THE PRESSOR RESPONSE OF THE SPINAL CAT TO DIFFERENT GROUPS OF GANGLION-STIMULATING AGENTS

¹ Department of Pharmacology, Harvard Medical School, Boston, Massachusetts

Intravenous injections of McN-A-343 and AHR-602 caused a transient fall and then a pronounced secondary rise of blood pressure. Ganglion block by depolarization, established by large amounts of nicotine or tetramethylammonium (TMA), abolished the pressor response to McN-A-343 and AHR-602; however, during the phase of "non-depolarizing ganglion block by nicotine" McN-A-343 and AHR-602 caused a marked pressor response at a time when nicotine and dimethylphenylpiperazinium (DMPP) produced no response. The pressor response to McN-A-343 and AHR-602 was potentiated after large amounts of nicotine, and hexamethonium subsequently reduced the response to the expected control magnitude.

Cocaine, morphine and methadone reduced the blood pressure rise caused by McN-A-343 and AHR-602 but were ineffective against nicotine and DMPP. Block of transmitter release from adrenergic nerve endings by TM 10 also prevented the pressor response to McN-A-343 and AHR-602.

It is concluded that the secondary rise of blood pressure caused by the intravenous injection of McN-A-343 and AHR-602 is due to an action of these agents on sympathetic ganglia. While stimulation of the adrenal medulla seems to be of some importance in the pressor response to McN-A-343, AHR-602 has a very weak action, if any, on the adrenal medulla and causes a pressor response mainly by the stimulation of sympathetic ganglion cells. McN-A-343 and AHR-602 resemble pilocarpine in their pharmacology and seem to produce stimulation of ganglia by an action on receptors different from those for nicotine and DMPP.