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1. The effect on coronary vascular resistance of selective stimulation of the A, B and sC fibre groups of the post-ganglionic cardiac sympathetic nerves was studied. The main left coronary artery was perfused at constant flow. The oxygen saturation of coronary sinus blood was measured continuously.

2. Stimulation of the peripheral ends of the cut A afferent fibres, normally excited by myocardial ischaemia, had no effect on coronary vascular resistance; these fibres do not evoke an axon reflex in the heart.

3. Stimulation of the preganglionic B fibres that run without synapse through the stellate ganglion also had no measurable effect on coronary resistance.

4. Stimulation of the post-ganglionic sC fibres of the cardiac sympathetic nerves caused coronary vasodilatation which occurred earlier than, and was initially independent of the decrease in coronary sinus oxygen saturation.

5. The injection of noradrenaline into the perfusion system had the same effect as stimulation of the sC fibres. In the K⁺-arrested heart, both noradrenaline and stimulation of the post-ganglionic nerves elicited coronary vasodilatation without changing the oxygen saturation of coronary sinus blood.

6. The intracoronary injection of acetylcholine caused coronary vasodilatation followed by an increase of coronary sinus oxygen saturation.

7. Vagal stimulation caused brady cardia and a fall in coronary resistance.

8. Propranolol blocked coronary vasodilatation elicited by sympathetic stimulation or noradrenaline without affecting the vasodilatation due to myocardial ischaemia or acetylcholine. Atropine blocked coronary vasodilatation evoked by acetylcholine without affecting that due to ischaemia or noradrenaline. Therefore smooth muscle of the coronary arteries has at least three different receptor sites from which vasodilatation can be elicited.

9. Hypertensin caused coronary vasoconstriction.

10. The presence of sympathetic cholinergic vasodilator fibres innervating the coronary arteries could not be demonstrated.

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