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The Effects of Adrenoceptor Agonists and Antagonists on Plasma Potassium Concentration in Anaesthetized Guinea-pigs, Rabbits and Rats

Overview
Journal Br J Pharmacol
Publisher Wiley
Specialty Pharmacology
Date 1985 Dec 1
PMID 4075019
Citations 6
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Abstract

An intravenous K+-sensitive electrode has been used to monitor plasma [K+] changes induced by alpha- and beta-adrenoceptor agonists in anaesthetized guinea-pigs, rabbits and rats. The effects of phentolamine and propranolol on these responses were studied. In the guinea-pig both alpha- and beta-adrenoceptor agonists produced a biphasic response consisting of an initial rapid increase in [K+] which was followed, within 1 min, by a fall below baseline. The antagonist studies indicated that in this species both phases of the response could be elicited by either alpha- or beta-adrenoceptor activation. In the rabbit the responses were both slower and smaller than those seen in the guinea-pig and required larger agonist doses. In addition it was found that the increase in plasma [K+] was alpha-adrenoceptor-mediated while the subsequent fall was seen only with beta-adrenoceptor activation. In the rat triphasic changes in plasma [K+] were seen consisting of an initial decrease which was alpha-adrenoceptor-mediated, followed by an increase and then a second fall which was elicited by beta-adrenoceptor stimulation. The increase in plasma [K+] was only slightly reduced by either alpha- or beta-adrenoceptor antagonists. Apamin, a toxin from bee venom which blocks Ca2+-activated K+-channels, was found to block the hyperkalaemic phase of the response in the guinea-pig and rabbit but had no effect in the rat. It is concluded that there are marked species differences in the effects of adrenoceptor agonists on plasma [K+] in vivo.

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References
1.
Craig Jr A . Observations on epinephrine and glucagon-induced glycogenolysis and potassium loss in the isolated perfused frog liver. Am J Physiol. 1958; 193(2):425-30. DOI: 10.1152/ajplegacy.1958.193.2.425. View

2.
Ellis S, BECKETT S . MECHANISM OF THE POTASSIUM MOBILIZING ACTION OF EPINEPHRINE AND GLUCAGON. J Pharmacol Exp Ther. 1963; 142:318-26. View

3.
Blackmore P, EXTON J . Evidence for two alpha-adrenergic binding sites in liver plasma membranes. Studies with [3H]epinephrine and [3H]dihydroergocryptine. J Biol Chem. 1979; 254(11):4375-86. View

4.
Haylett D, JENKINSON D . Effects of noradrenaline on potassium reflux, membrane potential and electrolyte levels in tissue slices prepared from guinea-pig liver. J Physiol. 1972; 225(3):721-50. PMC: 1331140. DOI: 10.1113/jphysiol.1972.sp009966. View

5.
BANKS B, Brown C, Burgess G, Burnstock G, Claret M, Cocks T . Apamin blocks certain neurotransmitter-induced increases in potassium permeability. Nature. 1979; 282(5737):415-7. DOI: 10.1038/282415a0. View