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The concentrations of dopamine (DA) in pituitary stalk plasma and the number of DA D-2 receptor sites in the anterior pituitary gland were evaluated in ovariectomized (OVX) rats treated for 48-78 h with estradiol (E2) or vehicle and for 2-30 h with progesterone (P) or vehicle. Only the combined administration of E2 for 72-78 h and P for 24-30 h altered the release of DA into pituitary stalk blood and the number of dopaminergic binding sites in the anterior pituitary gland. The DA concentrations in pituitary stalk plasma 72 h after initiation of treatment were 1.9 +/- 0.3 (mean +/- SEM), 2.6 +/- 0.2, and 2.4 +/- 0.3 ng/ml in OVX rats treated with vehicle, E2, and P alone, respectively, and were increased significantly to 4.3 +/- 0.4 ng/ml in E2- and P-treated rats. The binding of [3H] spiperone to DA D-2 receptors was measured by a single point assay in homogenates of the individual anterior pituitary glands obtained from the same rats. Anterior pituitary tissue was incubated with 0.4 nM [3H]spiperone in the presence or absence of 10(-6) M (+)butaclamol. Binding was similar in all animals except those treated with E2 and P, in which a significant increase occurred. Three days after initiation of treatment, binding was equivalent to 49.8 +/- 5.8, 51.3 +/- 5.1, and 55.4 +/- 4.9 fmol/mg protein in OVX rats treated with vehicle, E2, and P, respectively. In contrast, a significant increase in binding to 83.7 +/- 4.6 fmol/mg protein was observed in rats given E2 and P. No differences in either parameter were apparent 48 h after starting the steroid/vehicle treatment, nor were there any differences between morning and afternoon values in any single group. Scatchard analyses were made on the binding kinetics of DA receptors in anterior pituitary glands obtained from additional rats, and 1.5- to 2-fold increases in the density of sites were observed in animals that had received both E2 and P, while the apparent affinity of the receptors was unchanged. We conclude that treatment with the combination of E2 and P is required to increase the release of DA into hypophysial portal blood and that it also increases the density of DA receptors within the anterior pituitary gland.

After unilateral postganglionic parasympathetic denervation of rat parotid glands for 3, 6 or 16 days, the binding of [ 3 H] quinuclidinylbenzilate, a potent and specific muscarinic antagonist, was decreased by 28–45%. The largest part of the decrease was already present at 3 days, and thus appeared to coincide with the loss of parasympathetic terminals (as shown by a 94% reduction in choline acetyltransferase activity). The decrease in binding was expressed as a reduced number of membrane sites, with no significant change in affinity, and could be accounted for only in part by a reduction in the size of denervated glands. The rapid loss of binding suggests the existence of muscarinic receptors on parasympathetic terminals. The clear absence of any receptor increases at longer periods of denervation, when parotid glands are reported to give supersensitive secretory responses, suggests that mechanisms other than receptor increases are important in denervation supersensitivity in exocrine glands.