Endorphin-parasympathetic interactions in spinal shock.
We have recently shown that the opiate antagonist naloxone can partially reverse the hypotension which accompanies spinal cord transection, through actions on opiate receptors in the central nervous system. In the present studies we demonstrate that either vagotomy or atropine prevents the ability of naloxone to reduce the hypotension caused by spinal transection in the rat and cat. Since the peripherally acting methyl-atropine blocks the cardiovascular effects of centrally administered naloxone in this model, these findings imply an interaction between endorphin systems and central parasympathetic centers in spinal shock. This interaction results in a depression of cardiovascular function which is mediated through cholinergic vagal efferent pathways. Furthermore, the fact that naloxone reduces the hypotension following spinal transection, along with the role of the parasympathetic system in this process, appears to question the classic conception that such hypotension results entirely from interruption of descending sympathetic pressor pathways. Finally, the beneficial cardiovascular effects of naloxone in spinal shock may have important therapeutic implications in the management of spinal cord injury.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D002799:Cholinergic Fibers / Q000502:physiology; D004525:Efferent Pathways / Q000502:physiology; D004723:Endorphins / Q000502:physiology*; D005260:Female; D007276:Injections, Intraventricular; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009270:Naloxone / Q000494:pharmacology; D010275:Parasympathetic Nervous System / Q000502:physiology*; D051381:Rats; D011957:Receptors, Opioid / Q000502:physiology; D013116:Spinal Cord / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology
D004723:Endorphins; D011957:Receptors, Opioid; D009270:Naloxone