Actividad inducida por androsterona y hemisuccinato de androsterona sobre la presión de perfusión y la resistencia vascular

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.