Vascular Effects of Procaine Amide in the Dog: Predominance of the Inhibitory Effect on Ganglionic Transmission

• Published in: Circulation research 1974-12, Vol.35 (6), p.948-960
• Main Authors: SCHMID, PHILLIP G, NELSON, LOREN D, HEISTAD, DONALD D, MARK, ALLYN L, ABBOUD, FRANCOIS M
• Format: Article
• Language: English
• Subjects: Angiotensin II - pharmacology; Animals; Carotid Arteries - innervation; Dogs; Ganglia, Autonomic - drug effects; Hexamethonium Compounds - pharmacology; Hindlimb; Hypotension - chemically induced; Hypotension - drug therapy; Muscles - blood supply; Perfusion; Phenylephrine - pharmacology; Pressoreceptors; Procainamide - adverse effects; Procainamide - pharmacology; Serotonin; Synaptic Transmission - drug effects; Vascular Resistance - drug effects; Vasomotor System - drug effects
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.35.6.948

The mechanism of the vasodilator effect of procaine amide in dogs was investigated in isolated gracilis muscle and hindpaw perfused at constant flows with arterial blood. Inhibition of sympathetic ganglionic transmission contributed predominantly to the vasodilatation in muscle that accompanied intravenous administration of procaine amide (20 mg/kg). In contrast, comparable amounts of procaine amide administered locally had no detectable effects on resistance vessels; in both muscle and paw, no decreases in base-line perfusion pressures and no inhibition of constrictor responses to phenylephrine, angiotensin, and 5-hydroxytryptamine occurred. Also, procaine amide had no detectable effects on constrictor responses to stimulation of sympathetic postganglionic nerves. Procaine amide reduced the reflex vasoconstrictor response to carotid hypotension, but this reduction was comparable to the inhibition of sympathetic ganglionic transmission. The absence of direct inhibitory effects on baroreceptors and central reflex pathways was supported by the failure of intracarotid administration of procaine amide to alter detectably in gracilis muscle base-line perfusion pressures and reflex constrictor responses to carotid hypotension. Procaine amide reduced reflex responses to carotid chemoreceptor stimulation with nicotine but not those to stimulation with cyanide, suggesting a direct selective inhibitory action on the carotid body but not on the central pathways of the reflex. We conclude that the vasodilator effect of procaine amide results from inhibition of ganglionic transmission. A similar hexamethoniumlike effect may account for the inhibition of carotid chemoreceptor stimulation by nicotine.