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Involvement of the sympathetic nervous system in the cardiovascular effects of ACTH-(1-24) during hemorrhagic shock in rats

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Summary

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 mmHg and death of all animals within 22±5 min. The i.v. injection of ACTH-(1-24) in the dose range of 40–160 μg/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.

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Abbreviations

MAP:

mean arterial pressure

PP:

pulse pressure

i.c.v.:

intracerebroventricular

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Guarini, S., Ferrari, W. & Bertolini, A. Involvement of the sympathetic nervous system in the cardiovascular effects of ACTH-(1-24) during hemorrhagic shock in rats. Naunyn-Schmiedeberg's Arch Pharmacol 337, 556–560 (1988). https://doi.org/10.1007/BF00182731

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