Metabolic and haemodynamic effects of α2-adrenoceptor stimulation and antagonism in man

Author:

Brown M. J.1,Struthers A. D.1,Silvio L. Di2,Yeo T.3,Ghatei M.4,Burrin J. M.3

Affiliation:

1. Department of Clinical Pharmacology, Royal Postgraduate Medical School, London

2. Francis Fraser Laboratories, Hammersmith Hospital, London

3. Department of Medicine, Royal Postgraduate Medical School, London

4. Cobbold Laboratories, Middlesex Hospital, London

Abstract

1. Six healthy volunteers received a 60 min infusion of guanfacine (α2-agonist) on two occasions, preceded by either idazoxan (α2-antagonist) or vehicle. 2. Idazoxan elevated blood pressure by 8/7 mmHg, but there was no change on either day during guanfacine infusion. 3. Guanfacine reduced plasma noradrenaline by approximately 30%, and this was not antagonized by idazoxan. By contrast, the 30-fold increase in plasma growth hormone caused by guanfacine was almost completely blocked by idazoxan. 4. Guanfacine caused a two- to three-fold increase in plasma glucagon and a similar reduction in plasma insulin. Only the latter was antagonized by idazoxan. No consistent changes in plasma ACTH were observed after either idazoxan or guanfacine. 5. Idazoxan itself elevated plasma noradrenaline up to twice baseline values, but did not affect the other metabolic measurements. 6. α2-Adrenoceptor stimulation plays a minor role in control of hormone release but has a greater physiological role in regulating release of the neurotransmitter, noradrenaline.

Publisher

Portland Press Ltd.

Subject

Ocean Engineering

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