A comparison between the influence of pindolol and propranolol on the response of plasma potassium to catecholamines.
Jorge Castro-Tavares
Abstract
Jorge Castro-Tavares
Abstract
The influence of propranolol (0.3 and 1.0 mg/kg) and of D,L-4-(2-hydroxy-3-isopropylamino-propoxy)-indol-hydrochloride (pindolol, LB 46) (0.10, 0.25 and 0.50 mg/kg) on the responses of plasma potassium levels of anaesthetized dogs to slow i.v. infusions of adrenaline, noradrenaline and isoprenaline (5 mug/kg-min-1) was studied. Adrenaline and noradrenaline infusions regularly evoked a dual response (hyperkaliemia followed by hypokaliemia), whereas isoprenaline caused either similar effects or only a decrease of plasma potassium. Propranolol abolished the hypokaliemic phase of the responses to adrenaline, noradrenaline and isoprenaline; the lower dose used had no effect on the primary increase in plasma potassium, but the dose of 1.0 mg/kg modified this part of the response, which was reduced and became less steep. Pindolol antagonized in a dose dependent way the hypokaliemic phase of the responses to adrenaline, noradrenaline and isoprenaline, but did not interfere with the early rise in plasma potassium, thus being more specific than propranolol. It is concluded that the secondary decrease in plasma potassium is due to an activation of beta-receptors, whereas the initial increase is caused by alpha-receptor stimulation. Propranolol shows, in the 1.0 mg/kg dose, some alpha-blocking activity, thus contrasting with pindolol, which is devoid of this effect and therefore appears to be especially suitable for tentative characterization of adrenergic receptors.
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The influence of propranolol (0.3 and 1.0 mg/kg) and of D,L-4-(2-hydroxy-3-isopropylamino-propoxy)-indol-hydrochloride (pindolol, LB 46) (0.10, 0.25 and 0.50 mg/kg) on the responses of plasma potassium levels of anaesthetized dogs to slow i.v. infusions of adrenaline, noradrenaline and isoprenaline (5 mug/kg-min-1) was studied. Adrenaline and noradrenaline infusions regularly evoked a dual response (hyperkaliemia followed by hypokaliemia), whereas isoprenaline caused either similar effects or only a decrease of plasma potassium. Propranolol abolished the hypokaliemic phase of the responses to adrenaline, noradrenaline and isoprenaline; the lower dose used had no effect on the primary increase in plasma potassium, but the dose of 1.0 mg/kg modified this part of the response, which was reduced and became less steep. Pindolol antagonized in a dose dependent way the hypokaliemic phase of the responses to adrenaline, noradrenaline and isoprenaline, but did not interfere with the early rise in plasma potassium, thus being more specific than propranolol. It is concluded that the secondary decrease in plasma potassium is due to an activation of beta-receptors, whereas the initial increase is caused by alpha-receptor stimulation. Propranolol shows, in the 1.0 mg/kg dose, some alpha-blocking activity, thus contrasting with pindolol, which is devoid of this effect and therefore appears to be especially suitable for tentative characterization of adrenergic receptors.
Key concepts: Pindolol, Propranolol, Isoprenaline, Chemistry, Endocrinology, Internal medicine, Potassium, Stimulation