the lipid and hormonal profiles and decreased body weight, and testosterone therapy restored all of these parameters. Our results revealed an increase in SBP in the SUPRA group. In addition, our data led us to conclude that physiological concentrations of testosterone may play a beneficial role in the cardiovascular system by maintaining an environment that is favourable for the activity of an endothelium-dependent vasodilator without increasing SBP.
authors: Department of Physiological Sciences, Federal University of Espírito Santo (Universidade Federal do Espírito Santo-UFES), Vitória, Brazil.
authors: Wender Nascimento
authors: WN
authors: Rouver
authors: Department of Physiological Sciences, Federal University of Espírito Santo (Universidade Federal do Espírito Santo-UFES), Vitória, Brazil.
authors: Nathalie Tristão Banhos
authors: NT
authors: Delgado
authors: Department of Physiological Sciences, Federal University of Espírito Santo (Universidade Federal do Espírito Santo-UFES), Vitória, Brazil.
authors: Jussara Bezerra
authors: JB
authors: Menezes
authors: Department of Physiological Sciences, Federal University of Espírito Santo (Universidade Federal do Espírito Santo-UFES), Vitória, Brazil.
authors: Roger Lyrio
authors: RL
authors: Santos
authors: Department of Physiological Sciences, Federal University of Espírito Santo (Universidade Federal do Espírito Santo-UFES), Vitória, Brazil.
authors: Margareth Ribeiro
authors: MR
authors: Moyses
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001920:Bradykinin / Q000494:pharmacology; D002319:Cardiovascular System / Q000187:drug effects*; D002369:Castration / Q000009:adverse effects*; D003022:Clotrimazole / Q000494:pharmacology; D003331:Coronary Vessels / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000187:drug effects; D006321:Heart / Q000187:drug effects; D020249:Hormone Replacement Therapy / Q000379:methods; D007213:Indomethacin / Q000494:pharmacology; D008055:Lipids / Q000502:physiology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013739:Testosterone / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D008055:Lipids; D014665:Vasodilator Agents; D013739:Testosterone; D003022:Clotrimazole; D001920:Bradykinin; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin