Physostigmine, a choline-esterase inhibitor, is known to elevate endogenous levels of acetylcholine. Intravenously administered physostigmine causes a rise in blood pressure via its action in the central nervous system. Exact site of this action of physostigmine is not known. In this paper, it was demonstrated that microinjections of tetrodotoxin (a fast sodium channel blocker), lidocaine (a local anesthetic) and scopolamine (a cholinergic muscarinic receptor blocker) into the rostral ventrolateral medullary pressor area abolished the pressor action of intravenously administered physostigmine. These results demonstrate that the rostral ventrolateral medulla is the site of action of intravenously administered physostigmine and this action is mediated via cholinergic muscarinic receptors.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Clinical Neurology
- Developmental Biology
- cholinergic muscarinic receptor
- rostral ventrolateral medulla