Metabolic responses to selective β-adrenergic stimulation in man

I The effects of intravenously administered propranolol 0.01 and 0.03, pindolol 0.001 and 0.003, practolol 0.12 and 0.36, atenolol 0.03 and 0.09, metoprolol 0.045 and 0.135 and acebutolol 0.12 and 0.36 mg/kg, on isoprenaline-induced changes in heart rate, blood pressure, plasma free fatty acids, immunoreactive insulin plasma levels and plasma renin activity were determined in six healthy human subjects. 2 Propranolol, atenolol and metoprolol had a stronger effect on resting heart rate than practolol, acebutolol and pindolol, probably reflecting differences in intrinsic f,-sympathomimetic activity.Antagonist potencies against isoprenaline-induced changes in heart rate and blood pressure suggested cardioselectivity for practolol, atenolol, metoprolol and the lower dose of acebutolol and noncardioselectivity for propranolol, pindolol and the higher dose of acebutolol. 3 All six f-adrenoceptor blocking agents were able, to a varying extent, to antagonize the isoprenaline-induced increases in plasma free fatty acids and plasma immunoreactive insulin levels. In general, the cardioselective agents were relatively less effective antagonists than the non-cardioselective agents.4 Resting plasma renin activity was reduced by all six fJ-adrenoceptor blocking agents, suggestive of the presence of fJ1-adrenoceptors mediating renin release, but the non-cardioselective agents propranolol and pindolol seemed relatively more effective in antagonizing isoprenaline-induced increases in plasma renin activity than the cardioselective agents, which indicates that 62-adrenoceptors might also be involved.5 The results are compatible with the hypothesis that both #,-and fJ2-adrenoceptors are involved in the regulation oflipolysis, insulin release and renin release.

Section: Plasma Renin Activitymentioning

confidence: 99%

Blockade of isoprenaline‐induced changes in plasma free fatty acids, immunoreactive insulin levels and plasma renin activity in healthy human subjects, by propranolol, pindolol, practolol, atenolol, metoprolol and acebutolol.

Harms¹,

Gooren²,

Spoelstra³

et al. 1978

“…Low doses of the P2-adrenoceptor selective agonist salbutamol were found to have an almost specific effect on plasma free fatty acids (Goldberg et al, 1975); nonselective antagonists, like propranolol and pindolol are more potent than cardioselective agents such as metoprolol in blocking catecholamineinduced increases in plasma free fatty acids, not only on a mg for mg basis, but also relative to their cardiac (pl) effects. The relatively weak antilipolytic effect of cardioselective 3-adrenoceptor blocking agents has been found in studies using either isoprenaline or adrenaline as the agonist and was also reported in a study using exercise induced sympathetic activation as the agonist (Harms et al, 1978;William-Olsson et al, 1979;Lundborg et al, 1981;Raptis et al, 1981).…”

Section: Studies In Manmentioning

confidence: 99%

Beta‐adrenoceptor blocking agents and lipolysis.

Harms¹,

Vente²,

Zaagsma³

1982

1 The pharmacological characteristics of I-adrenoceptor subtypes on adipocytes of various mammalian species, including man, are reviewed. 2 Rat adipocytes possess a homogeneous population of 0-adrenoceptors with properties that clearly distinguish them from 'classic' ,13-and P2-adrenoceptors, although they share certain features with both. Thus, rat adipocyte P-adrenoceptors should be considered as non-pl-non-P2 receptors, like the atypical 1-adrenoceptors found on erythrocytes of turkey, chicken and frog. 3 Preliminary data suggest that adipocyte P-adrenoceptors of guinea pig and swine are different from 'classic' pl-and P2-adrenoceptors as well, whereas in the dog and possibly in the cat, a mixture of Pl-and P2-receptors mediates catecholamine induced lipolysis.

“…Increased glycogenolysis in the liver and skeletal muscle results in hyperglycaemia and hyperlactataemia (Kuo, Kamaka & Lum, 1977). Increased lipolysis in adipose tissue shown by Goldberg, Van As, Joffe, Krut, Bersohn & Seftel (1975), increases plasma free fatty acid and ketone concentrations. Hyperglycaemia and direct stimulation of pancreatic 1 cells (Day, 1975) cause insulin release.…”

Section: Introductionmentioning

confidence: 99%

Metabolic and cardiovascular side effects of the beta 2‐adrenoceptor agonists salbutamol and rimiterol.

Phillips¹,

Vedig²,

Jones³

et al. 1980

The metabolic and cardiovascular side‐effects of intravenous infusions of therapeutic doses of beta 2‐adrenoceptor agonists salbutamol and rimiterol have been determined in four healthy male subjects. There were dose‐related increases in plasma glucose, renin activity, serum insulin and heart rate, and significant hyperlactataemia and ketonaemia. There were dose‐related decreases in plasma potassium, phosphate and corticosteroids and significant hypocalcaemia and hypomagnesaemia. The effects of equivalent molar amounts of salbutamol and rimiterol were similar. Whichever drug is used, special care is required with patients who may have abnormal glucose tolerance, potassium depletion, or be predisposed to lactic acidosis. Rimiterol may be preferable for infusion because of its short plasma half‐life.