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Endocrinology, Vol 108, 1829-1836, Copyright © 1981 by Endocrine Society
ARTICLES |
T Kimura, L Share, BC Wang and JT Crofton
In order to investigate the role of central noradrenergic neurons in the control of vasopressin (ADH) release and cardiovascular regulation, norepinephrine (1.4 microgram/kg), clonidine (0.1 microgram/kg), and isoproterenol (1.4 microgram/kg were infused into the lateral cerebral ventricle of the anesthetized dog. The drugs were given over a 20-min period, dissolved in 0.9% saline at a volume rate of 10 microliter/min. Both norepinephrine and clonidine markedly reduced ADH release and lowered arterial blood pressure and heart rate. Isoproterenol had no effect on ADH release and produced a slight reduction in arterial pressure and a large increase in heart rate. Pretreatment with phenoxybenzamine (100 microgram/kg, iv) completely blocked the effects of norepinephrine on blood pressure and heart rate but only partially (about 50%) inhibited the norepinephrine effect on ADH release. Intravenous isoproterenol lowered blood pressure and increased ADH release and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality or plasma sodium and potassium concentrations. It is concluded that, in the anesthetized dog, intraventricular norepinephrine and clonidine decreased ADH release, blood pressure, and heart rate by stimulating alpha- adrenoreceptors. The increased release of ADH after peripheral administration of isoproterenol was presumably due to the reduction in blood pressure and decreased baroreceptor inhibition of ADH release.
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