The effects of acetylcholine, biogenic amines and other vasoactive agents on the cardiovascular functions of the Eel, Anguilla japonica.

The blood pressure in the cardinal vein, cardiac chambers and ventral and dorsal aortae have been recorded from conscious eels in water. At low doses, acetylcholine reduced the heart rate but increased the transbranchial differential blood pressure. The effects were abolished by atropine but not by tubocurarine. At doses in excess of 0.1 mug/kg, a secondary rise in arterial blood pressure was observed which could be abolished by bretylium, phentolamine or phenoxybenzamine. Catecholamines did not affect the heart rate although a transient bradycardia due to reflex inhibition could be observed with adrenaline and noradrenaline. Catecholamines increased the cardiac contractile force through an alpha-adrenergic mechanism which was blocked by phentolamine but not by propranolol. The relative potency was noradrenaline greater than adrenaline greater than isoprenaline. A beta-adrenergic receptor located in the branchial circulation led to vasodilation and decrease in transbranchial differential pressure. Both alpha-(vasoconstriction) and beta-(vasodilation) adrenergic receptors were present in the systemic circulation. Dopamine, 5-HT, GABA and bradykinin caused bradycardia abolishable by vagotomy or atropine treatment. Angiotensin II was hypertensive but did not affect the heart rate nor the transbranchial differential pressure. Tyramine caused release of endogenous catecholamines. With repeated doses, tachyphylaxis to the drug was observed. Histamine was without any obvious cardiovascular effects in the eel.