Methoctramine, a cardioselective muscarinic antagonist, stimulates phosphoinositide hydrolysis in rat cerebral cortex.
The cardioselective muscarinic antagonist methoctramine antagonized carbamylcholine-mediated phosphoinositide (PI) hydrolysis in a concentration-dependent fashion in dissociated rat cerebrocortical cells. However, as the concentration of methoctramine was increased above 5 microM, there was a reversal of the antagonism of the PI response. In the absence of carbamylcholine, methoctramine by itself significantly increased PI hydrolysis with a maximal effect at 30 microM. Various classes of receptor antagonists, including atropine, and ion-channel blockers were unable to block methoctramine-stimulated PI hydrolysis.
Lee
N H
NH
Department of Pharmacology and Toxicology, University of Maryland School of Pharmacy, Baltimore 21201.
Forray
C
C
el-Fakahany
E E
EE
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D003959:Diamines / Q000494:pharmacology*; D006868:Hydrolysis; D066298:In Vitro Techniques; D008297:Male; D010276:Parasympatholytics / Q000494:pharmacology*; D010716:Phosphatidylinositols / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D003959:Diamines; D010276:Parasympatholytics; D010716:Phosphatidylinositols; D001285:Atropine; D002217:Carbachol; C054938:methoctramine