Involvement of the sympathetic nervous system in the cardiovascular effects of ACTH-(1-24) during hemorrhagic shock in rats.
In urethane-anesthetized rats, removal of about 50% of the total blood volume over a period of 25-30 min caused hypovolemic shock, with extreme hypotension (MAP = 18-25 mm Hg and death of all animals within 22 +/- 5 min. The i.v. injection of ACTH-(1-24) in the dose range of 40-160 micrograms/kg induced a sustained, dose-dependent, and, at the highest dose used, an almost complete recovery of blood pressure, and 100% survival, at least for 2 h after treatment. The effect of ACTH-(1-24) was completely prevented by reserpine (5 mg/kg) and clonidine (0.1 mg/kg), significantly reduced by prazosin (0.1 mg/kg), dibenamine (15 mg/kg) and i.v. yohimbine (1 mg/kg) and unaffected by i.c.v. yohimbine (0.2 mg/kg) and i.v. practolol (15 mg/kg). These data suggest that the effect of ACTH-(1-24) in hypovolemic shock depends on the functional integrity of the sympathetic nervous system and is mediated through an activation of peripheral alpha-adrenoceptors.
Guarini
S
S
Institute of Pharmacology, University of Modena, Italy.
Ferrari
W
W
Bertolini
A
A
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003366:Cosyntropin / Q000494:pharmacology*; D003983:Dibenzylchlorethamine / Q000494:pharmacology; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D011674:Pulse / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000502:physiology*; D013997:Time Factors
D003366:Cosyntropin; D003983:Dibenzylchlorethamine