title: Influences of thyroid status and sympathoadrenal system on extrarenal potassium disposal.
abstract: Effects of hyper- and hypothyroidism on the ability of rats to transfer acute intravenous loads of potassium from the extracellular to the intracellular milieu (extrarenal potassium disposal, ERPD) were studied. We also examined the effects of the sympathoadrenal system on ERPD, as well as the manner in which it interacts with thyroid status. Experiments were performed in thyroidectomized (hypothyroid), sham-operated (euthyroid), or 3,5,3'-triiodo-L-thyronine-treated (thyrotoxic) rats. In anesthetized, acutely nephrectomized animals given a constant infusion of KCl over a 90-min period, ERPD was assessed as an inverse function of the increase in plasma potassium concentration. Some animals were subjected to chemical sympathectomy, adrenalectomy, the administration of adrenergic antagonists, or the infusion of adrenergic agonists. The effects of these treatments in various combinations on ERPD in animals of differing thyroid status were determined and the following conclusions could be drawn: 1) beta 2-adrenergic influences increase ERPD; 2) alpha 1- and alpha 2-adrenergic influences decrease ERPD; 3) these influences of the sympathoadrenal system on ERPD are qualitatively independent of thyroid status, and in all three thyroid states, beta-adrenergic enhancement predominates over alpha-adrenergic inhibition; 4) thyrotoxicosis increases and hypothyroidism decreases ERPD, and these effects are qualitatively independent of the presence of sympathoadrenal activity; 5) the intrinsic effect of thyroid hormone insufficiency and increased alpha-adrenergic tone and/or responsiveness together account for the decreased ERPD observed in hypothyroid animals; and 6) the intrinsic effect of thyroid hormone excess and increased beta-adrenergic tone and/or responsiveness, as well as decreased alpha-adrenergic tone and/or responsiveness, together account for the increased ERPD found in thyrotoxic animals.
authors.affiliation: Charles A. Dana Research Institute, Boston, Massachusetts.
authors.forename: K
authors.initials: K
authors.lastname: Kubota
authors.forename: S H
authors.initials: SH
authors.lastname: Ingbar
mesh_terms: D000311:Adrenal Glands / Q000502:physiology* / Q000503:physiopathology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D004837:Epinephrine / Q000494:pharmacology; D006980:Hyperthyroidism / Q000378:metabolism*; D007668:Kidney / Q000502:physiology / Q000503:physiopathology; D008297:Male; D010643:Phenoxybenzamine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011188:Potassium / Q000097:blood / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D013961:Thyroid Gland / Q000502:physiology*; D013965:Thyroidectomy; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D014284:Triiodothyronine; D010643:Phenoxybenzamine; D010656:Phenylephrine; D013974:Thyroxine; D011188:Potassium; D004837:Epinephrine; D010646:Phentolamine