Developmental changes in β‐adrenergic and cholinergic interactions on calcium‐dependent slow action potentials in rat ventricular muscles

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Abstract
Developmental changes in the effect of isoprenaline (Iso) and acetylcholine (ACh) interactions on Ca2+‐dependent slow action potentials (APs) were studied in the ventricular muscles of foetal (12–20 days post‐gestation), neonatal (0–20 days old), and adult (2–3 months old) rats. The slow APs were recorded at 0.2 Hz in partially depolarized preparations (an extracellular K+ concentration of 25 mm). Iso (1 nm to 10 μm) began to increase the of the slow APs (an approximate indicator of Ca2+ current) on foetal day 18; its potentiating effect became greater with age and reached the adult level about 2 weeks after birth. ACh (10 μm) abolished the Iso (1 μm)‐induced increased in the observed in the late foetal and neonatal periods. The inhibitory effect of ACh on the was antagonized by atropine but not by pirenzepine, suggesting that ACh reduces Ca2+ current (in the presence of β‐adrenoceptor agonists) by stimulating muscarinic (M2) cholinoceptors. These results suggest that developmental changes in the modulatory effects of β‐adrenoceptor and cholinoceptor agonists on Ca2+ channels occur from a few days before birth to 2 weeks after birth and that the functional coupling between muscarinic cholinoceptors and Ca2+ channels has already been established when the coupling between β‐adrenoceptors and Ca2+ channels starts to operate.