Microelectrode recording of the effects of agonists and antagonists on α‐adrenoceptors on rat somatic nerve terminals

Abstract

The effects of apomorphine, catechol, clonidine, isoprenaline, (‐)‐and (±)‐noradrenaline, phenylephrine, pyrogallol and xylazine were investigated on the frequency and amplitude of miniature endplate potentials (m.e.p.ps) and, with the exception of apomorphine, catechol and pyrogallol, on the amplitude of endplate potentials (e.p.ps) in the rat phrenic nerve diaphragm preparation. Clonidine, (‐)‐noradrenaline, phenylephrine and xylazine (each at 1.5 × 10−5M) increased m.e.p.p. frequency but not amplitude. The other drugs were ineffective, except isoprenaline (1.5 × 10−5 M) which enhanced m.e.p.p. amplitude but not frequency. The increase in m.e.p.p. frequency was inhibited by phentolamine, prazosin and yohimbine (each 1.5 × 10−9M). Prazosin and yohimbine alone each reduced m.e.p.p. frequency but failed to abolish m.e.p.ps even at high concentrations (10−3M). Clonidine, (‐)‐noradrenaline, phenylephrine and xylazine (each 3 × 10−6M) enhanced e.p.p. amplitude; this enhancement was blocked by prazosin and by yohimbine (each 3 × 10−6M). In preparations fatigued by prolonged continuous nerve stimulation (5 Hz, 0.05 ms for 30 min), (‐)‐noradrenaline (3.3 × 10−4M) restored m.e.p.p. frequency. The results indicate that adrenoceptors on somatic nerve terminals interact with both α1‐ and α2‐agonists and antagonists and show different characteristics from those at autonomic neuroeffector junctions. The α‐adrenoceptors on somatic nerve terminals may have an ancilliary physiological role in influencing but not controlling transmitter release. 1983 British Pharmacological Society