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      Presynaptic Muscarinic and α-Adrenergic Receptor Blocking Effect of Atropine on the Noradrenergic Neurones of the Rabbit Pulmonary Artery

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          The effect of atropine on the electrical-field stimulation-evoked overflow of tritium from isolated rabbit pulmonary arteries preincubated with <sup>3</sup>H-noradrenaline was studied. Atropine (10<sup>–4</sup> M) and phentolamine (10<sup>–6</sup> M) increased stimulation-induced overflow of tritium. Clonidine (10<sup>–6</sup> to 10<sup>-5</sup> M) and acetylcholine (10<sup>–6</sup> M) diminished the stimulation-evoked overflow of tritium. After the overflow had been raised by either atropine (10<sup>–4</sup> M) or phentolamine (10<sup>–6</sup> M), clonidine (10<sup>–6</sup> M) decreased the overflow below control values. Clonidine (10<sup>–5</sup> M) prevented the enhancement of tritium overflow evoked by atropine (10<sup>–4</sup> M). A lower concentration of clonidine (10<sup>–6</sup> M) only caused a partial prevention. Enhancement of the overflow by phentolamine (10<sup>–6</sup> and 3 × 10<sup>–5</sup> M) was not altered by atropine (10<sup>–4</sup> M). Atropine (10<sup>–7</sup> M), in a concentration which was without any effect on the stimulation-induced tritium overflow, prevented the reduction evoked by acetylcholine (10<sup>–6</sup> M). It is concluded that atropine in a low concentration blocks presynaptic inhibitory muscarinic receptors; at higher concentrations it blocks in addition presynaptic α-adrenoceptors.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          19 September 2008
          : 16
          : 3
          : 163-168
          Department of Pharmacology, Odense University, Odense
          158203 Blood Vessels 1979;16:163–168
          © 1979 S. Karger AG, Basel

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