title: [Activity induced by androsterone and hemisuccinate of androsterone on perfusion pressure and vascular resistance].
abstract: BACKGROUND
  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.
  
  
  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.
authors.affiliation: Laboratorio de Fármaco-Química, Facultad de Ciencias Químico-Biológicas, Universidad Autónoma de Campeche, Campeche, México. lauro_1999@yahoo.com
authors.forename: Lauro
authors.initials: L
authors.lastname: Figueroa
authors.forename: Francisco
authors.initials: F
authors.lastname: Díaz
authors.forename: Abelardo
authors.initials: A
authors.lastname: Camacho
authors.forename: Eliseo
authors.initials: E
authors.lastname: Díaz
authors.forename: Rolando
authors.initials: R
authors.lastname: Marvin
mesh_terms: D000738:Androsterone / Q000031:analogs & derivatives / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005485:Flutamide / Q000494:pharmacology; D006321:Heart / Q000187:drug effects*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009543:Nifedipine / Q000494:pharmacology; D011284:Pregnenolone / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D016861:Cyclooxygenase Inhibitors; C552059:androsterone hemisuccinate; D011284:Pregnenolone; D005485:Flutamide; D000738:Androsterone; D009543:Nifedipine; D007213:Indomethacin