Pharmacological evidence that alpha 1-adrenoceptors mediate metamorphosis of the Pacific oyster, Crassostrea gigas.

Oyster larvae can be induced to metamorphose by exposure to the natural vertebrate adrenergic agonists, epinephrine and norepinephrine. The larval receptors mediating this induction were pharmacologically characterized by testing the ability of a variety of adrenergic agonists and selected structural analogs of epinephrine and norepinephrine to induce oyster metamorphosis, and by testing the ability of various adrenergic antagonists to block the induction of metamorphosis by epinephrine. Oyster metamorphosis can be induced by vertebrate adrenergic agonists with relative potencies: cirazoline greater than epinephrine greater than phenylephrine greater than or equal to norepinephrine greater than alpha-methylnorepinephrine greater than isoproterenol much greater than methoxamine = clonidine. Other structural analogs of epinephrine and norepinephrine, including dopamine and octopamine, were ineffective at inducing metamorphosis. Induction of metamorphosis by epinephrine can be blocked by vertebrate adrenergic antagonists with relative potencies: chlorpromazine greater than or equal to prazosin greater than phentolamine greater than WB4101 greater than propranolol greater than yohimbine greater than metoprolol. These data demonstrate that receptors similar to vertebrate-type alpha 1-adrenoceptors mediate oyster metamorphosis. This is the first evidence for alpha 1-adrenoceptors in molluscs, and provides an important clue to the control of the complex process of molluscan metamorphosis and to the evolution of vertebrate adrenergic receptors.