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Abstract
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.