RESUMO
Introducción. Existen pocos datos sobre los efectos de la androsterona y sus derivados a nivel cardiovascular. Además, el mecanismo molecular de estos andrógenos y su sitio de acción celular son poco claros. Objetivo. Evaluar el efecto inducido por la androsterona y el hemisuccinato de androsterona sobre la presión de perfusión y la resistencia vascular. Materiales y métodos. Los efectos de la androsterona y del derivado de androsterona sobre la presión de perfusión y la resistencia vascular fueron evaluados en un modelo de corazón aislado de rata (Langendorff). Resultados. Los resultados mostraron que: 1) el hemisuccinato de androsterona [10-9 M] incrementa la presión de perfusión y la resistencia vascular en comparación con la androsterona [10-9 M]; 2) los efectos del derivado de androsterona [10-9 M-10-5 M] sobre la presión de perfusión no fueron inhibidos por indometacina [10-6 M]; 3) la nifedipina [10-6M] bloquea los efectos ejercidos por el hemisuccinato de androsterona [10-9 M-10-5 M] sobre la presión de perfusión, y 4) el efecto del derivado de androsterona [10-9 M-10-5 M] sobre la presión de perfusión en presencia de flutamida [10-6 M] fue inhibido. Conclusiones. Los efectos inducidos por androsterona y hemisuccinato de androsterona sobre la presión de perfusión y la resistencia vascular pueden depender de su estructura química. En el caso de la actividad ejercida por el análogo de androsterona, podría involucrar la interacción del esteroide-receptor androgénico e, indirectamente, la activación del canal de calcio y, consecuentemente, inducir variaciones en la presión de perfusión.
Introduction. Few data exist with respect to the effects of androsterone and their derivatives at cardiovascular level. In addition, the molecular mechanisms and cellular site of action of these androgens are still unclear. Objective. An evaluation was conducted on the effects induced by androsterone and hemisuccinate of androsterone on perfusion pressure and vascular resistance. Materials and methods. The effects of both androsterone and hemisuccinate of androsterone on the perfusion pressure and vascular resistance in isolated rat hearts (Langendorff model) were evaluated. Results. The results showed that: (1) the hemisuccinate of androsterone [10-9 M] increases the perfusion pressure and vascular resistance in comparison with the androsterone [10-9 M]; (2) the effect of androsterone-derivative [10-9 M-10-5 M] on perfusion pressure not was inhibited by indometacin [10-6 M]; (3) nifedipine [10-6 M] blocks the effects exerted by hemisuccinate of androsterone [10-9 M-10-5 M] on perfusion pressure; and (4) the effect of androsterone-derivative [10-9 M-10-5 M] on perfusion pressure in presence of flutamide [10-6 M] was inhibited. Conclusions. The effects induced by androsterone and hemisuccinate of androsterone on the perfusion pressure and resistance vascular probably involve the interaction of steroid-receptor androgenic and, indirectly, activation of the calcium channel to induce variations in the perfusion pressure.
Assuntos
Ratos , Androsterona , Flutamida , Ratos Wistar , Resistência Vascular , PerfusãoRESUMO
INTRODUCTION: Few data exist with respect to the effects of androsterone and their derivatives at cardiovascular level. In addition, the molecular mechanisms and cellular site of action of these androgens are still unclear. OBJECTIVE: An evaluation was conducted on the effects induced by androsterone and hemisuccinate of androsterone on perfusion pressure and vascular resistance. MATERIALS AND METHODS: The effects of both androsterone and hemisuccinate of androsterone on the perfusion pressure and vascular resistance in isolated rat hearts (Langendorff model) were evaluated. RESULTS: The results showed that: (1) the hemisuccinate of androsterone [10(-9) M] increases the perfusion pressure and vascular resistance in comparison with the androsterone [10(-9) M]; (2) the effect of androsterone-derivative [10(-9) M-10(-5) M] on perfusion pressure not was inhibited by indometacin [10(-6) M]; (3) nifedipine [10(-6) M] blocks the effects exerted by hemisuccinate of androsterone [10(-9) M-10(-5) M] on perfusion pressure; and (4) the effect of androsterone-derivative [10(-9) M-10(-5) M] on perfusion pressure in presence of flutamide [10(-6) M] was inhibited. CONCLUSIONS: The effects induced by androsterone and hemisuccinate of androsterone on the perfusion pressure and resistance vascular probably involve the interaction of steroid-receptor androgenic and, indirectly, activation of the calcium channel to induce variations in the perfusion pressure.