In unanaesthetized rats chronically prepared with venous and intracerebral cannulae, noradrenaline injected into the region of the supraoptic nuclei caused a dose-dependent increase in plasma vasopressin, measured by radioimmunoassay. A similar response was obtained with phenylephrine, but not with either clonidine or isoprenaline. The secretion of vasopressin was not secondary to change in arterial pressure, since similar injections of noradrenaline resulted in a small increase in arterial pressure, measured in the anaesthetized rat. These results suggest that noradrenaline stimulates alpha-1-adrenoceptors, presumably located on vasopressin-secreting neurones, thereby causing these cells to secrete vasopressin into the circulation. Tyramine injections also resulted in a prompt elevation in plasma vasopressin, indicating that endogenous noradrenaline is capable of releasing vasopressin.

No abstract

No abstract

GH and PRL levels were measured by RIA in plasma samples taken from genetically obese and nonobese rats over a 6-h period at consecutive 15-min intervals. The mean GH level was 204 ng/ml for lean animals and 48 ng/ml for obese rats; the difference is significant (t = 5.8; P less than 0.01). For the group of 5 lean rats, there were 10 GH peaks that exceeded the upper limit of the assay (800 ng/ml), whereas for the group of 6 obese rats, there were only 2 peaks that exceeded the upper limit. In some of the obese rats, peaks of very small amplitude were present. No differences were seen in PRL levels. The mean plasma PRL level was 3.6 ng/ml for lean animals and 3.3 ng/ml for obese rats. Abnormalities in GH in obese rats may be related to an imbalance between hypothalamic releasing and inhibiting factors or a defect in the pituitary.

Amitraz inhibited basal and hCG-stimulated progesterone but not estrogen production. The inhibitory action of amitraz and its antagonism by yohimbine suggest that alpha2-adrenergic receptors are expressed by luteinized human granulosa cells.