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Effects of almitrine on the release of catecholamines from the rabbit carotid body in vitro

1 . Almitrine increases ventilation by stimulating the carotid body (CB) arterial chemoreceptors but neither its intraglomic target nor its mechanism of action have been elucidated. 2 . We have tested the hypothesis that chemoreceptor cells are targets for almitrine by studying its effects on the release of 3H‐catecholamines in an in vitro rabbit CB preparation. 3 . It was found that almitrine (0.3 and 1.5 × 10−6 m; i.e. 0.2 and 1 mg l−1) increases the resting release of 3H‐catecholamines from CBs (previously loaded with [3H]‐tyrosine) incubated in a balanced 95% O2/5% CO2‐equilibrated solution. 4 . Almitrine at a concentration of 3×10−6 m (2mg l−1) also augmented the release of 3H‐catecholamines elicited by incubating the CBs in a hypoxic solution (equilibrated with 7% O2/5% CO2 in N2), by high external K+ (35 mm) and by veratridine (2 × 10−5 m), but did not modify release induced by dinitrophenol (7.5 × 10−5 m). 5 . At the same concentration (3 × 10−6 m), almitrine increased the rate of dopamine synthesis and was ineffective in modifying the cyclic AMP levels in either normoxic or hypoxic CBs. 6 . It is concluded that chemoreceptor cells are the intraglomic targets for almitrine. The mechanisms of action of almitrine on chemoreceptor cells are discussed.