Cholinergic mechanisms and the response to ATP in the systemic vasculature of the rainbow trout

1. Cholinergic mechanisms in the systemic vasculature of the rainbow trout have been pharmacologically analysed using an isolated trunk preparation perfused at constant flow. 2. Acetylcholine (ACh) causes a two component vasoconstriction comprising a rapid initial peak (response A) and a long-lasting tail on the initial peak (response B). Skeletal muscle contraction is not involved in either response. 3. Response B has a high dose threshold, is nicotinic in nature, and is blocked by α-adrenoreceptor antagonists, procaine, and 0 mM Ca⁺⁺ plus 20 mM Mg⁺⁺, indicating a classical indirect action of ACh on sympathetic neurons or chromaffin tissue to cause the release of an adrenergic transmitter. 4. Response A has a lower dose threshold, is nicotinic in nature, is resistant to α-adrenergic, muscarinic cholinergic, and adrenergic neuron blockade, is insensitive to tetrotoxin and 0 mM Ca⁺⁺ plus 20 mM Mg⁺⁺, but is blocked with some specificity by procaine. 5. The properties of the nicotinic receptors of response A differ from those of the traditional ganglionic and skeletal muscle types of higher vertebrates. 6. Response A is mimicked by ATP, which appears to act by a direct mechanism in the preparation. 7. It is concluded that response A reflects either direct stimulation of nicotinic receptors on vascular tissue or an indirect nicotinic effect resulting in the release of a non-adrenergic, non-cholinergic transmitter such as ATP. 8. Unlike the situation in higher vertebrates, no muscarinic dilatory responses to ACh occur in the preparation.