The role of skeletal muscle in the biphasic response of plasma potassium to epinephrine and norepinephrine

Castro-Tavares, J.; Garrett, J

doi:10.1016/0024-3205(73)90343-3

Cited by 2 publications

(2 citation statements)

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“…These conclusions are in accordance with those presented by Osswald (1958); this author proposed that a modification in the reactional characteristics of the trigger cells, induced by adrenergic antagonists, could be responsible for the vasomotor inversion observed during the administration of the same agonist. Noradrenergic stimulation in the liver (Castro-Tavares and Cardoso, 1974) and skeletal muscle cells (Castro-Tavares and Garrett, 1973) induces a transmem brane flux of potassium, the sense of which is dependent, as least in part, on the extracellular concentration of this ion. It may be concluded that the different alterations of the metabolic states of different effector cells during the infusion of adrenergic agonists and/or antagonists must be kept in mind in the analysis of the kalemotropic responses to adrenergic stimulation, and the interpretative difficulties discussed above may result from this fact.…”

Section: Discussionmentioning

confidence: 99%

“…in arterial plasma potassium, followed by a sustained decrease to values lower than controls, has been observed with adrenaline (D'Silva, 1934;Todd et al, 1968;Castro-Tavares, 1971b;Castro-Tavares and Garrett, 1973) and with nor adrenaline {Muirhead et al., 1954\ Castro-Tavares, 1971Todd and Vick, 1971). Isoprenaline is also able to evoke a similar dual response, but only in some of the dogs infused (Dresel and Nickerson, 1959;Mendez et al, 1964.Castro-Tavares, 1974.…”

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confidence: 89%

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

Jc¹

1975

Pharmacology

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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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Section: Discussionmentioning

confidence: 99%

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confidence: 89%

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

Jc¹

1975

Pharmacology

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Effect of propranolol on some adrenaline- and insulin-induced metabolic changes in man

1975

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The effect of propranolol on adrenaline- and insulin-induced changes in blood glucose pyruvate, lactate, phosphorus and potassium were examined in 29 apparently healthy volunteers. A slight, but significant reduction in adrenaline-induced hyperglycaemia was noted, along with suppression of both the increase in pyruvate and lactate and the decrease in phosphorus and potassium attributable to this catecholamine. There was no significant change in the blood glucose curve after insulin whereas insulin-induced increases in pyruvate and lactate were reduced by 44% +/- 17.7 (mean +/- SEM) and 78% +/- 5.4 respectively, and the fall in phosphorus by 48% +/- 3.1; the decrease in potassium, however, was not significantly modified. These findings suggest that changes in plasma pyruvate, lactate and inorganic phosphates induced by insulin, and regarded as espressions of its peripheral metabolism, are greatly dependent on the beta-adrenergic effect of the endogenous catecholamines released during the time when blood glucose values are low.

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The role of skeletal muscle in the biphasic response of plasma potassium to epinephrine and norepinephrine

Cited by 2 publications

References 6 publications

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

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

Effect of propranolol on some adrenaline- and insulin-induced metabolic changes in man

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