Intrathecal dynorphin A (1-13) and (3-13) reduce spinal cord blood flow by non-opioid mechanisms.
Dynorphin A (Dyn A)-related peptides have been implicated in the pathophysiology of spinal cord injury in part because their intrathecal (i.t.) injection causes hindlimb paralysis. The effects of paralytic doses of i.t. Dyn A (1-13) and Dyn A (3-13) on spinal cord blood flow and cardiac output were examined in rats using radiolabeled microspheres. Both Dyn A (1-13) and Dyn A (3-13) significantly reduced blood flow in lumbosacral spinal cord without altering cardiac output. Pretreatment with naloxone failed to block these reductions in blood flow. Thus, the paralytic effects of Dyn A may result from non-opioid actions of Dyn A to reduce spinal cord perfusion.
D000818:Animals; D002302:Cardiac Output / Q000187:drug effects; D002552:Cerebral Ventricles / Q000187:drug effects / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D004399:Dynorphins / Q000008:administration & dosage / Q000494:pharmacology*; D007276:Injections, Intraventricular; D008297:Male; D010446:Peptide Fragments / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012039:Regional Blood Flow / Q000187:drug effects; D013116:Spinal Cord / Q000098:blood supply*
D010446:Peptide Fragments; C026843:dynorphin (1-13); D004399:Dynorphins; C045478:dynorphin (3-13)