Further characterization of putative alpha--adrenergic receptors in brain that affect blood pressure and the secretion of ACTH, GH and renin in dogs.

To determine if alpha 1-or alpha 2-adrenergic receptors mediate the inhibition of ACTH stimulation of growth hormone secretion, decrease in blood pressure and inhibition of renin secretion produced by release of catecholamines in the brain, drugs with varying amounts of alpha 1- and alpha 2-adrenergic activity were injected directly into the third ventricle in pentobarbital anesthetized dogs. To determine whether the receptors mediating the responses to clonidine were pre- or postsynaptic, the effect of intravenous clonidine was determined 2 weeks after intraventricular 6-hydroxydopamine, and 24 h after intravenous alpha-metyl-p-tyrosine. Norepinephrine, epinephrine and clonidine, but not methoxamine and phenylephrine inhibited ACTH secretion. None of these alpha-agonists affected growth hormone secretion. Epinephrine and clonidine lowered blood pressure. Clonidine decreased plasma renin activity, but the other agonists increased it. In dogs treated with 6-hydroxydopamine, the decrease in blood pressure and ACTH and renin secretion produced by clonidine was not altered but the growth hormone response was reduced. alpha-methyl-p-tyrosine had no effect on the ACTH and growth hormone responses to clonidine. The data suggest that postsynaptic alpha-adrenergic receptors mediate inhibition of ACTH secretion and stimulation of growth hormone secretion, although in the case of growth hormone secretion, a presynaptic receptor is also involved. In addition, postsynaptic alpha 2-adrenergic receptors mediate a decrease in blood pressure, and they may mediate decreased renin secretion.