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1. 1. Adrenalin (5.0 × 10-5M) increases gill vascular resistance up to 23.2 ± 6.8% in the isolated and perfused head of the european eel (Anguilla anguilla L.). 2. 2. This vasoactive response is nearly abolished by the α-adrenergic blocking agent phentolamine mesylate (5.0 × 10-4M), while it is increased by the β-blocker propranolol (5.0 × 10-5M). 3. 3. From these results it may be inferred that, in our experimental conditions, the major response to the catecholamine is a vasoconstriction mediated via α-adrenoceptors. © 1983.

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.

An investigation was carried out to determine the adrenoceptor types in isolated places of the guinea-pig pulmonary artery. The results indicated a predominance of α-adrenoceptors and the presence of a paucity of β- adrenoceptors in the tissue which may increase at the level of the pulmonary arterioies. The eympathomimetics used acted principally on the of α-adrenoceptors to produce contraction of the preparation. &nbsp

The regulation of triglyceride mobilization by catecholamines was investigated in the teleost fish Oreochromis mossambicus (tilapia) in vivo and in vitro. In vitro experiments were carried out with adipocytes that were isolated for the first time from fish adipose tissue. For the in vivo experiments, cannulated tilapia were exposed to stepwise decreasing oxygen levels (20, 10, and 5% air saturation; 3.9, 1.9, and 1.0 kPa PO2, respectively), each level being maintained for 2 h. Blood samples were taken at timed intervals and analyzed for plasma lactate, glucose, free fatty acids, epinephrine, norepinephrine, and cortisol. Hypoxia exposure did not change plasma epinephrine levels. In contrast, the plasma norepinephrine concentration markedly increased at all hypoxia levels. Over the same period, plasma free fatty acid levels showed a significant continuous decrease, suggesting that norepinephrine is responsible for the reduced plasma free fatty acid concentration, presumably through inhibition of lipolysis in adipose tissue. To elucidate the mechanism, adipocytes were isolated from mesenteric adipose tissue of tilapia and incubated with 1) norepinephrine, 2) norepinephrine + phentolamine (alpha(1),alpha(2)-antagonist), 3) isoproterenol (nonselective beta-agonist), 4) isoproterenol + timolol (beta(1),beta(2)-antagonist), 5) norepinephrine + timolol, and 6) BRL-35135A (beta(3)-agonist). The results demonstrate for the first time that norepinephrine and isoproterenol suppress lipolysis in isolated adipocytes of tilapia. The effect of norepinephrine is not mediated through alpha(2)-adrenoceptors but, like isoproterenol, via beta-adrenoceptors. Furthermore, this study provides strong indications that beta(3)-adrenoceptors are involved.

Background eIF3f is a multifunctional protein capable of interacting with proteins involved in different cellular processes, such as protein synthesis, DNA repair, and viral mRNA edition. In human cells, eIF3f is related to cell cycle and proliferation, and its deregulation compromises cell viability. Results We here report that, in native conditions, eIF3f physically interacts with the alpha 1B-adrenergic receptor, a plasma membrane protein considered as a proto-oncogene, and involved in vasoconstriction and cell proliferation. The complex formed by eIF3f and alpha 1B-ADR was found in human and mouse cell lines. Upon catecholamine stimulation, eIF3f promotes adrenoceptor activity in vitro, independently of the eIF3f proline- and alanine-rich N-terminal region. Conclusions The eIF3f/alpha adrenergic receptor interaction opens new insights regarding adrenoceptor-related transduction pathways and proliferation control in human cells. The eIf3f/alpha 1B-ADR complex is found in mammals and is not tissue specific.