Catecholamine-sensitive adenylate cyclase in the developing golden hamster palate.

The present study was initiated to determine whether specific hormones would influence adenylate cyclase activity within the maxillary-palatal complex during formation of the hamster secondary palate. Stages from initial appearance of the palatal processes to shortly after birth were studied. Highest basal adenylate cyclase activities occurred during the earliest periods of palate development. This basal enzyme activity began to diminish as palatal fusion occurred and remained lowered until birth. Activation of adenylate cyclase by fluoride was maximal at concentrations of 5-10 mM, and was observed throughout the span of palatal development. Fluoride activation of adenylate cyclase was greatest prior to fusion of the palatal processes, then decreased until birth when a slightly increased enzymatic stimulation was seen. Norepinephrine and epinphrine were the catecholamines most capable of inducing increased activation of adenylate cyclase at most periods of palatal growth. Increased enzyme activity in the presence of norepinephrine was more susceptible to antagonism by the beta adrenergic agent, propranolol, than to the alpha adrenergic agent, phentolamine. The remaining catecholamines, namely isoproterenol and dopamine, displayed a lesser ability to activate the enzyme, and adenylate cyclase was not equally responsive to these catecholamines at identical developmental stages. Other hormones, i.e. histamine, serotonin, thyrotropin, growth hormone, thyroxine and glucagon were generally ineffective in activating the enzyme. Phosphodiesterase activity was not detected until shortly before birth.