α‐Adrenoceptor involvement in catecholamine‐induced hyperglycaemia in conscious fasted rabbits

Abstract

1 In conscious fasted rabbits an intravenous infusion of phenylephrine (20 ptg kg-' min-) induced hyperglycaemia. The increase in blood glucose was accompanied by a modest increase in insulin secretion and a reduction of liver glycogen. Muscle glycogen and blood lactate levels were not altered by treatment with phenylephrine. 2 Prazosin, 1 mg kg-I s.c., partially attenuated phenylephrine-induced hyperglycaemia.3 Phenoxybenzamine infusion (16.6pgkg-'min-') for 15min suppressed the increase in blood glucose and the reduction in liver glycogen evoked by phenylephrine. This a-adrenoceptor blocker also clearly attenuated the blood glucose elevation observed on infusing adrenaline at 0.3 fig kg'-min -. 4 Blockade by phenoxybenzamine of phenylephrine-and adrenaline-induced hyperglycaemia was not accompanied by a significant increase in immunoreactive insulin plasma levels.5 Yohimbine infused at a rate of 20 g kg-lmin', also completely blocked phenylephrine-induced hyperglycaemia. This suppressor effect was accompanied by a marked rebound in insulin secretion. 6 It is concluded that in normal fasted rabbits stimulation of a-adrenoceptors induces hyperglycaemia. The increase in blood glucose depends mainly on liver glycogenolysis and inhibition of insulin secretion. Separate blockade of each component suffices to reduce a-adrenoceptor-mediated hyperglycaemia.

Role of α1‐ and α2‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

“…According to circulating substrate levels, rabbits could be classified into two groups ( Table 1). The larger one showed no change in glycerol levels thus confirming lack of effect of Yoh, as had already been described by Moratinos et al (1986). In the smaller group, Yoh did raise blood glycerol.…”

“…For more details see text and legend to Figure 1. (see Moratinos et al, 1986). PE also significantly reduced the metabolic effects derived from ,Badrenoceptor stimulation when both agonists were infused together (Figure 4a and b) (A in blood glycerol at 45 min after PE + Iso combined infusion was:…”

“…A reduction (Metz et al, 1978;Hsu & Kummel, 1981;Brown et al, 1985) and no change (Ditullio et al, 1984;Thompson et al, 1984) in basal IRI plasma levels has been reported after the administration of Clo, xylazine and guanfacine. Therefore using the rabbit as a suitable experimental model (animal adipose tissue and Pi-cells possess a2-adrenoceptor receptivity, Lafontan, 1981;Moratinos et al, 1986) we intended to explore in more detail the nature and functional relevance of these a2-adrenoceptors. The effects of Clo on basal and fi-adrenoceptor promoted lipid mobilization and insulin secretion have also been studied.…”

Effects of catecholamines on plasma potassium: the role of alpha‐ and beta‐adrenoceptors

“…As mentioned above, the effects of CA and selective alpha-AR agonists are independent of insulin secretion. Adrenaline can exert a hypokaliemic effect in pancreatectomized animals (Pettit and Vick, 1974) or, when insulin secretion is inhibited (Moratinos et al, 1986). Amidephrine and clonidine increase plasma K+ in rabbits though the first stimulates and the last inhibits insulin release (Moratinos et al, 1988;Reverte et al, 1991a).…”

Benzylamine Exhibits Insulin-Like Effects on Glucose Disposal, Glucose Transport, and Fat Cell Lipolysis in Rabbits and Diabetic Mice

“…These differences in the vanadate requirement for the observation of insulin-mimicking effects with benzylamine led us to further study in vivo the putative antihyperglycemic properties of benzylamine in species other than rat. To this aim, we have studied the effects of benzylamine on glucose tolerance tests (GTTs) in the rabbit, an excellent model for the human glucose homeostasis (Moratinos et al, 1986(Moratinos et al, , 1988, and in the mouse, which accounts for a growing number of either genetically or nutritionally induced models of diabetes and/or obesity . Then, we explored the mechanisms of the antihyperglycemic effects of benzylamine.…”