RT Journal Article
SR Electronic
T1 ANTAGONISM OF GANGLIONIC STIMULANTS BY α,ά-BIS-(DIMETHYLAMMONIUMACETALDEHYDE DIETHYLACETAL)-<em>p</em>,<em>p''</em>-DIACETYLBIPHENYL BROMIDE (DMAE)
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 176
OP 184
VO 164
IS 1
A1 WONG, S.
A1 LONG, J. P.
YR 1968
UL http://jpet.aspetjournals.org/content/164/1/176.abstract
AB α,ά-Bis-(dimethylammoniumacetaldehyde diethylacetal)-p,p-diacetylbiphenyl bromide (DMAE) has been found to antagonize the ganglionic stimulating actions of nicotine (NIC), tetramethylammonium bromide (TMA), dimethylphenylpiperazinium iodide (DMPP) and acetylcholine (ACh). Pressor responses to splanchnic nerve stimulation and central vagal nerve stimulation indicated that transmission through ganglia remained unimpaired at levels of DMAE sufficient to block the ganglionic stimulants. NIC was most readily blocked, while KCl and nerve stimulation resisted blockade by DMAE. The sequence of sensitivity to blockade is: NIC &gt; TMA &gt; DMPP &gt; ACh &gt; KC1 and nerve stimulations. The respiratory stimulating action of NIC was completely abolished by DMAE (400 µg/kg). By using the cat nictitating membrane-cervical sympathetic ganglion preparation, the sequence of sensitivity to blockade by DMAE was confirmed, i.e., NIC &gt; TMA &gt; ACh &gt; nerve stimulation. The ED5O for nerve stimulation was estimated to be 1000 times greater than that for NIC. The sequence of sensitivity to blockade by hexamethonium (C6) was also found to be: NIC &gt; TMA &gt; ACh &gt; nerve stimulation. However, the ED5O for nerve stimulation was 50 times greater than that for NIC. Low-frequency (0.1-1.0 cps) stimulations of the cervical sympathetic nerve were completely blocked by C6, whereas single-shock stimulations were potentiated and 1.0-cps stimulations were not affected by DMAE. DMAE is the Only known derivative of the hemicholinium (HC-3) structure that exhibits either catecholamine-potentiating actions or the selective antinicotinic action. © 1968, by The Williams &amp; Wilkins Company