Metabolic and hormonal effects of preferential beta1 and beta2-adrenoceptor stimulation in man

The changes of blood glucose, serum potassium (K+), plasma non-esterified fatty acids (NEFA), plasma insulin and plasma renin activity (PRA) following the preferential stimulation of beta-1 and beta-2 adrenoceptors were studied in 7 healthy subjects during a 60-min infusion of prenalterol, a new, relatively beta-1 selective agonist and salbutamol, a well known, relatively beta-2 selective agonist. Two different high and low doses were used for both agents: 300 μg and 600 μg and 1 mg and 2 mg for salbutamol and prenalterol, respectively. The levels of PRA seemed equally increased by the two agents in proportion to the dose infused, thus suggesting an equally important role for beta-1 and beta-2 adrenoceptors in renin release. Blood glucose did not change during prenalterol infusions, while increased by 12±2 mg/100ml (mean ± SE; p< 0.01) and 25±3mg/100ml (p< 0.01) on salbutamol, at low and high dose, respectively. Similarly the decrement of serum K+ was significantly more pronounced (p< 0.01 ) after salbutamol infusion (0.6 ± 0.07 mEq/Land 1.0 < 0.09 mEq/L, at low and high dose, respectively) than after prenalterol (0.1 + 0.07 mEq/L and 0.3 ± 0.05 mEq/L). These metabolic effects should suggest a main beta-2 adrenoceptor involvement. Although both agonists determined a significant rise of plasma NEFA (p < 0.01), surprisingly the increase was significantly greater after salbutamol (441 ± 20 μEq/ L and 492 ± 25 μEq/ L, at low and high dose, respectively) than after prenalterol infusion (218 ± 25μEq/Land 269 ± 28μEq/L). Plasma insulin levels were unchanged on low dose prenalterol infusion, with a transient increment on high dose infusion, while increased significantly during both low and high dose salbutamol infusion at all observation times (12 ± 2 μU/ml and 16 ± 2 μU/ml at the end of low and high dose salbutamol infusion, respectively). This behavior might suggest a prevalent involvement of beta-2 adrenoceptors in the mechanism of the pancreatic release of insulin on sympathoadrenergic stimulation. © 1988, Italian Society of Endocrinology (SIE). All rights reserved.