Effects of Phentolamine on the Adrenergic-Induced Changes in Arterial Plasma Potassium

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Abstract
Phentolamine was used as a pure α-adrenergic blocking agent in the study of the arterial plasma potassium responses to adrenergic stimulation in dogs. Both the hyperkalemia and hypokalemia evoked by the intravenous infusion of noradrenaline, 5 μg/kg·min–1, were reduced by phentolamine (1–3 mg/kg), the response being completely abolished by increasing the dose of this α-blocker (9 mg/kg). The decrease of both parts of this dual response was parallel, and it was not possible to abolish the secondary hypokalemia without abolishing the early rise. The secondary decrease in arterial plasma potassium evoked by the intravenous infusion of the same dose of adrenaline was reduced, but not abolished, by the pretreatment with increasing doses of phentolamine, although the initial increase was completely abolished. These results agree with those that attribute an α-adrenergic nature to the adrenergic-evoked hyperkalemia, and a complex origin to the secondary hypokalemia. The different interpretations of the results obtained for these kalemotropic adrenergic effects are discussed, in the light of the Ahlquist hypothesis for adrenergic receptors. It is concluded that the alterations in the metabolic state of the effector cells observed during the administration of either adrenergic agonists or antagonists may influence the results obtained and may be considered as one of the factors responsible for interpretative difficulties described.

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