Blockade of cholinergic receptors in the C1 area abolishes hypertensive response to opiates in the A1 area of the ventrolateral medulla.
Opiate receptor stimulation by microinjections of a delta-receptor agonist, D-Ala2-D-Leu5-enkephalin (DADLE) into the caudal depressor (A1) area of the ventrolateral medulla produced a hypertensive response which was prevented as well as reversed by the blockade of cholinergic receptors in the rostral pressor (C1) area. These results suggest that the hypertensive responses to opiates in the A1 area are mediated via cholinergic mechanisms in the rostral C1 area of the ventrolateral medulla and acetylcholine may be the neurotransmitter released in the ventrolateral pressor area.
D000109:Acetylcholine / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001931:Brain Mapping; D004743:Enkephalin, Leucine / Q000031:analogs & derivatives* / Q000494:pharmacology; D016308:Enkephalin, Leucine-2-Alanine; D008297:Male; D008526:Medulla Oblongata / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D011950:Receptors, Cholinergic / Q000187:drug effects*; D012154:Reticular Formation / Q000187:drug effects; D014666:Vasomotor System / Q000502:physiology
D011950:Receptors, Cholinergic; D004743:Enkephalin, Leucine; D016308:Enkephalin, Leucine-2-Alanine; D000109:Acetylcholine