Adrenoceptor specificity in the central regulation of adrenocortical secretion.
Electrical stimulation of the ventral noradrenergic ascending bundle, through chronically implanted electrodes, resulted in significant elevations of the levels of plasma corticosterone in rats. Injection of either alpha 1- or alpha 2-adrenergic antagonists, at doses of 20 nmol, through chronic cannulae, implanted above the dorsal aspect of the hypothalamic paraventricular nucleus prior to stimulation of the ventral noradrenergic ascending bundle attenuated the stimulation-evoked increases in corticosterone in plasma levels. For alpha 1-antagonists, ergotamine tartrate was more effective than was prazosin hydrochloride and for alpha 2-antagonists, yohimbine hydrochloride was more effective than tolazoline hydrochloride; these results being consistent with the pharmacological binding characteristics. The beta-antagonist, propranolol hydrochloride was without effect upon the stimulation-evoked increases in levels of corticosterone in plasma. Injection of 6-hydroxydopamine hydrobromide into the paraventricular nucleus, a few days before the stimulation, prevented the corticosterone response. In rats with cannulae in the paraventricular nucleus alone, noradrenaline bitartrate (10 and 20 nmol) increased levels of corticosterone in plasma in a dose-dependent manner, as did the postulated co-transmitter, neuropeptide Y, at doses of 10 and 20 pmol. Noradrenaline (10 nmol) and neuropeptide Y (10 pmol), administered together, were found to potentiate each other. The alpha 1-agonist, 1-phenylephrine hydrochloride, and the alpha 2-agonist, clonidine hydrochloride, significantly increased levels of corticosterone in plasma as did the beta-agonist, isoproteronol hydrochloride. The data obtained demonstrate a facilitatory action of noradrenaline at the level of the paraventricular nucleus upon adrenocortical secretion and that this effect was probably mediated by both alpha 1- and alpha 2-adrenoceptors, the role of beta-receptors being unclear.2 +
Saphier
D
D
Department of Neurology, Hadassah University Hospital, Jerusalem, Israel.
Feldman
S
S
D000302:Adrenal Cortex / Q000502:physiology*; D000818:Animals; D003345:Corticosterone / Q000502:physiology; D007150:Immunohistochemistry; D008297:Male; D009478:Neuropeptide Y / Q000494:pharmacology; D009638:Norepinephrine / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000502:physiology; D051381:Rats; D011941:Receptors, Adrenergic / Q000502:physiology*; D013238:Stereotaxic Techniques
D009478:Neuropeptide Y; D011941:Receptors, Adrenergic; D003345:Corticosterone; D009638:Norepinephrine